FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2022242531> ?p ?o ?g. }

• W2022242531 endingPage "223" @default.
• W2022242531 startingPage "215" @default.
• W2022242531 abstract "The recent findings that adult stem cells are capable of generating new blood vessels and parenchymal cells within tissues they have colonized has raised immense optimism that these cells may provide functional recovery of damaged organs. The use of adult stem cells for regenerative therapy poses the challenging task of getting these cells into the requisite sites with minimum morbidity and maximum efficiency. Ideally, tissue-specific colonization could be achieved by introducing the stem cells intravascularly and exploiting the native physiologic processes governing cell trafficking. Critical to the success of this approach is the use of stem cells bearing appropriate membrane molecules that mediate homing from vascular to tissue compartments. Hematopoietic stem cells (HSC) express a novel glycoform of CD44 known as hematopoietic cell E-/L-selectin ligand (HCELL). This molecule is the most potent E-selectin ligand natively expressed on any human cell. This article reviews our current understanding of the molecular basis of HSC homing and will describe the fundamental “roll” of HCELL in opening the avenues for efficient HSC trafficking to the bone marrow, the skin and other extramedullary sites. The recent findings that adult stem cells are capable of generating new blood vessels and parenchymal cells within tissues they have colonized has raised immense optimism that these cells may provide functional recovery of damaged organs. The use of adult stem cells for regenerative therapy poses the challenging task of getting these cells into the requisite sites with minimum morbidity and maximum efficiency. Ideally, tissue-specific colonization could be achieved by introducing the stem cells intravascularly and exploiting the native physiologic processes governing cell trafficking. Critical to the success of this approach is the use of stem cells bearing appropriate membrane molecules that mediate homing from vascular to tissue compartments. Hematopoietic stem cells (HSC) express a novel glycoform of CD44 known as hematopoietic cell E-/L-selectin ligand (HCELL). This molecule is the most potent E-selectin ligand natively expressed on any human cell. This article reviews our current understanding of the molecular basis of HSC homing and will describe the fundamental “roll” of HCELL in opening the avenues for efficient HSC trafficking to the bone marrow, the skin and other extramedullary sites. cutaneous lymphocyte antigen hematopoietic cell E-/L-selectin ligand high endothelial venules Hematopoietic stem cells monoclonal antibodies P-selectin glycoprotein ligand-1 Substantial evidence has accumulated over the past several years that “adult” (i.e., postnatal) stem cells are capable of generating cells not only of their usual somatic lineage but also, depending on where they reside, that of diverse tissues/organs (Azizi et al., 1998Azizi S.A. Stokes D. Augelli B.J. DiGirolamo C. Prockop D.J. Engraftment and migration of human bone marrow stromal cells implanted in the brains of albino rats—similarities to astrocyte grafts.Proc Natl Acad Sci USA. 1998; 95: 3908-3913Crossref PubMed Scopus (774) Google Scholar;Orlic et al., 2001Orlic D. Kajstura J. Chimenti S. et al.Bone marrow cells regenerate infarcted myocardium.Nature. 2001; 410: 701-705Crossref PubMed Scopus (3860) Google Scholar;Hess et al., 2002Hess D.C. Hill W.D. Martin-Studdard A. Carroll J. Brailer J. Carothers J. Bone marrow as a source of endothelial cells and NeuN-expressing cells after stroke.Stroke. 2002; 33: 1362-1368Crossref PubMed Scopus (220) Google Scholar;Hofstetter et al., 2002Hofstetter C.P. Schwarz E.J. Hess D. Widenfalk J. El Manira A. Prockop D.J. Olson L. Marrow stromal cells form guiding strands in the injured spinal cord and promote recovery.Proc Natl Acad Sci USA. 2002; 99: 2199-2204Crossref PubMed Scopus (689) Google Scholar;Jin et al., 2002Jin H.K. Carter J.E. Huntley G.W. Schuchman E.H. Intracerebral transplantation of mesenchymal stem cells into acid sphingomyelinase-deficient mice delays the onset of neurological abnormalities and extends their life span.J Clin Invest. 2002; 109: 1183-1191Crossref PubMed Google Scholar;Toma et al., 2002Toma C. Pittenger M.F. Cahill K.S. Byrne B.J. Kessler P.D. Human mesenchymal stem cells differentiate to a cardiomyocyte phenotype in the adult murine heart.Circulation. 2002; 105: 93-98Crossref PubMed Scopus (1432) Google Scholar;Hess et al., 2003Hess D. Li L. Martin M. et al.Bone marrow-derived stem cells initiate pancreatic regeneration.Nat Biotechnol. 2003; 21: 763-770Crossref PubMed Scopus (435) Google Scholar). Although it is debated whether this effect is due to stem cell “plasticity” (the capacity to transdifferentiate across typical lineage commitments, even across derivative embryonic layers) or due to fusion and provoked proliferation of resident tissue-specific cells (Wulf et al., 2001Wulf G.G. Jackson K.A. Goodell M.A. Somatic stem cell plasticity: Current evidence and emerging concepts.Exp Hematol. 2001; 29: 1361-1370Abstract Full Text Full Text PDF PubMed Scopus (78) Google Scholar;Terada et al., 2002Terada N. Hamazaki T. Oka M. et al.Bone marrow cells adopt the phenotype of other cells by spontaneous cell fusion.Nature. 2002; 416: 542-545Crossref PubMed Scopus (1531) Google Scholar;Ianus et al., 2003Ianus A. Holz G.G. Theise N.D. Hussain M.A. In vivo derivation of glucose-competent pancreatic endocrine cells from bone marrow without evidence of cell fusion.J Clin Invest. 2003; 111: 843-850Crossref PubMed Scopus (576) Google Scholar;Vassilopoulos et al., 2003Vassilopoulos G. Wang P.R. Russell D.W. Transplanted bone marrow regenerates liver by cell fusion.Nature. 2003; 422: 901-904Crossref PubMed Scopus (965) Google Scholar), it is indisputable that remarkable new blood vessel and tissue growth can occur. Justifiably, these findings have engendered great hope that adult stem cells will prove useful in curing previously incurable illnesses affecting millions of people across all ages. The most plentiful source of adult stem cells in the body is the bone marrow. Two populations of stem cells are marrow residents: the hematopoietic stem cells (HSC) and the non-hematopoietic mesenchymal stem cells (MSCs). Both of these have broad developmental potential and display “plasticity” (Caplan and Dennis, 1996Caplan A.I. Dennis J.E. Mesenchymal stem cells: Progenitors, progeny, and pathways.J Bone Miner Metab. 1996; 14: 193-201Crossref Google Scholar;Wulf et al., 2001Wulf G.G. Jackson K.A. Goodell M.A. Somatic stem cell plasticity: Current evidence and emerging concepts.Exp Hematol. 2001; 29: 1361-1370Abstract Full Text Full Text PDF PubMed Scopus (78) Google Scholar;Jiang et al., 2002aJiang Y. Jahagirdar B.N. Reinhardt R.L. et al.Pluripotency of mesenchymal stem cells derived from adult marrow.Nature. 2002; 418: 41-49Crossref PubMed Scopus (3996) Google Scholar). MSCs are relatively rare in situ and must be expanded in culture to achieve sufficient numbers, whereas bone marrow natively contains large numbers of HSC. HSC can be obtained readily by direct extraction (harvesting) or by cytokine-stimulated mobilization of the cells into the circulation with subsequent collection by pheresis, and the techniques for collection and processing of highly enriched populations of HSC are clinically routine. Thus, ex vivo expansion of HSC is not required, and these cells are imminently available. A major issue still facing the clinical use of HSC for regenerative therapy, however, is how to achieve sufficient colonization of these cells within the relevant site(s) of tissue damage. Although the direct injection of HSC has already shown promise in recovery of blood supply and function in ischemic heart disease in rodent models (Orlic et al., 2001Orlic D. Kajstura J. Chimenti S. et al.Bone marrow cells regenerate infarcted myocardium.Nature. 2001; 410: 701-705Crossref PubMed Scopus (3860) Google Scholar) and in humans (Stamm et al., 2003Stamm C. Westphal B. Kleine H.D. et al.Autologous bone-marrow stem-cell transplantation for myocardial regeneration.Lancet. 2003; 361: 45-46Abstract Full Text Full Text PDF PubMed Scopus (1048) Google Scholar;Tse et al., 2003Tse H.F. Kwong Y.L. Chan J.K. Lo G. Ho C.L. Lau C.P. Angiogenesis in ischemic myocardium by intramyocardial autologous bone marrow mononuclear cell implantation.Lancet. 2003; 361: 11-12Abstract Full Text Full Text PDF PubMed Scopus (685) Google Scholar), this approach is hampered by the need to specifically map affected zones and to perform invasive procedure(s). Clearly, the cost(s) of these intervention(s) and risk(s) of procedure-related morbidity must always be considered. Moreover, in general, direct injection is only feasible for affected organs/tissues with distinct margins and anatomic localization. An alternative method to achieve tissue infiltration is to introduce HSC into the systemic circulation thereby relying on physiologic homing to deliver the cells to the relevant site(s). This approach has already shown promise in preclinical models of stroke and myocardial infarction (Chen et al., 2001Chen J. Li Y. Wang L. Zhang Z. Lu D. Lu M. Chopp M. Therapeutic benefit of intravenous administration of bone marrow stromal cells after cerebral ischemia in rats.Stroke. 2001; 32: 1005-1011Crossref PubMed Google Scholar;Wang et al., 2001Wang J.S. Shum-Tim D. Chedrawy E. Chiu R.C. The coronary delivery of marrow stromal cells for myocardial regeneration: Pathophysiologic and therapeutic implications.J Thorac Cardiovasc Surg. 2001; 122: 699-705Abstract Full Text Full Text PDF PubMed Scopus (232) Google Scholar). In particular, for regeneration of large tissue areas such as skin affected by burns or by autoimmune or congenital/genetic degenerative disease(s), the requisite colonization of stem cells could only be accomplished through a systemic approach. To migrate to tissue(s), all circulating cells must first be capable of adhering to vascular endothelium with sufficient strength to overcome the shear forces of blood flow in a process known as “rolling”. This primary adhesive interaction dictates the trafficking of blood-borne cells to any tissue. Accordingly, to attain successful tissue colonization of infused stem cells requires that this process be functionally intact and, preferably, optimized. This review will consider this issue, and will discuss the emerging evidence that a newly discovered E-selectin ligand, hematopoietic cell E-/L-selectin ligand (HCELL), may function as the principal “homing receptor” directing migration of HSC to the bone marrow, the skin and other extramedullary sites of tissue injury/inflammation. The term “homing receptor” is an historical, operational definition, first coined to describe the migration patterns of circulating lymphocytes (Gowans, 1957Gowans J.L. The effect of continuous reinfusion of lymph and lymphocytes on the output of lymphocytes from the thoracic duct of unanaesthetised rats.Br J Exp Pathol. 1957; 38: 67PubMed Google Scholar,Gowans, 1959Gowans J.L. The recirculation of small lymphocytes from blood to lymph in the rat.J Physiol. 1959; 146: 54Crossref PubMed Google Scholar;Gowans and Steer, 1980Gowans J.L. Steer H.W. The function and pathways of lymphocyte recirculation.Ciba Found Symp. 1980; 71: 113-126PubMed Google Scholar). Early studies in rodent and sheep models demonstrated that lymphocyte migration to lymphoid tissues was conspicuously non-random: lymphocytes isolated from intestinal lymph tended to migrate through gut-associated lymphoid tissues whereas lymphocytes isolated from peripheral lymph node tended to migrate to those sites (reviewed inChin et al., 1991Chin Y.H. Sackstein R. Cai J.P. Lymphocyte-homing receptors and preferential migration pathways.Proc Soc Exp Biol Med. 1991; 196: 374-380Crossref PubMed Google Scholar). Later it became clear that specificity in migration to different lymphoid compartments depended on the ability of circulating lymphocytes to bind to the specialized post-capillary venules of lymph nodes known as “high endothelial venules” (HEV). Monoclonal antibodies (mAb) were raised against lymphocyte membrane glycoproteins that mediated high affinity adhesion to lymphoid organ-specific HEV ligand(s), and these mAb blocked the migration of lymphocytes to peripheral lymph nodes and Peyer's patches (Gallatin et al., 1983Gallatin W.M. Weissman I.L. Butcher E.C. A cell-surface molecule involved in organ-specific homing of lymphocytes.Nature. 1983; 304: 30-34Crossref PubMed Google Scholar;Rasmussen et al., 1985Rasmussen R.A. Chin Y.H. Woodruff J.J. Easton T.G. Lymphocyte recognition of lymph node high endothelium. VII. Cell surface proteins involved in adhesion defined by monoclonal anti-HEBFLN (A.11) antibody.J Immunol. 1985; 135: 19-24PubMed Google Scholar;Chin et al., 1986Chin Y.H. Rasmussen R.A. Woodruff J.J. Easton T.G. A monoclonal anti-HEBFPP antibody with specificity for lymphocyte surface molecules mediating adhesion to Peyer's patch high endothelium of the rat.J Immunol. 1986; 136: 2556-2561PubMed Google Scholar;Woodruff et al., 1987Woodruff J.J. Clarke L.M. Chin Y.H. Specific cell-adhesion mechanisms determining migration pathways of recirculating lymphocytes.Annu Rev Immunol. 1987; 5: 201-222Crossref PubMed Google Scholar;Holzmann et al., 1989Holzmann B. McIntyre B.W. Weissman I.L. Identification of a murine Peyer's patch-specific lymphocyte homing receptor as an integrin molecule with an alpha chain homologous to human VLA-4 alpha.Cell. 1989; 56: 37-46Abstract Full Text PDF PubMed Scopus (239) Google Scholar). These functionally defined homing receptors were then characterized at a molecular level. The biochemical studies revealed that the principal peripheral lymph node homing receptor was a molecule of the selectin class of adhesion molecules named “L-selectin”, whereas the homing receptor for gut-associated lymphoid tissue was another structure of the integrin class called α4β7 (LPAM-1). Had it not been for the fact that L-selectin expression is not restricted to lymphocytes, our understanding of tissue-specific homing would have been complete two decades ago. But it was soon clear that all mature leukocytes and, in fact, primitive hematopoietic progenitor cells (but not intermediate differentiating myeloid or lymphoid cells), characteristically express L-selectin (Sackstein, 1993Sackstein R. Physiologic migration of lymphocytes to lymph nodes following bone marrow transplantation: Role in immune recovery.Semin Oncol. 1993; 20: 34-39PubMed Google Scholar). Importantly, in vitro adherence assays under shear conditions showed that L-selectin expressed on neutrophils was capable of directing the binding of these cells to HEV ligands (Lawrence et al., 1995Lawrence M.B. Berg E.L. Butcher E.C. Springer T.A. Rolling of lymphocytes and neutrophils on peripheral node addressin and subsequent arrest on ICAM-1 in shear flow.Eur J Immunol. 1995; 25: 1025-1031Crossref PubMed Google Scholar), yet these cells do not routinely migrate into lymph nodes. These findings raised doubts about the function of L-selectin as the lymph node homing receptor: How could a molecule serve as a homing receptor on one cell and not another? This puzzle was solved with the understanding that physiologic migration of blood-borne cells into tissues requires a cascade of multiple steps. Leukocytes typically exit the vasculature at post-capillary venules, where shear stress ranges from 1 to 4 dynes per cm2 (Jones et al., 1996Jones D.A. Smith C.W. McIntire L.V. Leucocyte adhesion under flow conditions: Principles important in tissue engineering.Biomaterials. 1996; 17: 337-347Crossref PubMed Scopus (45) Google Scholar). In this state of motion, leukocytes must first make contact along the endothelial surface with adhesive interactions of sufficient strength to overcome the shear forces of blood flow (initial tethering and rolling, Step 1; see Figure 1). During this initial stage, leukocytes are exposed to chemical signals (chemokines, cytokines, and other pro-inflammatory mediators) in the local milieu (Step 2), thereby leading to activation-dependent upregulation of integrin adhesive capabilities resulting in firm arrest (Step 3). Firm arrest is then followed by transmigration (Step 4) (see Figure 1). This “multi-step paradigm” (Butcher, 1991Butcher E.C. Leukocyte-endothelial cell recognition: Three (or more) steps to specificity and diversity.Cell. 1991; 67: 1033-1036Abstract Full Text PDF PubMed Google Scholar;Springer, 1994Springer T.A. Traffic signals for lymphocyte recirculation and leukocyte emigration: The multistep paradigm.Cell. 1994; 76: 301-314Abstract Full Text PDF PubMed Scopus (5540) Google Scholar) holds that cells capable of homing to any given tissue must possess the capacity to crawl along the endothelium with sufficient time to “taste” the local milieu and must possess the requisite receptors for the environmental chemoattractants such as chemokines, thus leading to activation-induced upregulation of the surface integrins mediating firm adherence. Chemokines are a superfamily of small proteins that function as potent chemotactic agents, some of which have a tissue- and inflammation-specific distribution, and others which are widely distributed (Campbell and Butcher, 2000Campbell J.J. Butcher E.C. Chemokines in tissue-specific and microenvironment-specific lymphocyte homing.Curr Opin Immunol. 2000; 12: 336-341Crossref PubMed Scopus (488) Google Scholar;Moser and Loetscher, 2001Moser B. Loetscher P. Lymphocyte traffic control by chemokines.Nat Immunol. 2001; 2: 123-128Crossref PubMed Scopus (832) Google Scholar;D'Ambrosio et al., 2003D'Ambrosio D. Panina-Bordignon P. Sinigaglia F. Chemokine receptors in inflammation: An overview.J Immunol Methods. 2003; 273: 3-13Crossref PubMed Scopus (114) Google Scholar). The activation signal(s) for firm adherence are typically mediated by G-protein-coupled chemokine receptors, which have a cell-specific distribution. For the case of lymphocyte homing to peripheral lymph nodes, HEV constitutively express the chemokine SLC (CCL21) that binds the lymphocyte receptor known as CCR7 (Gunn et al., 1998Gunn M.D. Tangemann K. Tam C. Cyster J.G. Rosen S.D. Williams L.T. A chemokine expressed in lymphoid high endothelial venules promotes the adhesion and chemotaxis of naive T lymphocytes.Proc Natl Acad Sci USA. 1998; 95: 258-263Crossref PubMed Scopus (718) Google Scholar;Tangemann et al., 1998Tangemann K. Gunn M.D. Giblin P. Rosen S.D. A high endothelial cell-derived chemokine induces rapid, efficient, and subset-selective arrest of rolling T lymphocytes on a reconstituted endothelial substrate.J Immunol. 1998; 161: 6330-6337PubMed Google Scholar;Willimann et al., 1998Willimann K. Legler D.F. Loetscher M. et al.The chemokine SLC is expressed in T cell areas of lymph nodes and mucosal lymphoid tissues and attracts activated T cells via CCR7.Eur J Immunol. 1998; 28: 2025-2034Crossref PubMed Scopus (208) Google Scholar). Neutrophils do not express CCR7, and, therefore, while able to undergo rolling interactions on HEV, they cannot convert these contacts into firm adherence (Warnock et al., 1998Warnock R.A. Askari S. Butcher E.C. von Andrian U.H. Molecular mechanisms of lymphocyte homing to peripheral lymph nodes.J Exp Med. 1998; 187: 205-216Crossref PubMed Scopus (335) Google Scholar). This example emphasizes the fact that the “address” directing cellular trafficking to relevant tissues is created by the combined expression of leukocyte and endothelial adhesion molecules and their respective chemokine receptors and chemokines. Although the appropriate display of chemokines and chemokine receptors is required for passage through the endothelium, no cellular emigration from the vascular compartment can occur without the initial (Step 1) molecular adhesive interactions that cause decelerative braking (“tethering”) of the flowing cells and organized sustained contact (“rolling”) of these cells against the endothelial surface. These critical contacts are created by leukocyte surface molecules possessing the requisite chemical characteristics to achieve fast on-off bond times with their respective endothelial co-receptors; in the setting of fluid shear forces and consequent cellular torque, this translates into a rolling interaction (Lawrence et al., 1997Lawrence M.B. Kansas G.S. Kunkel E.J. Ley K. Threshold levels of fluid shear promote leukocyte adhesion through selectins (CD62L,P,E).J Cell Biol. 1997; 136: 717-727Crossref PubMed Scopus (238) Google Scholar). Thus, Step 1 is the physiologic linchpin for all downstream events and is a key regulatory step in the composition of the infiltrate: only those cells in blood flow that are capable of participating in tethering and rolling interactions will become tissue residents. Indeed, all “homing receptors” are effectors of Step 1 interactions. Thus, despite the selectivity implied by the name, a broader view based on biophysics holds that a homing receptor is, principally, a molecule specialized to allow blood-borne cells to brake, contact and roll along the endothelium at velocities below the prevailing hydrodynamic flow. A number of well-characterized adhesion molecules serve as mediators of Step 1 rolling interactions: the three members of the selectin family (E-, P-, and L-selectin, also known as CD62E, CD62P, and CD62L, respectively), the “hyaluronate receptor” CD44, and a small subset of the integrin superfamily, principally VLA-4, α4β7, and LFA-1 (Berlin et al., 1993Berlin C. Berg E.L. Briskin M.J. et al.Alpha 4 beta 7 integrin mediates lymphocyte binding to the mucosal vascular addressin MAdCAM-1.Cell. 1993; 74: 185-195Abstract Full Text PDF PubMed Scopus (944) Google Scholar;Springer, 1994Springer T.A. Traffic signals for lymphocyte recirculation and leukocyte emigration: The multistep paradigm.Cell. 1994; 76: 301-314Abstract Full Text PDF PubMed Scopus (5540) Google Scholar;Alon et al., 1995Alon R. Kassner P.D. Carr M.W. Finger E.B. Hemler M.E. Springer T.A. The integrin VLA-4 supports tethering and rolling in flow on VCAM-1.J Cell Biol. 1995; 128: 1243-1253Crossref PubMed Scopus (515) Google Scholar;DeGrendele et al., 1996DeGrendele H.C. Estess P. Picker L.J. Siegelman M.H. CD44 and its ligand hyaluronate mediate rolling under physiologic flow: A novel lymphocyte-endothelial cell primary adhesion pathway.J Exp Med. 1996; 183: 1119-1130Crossref PubMed Scopus (310) Google Scholar;Knorr and Dustin, 1997Knorr R. Dustin M.L. The lymphocyte function-associated antigen 1 I domain is a transient binding module for intercellular adhesion molecule (ICAM)-1 and ICAM-3 in hydrodynamic flow.J Exp Med. 1997; 186: 719-730Crossref PubMed Scopus (59) Google Scholar;Lichtman et al., 1997Lichtman A.H. Ding H. Henault L. Vachino G. Camphausen R. Cumming D. Luscinskas F.W. CD45RA-RO+ (memory) but not CD45RA+RO- (naive) T cells roll efficiently on E- and P-selectin and vascular cell adhesion molecule-1 under flow.J Immunol. 1997; 158: 3640-3650PubMed Google Scholar;Sackstein, 1997Sackstein R. Expression of an L-selectin ligand on hematopoietic progenitor cells.Acta Haematol. 1997; 97: 22-28Crossref PubMed Google Scholar;de Chateau et al., 2001de Chateau M. Chen S. Salas A. Springer T.A. Kinetic and mechanical basis of rolling through an integrin and novel Ca2+-dependent rolling and Mg2+-dependent firm adhesion modalities for the alpha 4 beta 7-MAdCAM-1 interaction.Biochemistry. 2001; 40: 13972-13979Crossref PubMed Scopus (32) Google Scholar). The selectins are a family of integral membrane glycoproteins that function as Ca2+-dependent lectins in binding to carbohydrate determinants expressed on their respective ligands. E- and P-selectin are the “vascular” selectins, which are typically inducible molecules expressed on activated endothelium (and on platelets, for P-selectin), yet are also expressed constitutively on bone marrow and dermal microvasculature (Schweitzer et al., 1996Schweitzer K.M. Drager A.M. van der Valk P. et al.Constitutive expression of E-selectin and vascular cell adhesion molecule-1 on endothelial cells of hematopoietic tissues.Am J Pathol. 1996; 148: 165-175PubMed Google Scholar;Frenette et al., 1998Frenette P.S. Subbarao S. Mazo I.B. von Andrian U.H. Wagner D.D. Endothelial selectins and vascular cell adhesion molecule-1 promote hematopoietic progenitor homing to bone marrow.Proc Natl Acad Sci USA. 1998; 95: 14423-14428Crossref PubMed Scopus (247) Google Scholar;Weninger et al., 2000Weninger W. Ulfman L.H. Cheng G. Souchkova N. Quackenbush E.J. Lowe J.B. von Andrian U.H. Specialized contributions by alpha(1,3)-fucosyltransferase-IV and FucT-VII during leukocyte rolling in dermal microvessels.Immunity. 2000; 12: 665-676Abstract Full Text Full Text PDF PubMed Google Scholar). L-selectin is the “leukocyte” selectin and, as mentioned above, is expressed on granulocytes and monocytes, as well as on lymphocytes. The selectins are the most effective molecules in mediating leukocyte tethering and rolling interactions on endothelium in the hydrodynamic conditions of blood flow and are capable of maintaining rolling at higher fluid shear stresses than any other structures (Lawrence et al., 1997Lawrence M.B. Kansas G.S. Kunkel E.J. Ley K. Threshold levels of fluid shear promote leukocyte adhesion through selectins (CD62L,P,E).J Cell Biol. 1997; 136: 717-727Crossref PubMed Scopus (238) Google Scholar). Moreover, the selectins bear the unique property of binding optimally to their ligands under physiologic shear conditions, and, in fact, L-selectin–ligand interactions require a threshold shear level (Finger et al., 1996Finger E.B. Puri K.D. Alon R. Lawrence M.B. von Andrian U.H. Springer T.A. Adhesion through L-selectin requires a threshold hydrodynamic shear.Nature. 1996; 379: 266-269Crossref PubMed Google Scholar;Alon et al., 1997Alon R. Chen S. Puri K.D. Finger E.B. Springer T.A. The kinetics of l-selectin tethers and the mechanics of selectin-mediated rolling.J Cell Biol. 1997; 138: 1169-1180Crossref PubMed Scopus (256) Google Scholar;Lawrence et al., 1997Lawrence M.B. Kansas G.S. Kunkel E.J. Ley K. Threshold levels of fluid shear promote leukocyte adhesion through selectins (CD62L,P,E).J Cell Biol. 1997; 136: 717-727Crossref PubMed Scopus (238) Google Scholar). The selectin ligands comprise a diverse group of glycosylated molecules. Lymph node HEV express several glycoprotein L-selectin ligands and each of these is recognized by the mAb MECA79 (Streeter et al., 1988Streeter P.R. Rouse B.T. Butcher E.C. Immunohistologic and functional characterization of a vascular addressin involved in lymphocyte homing into peripheral lymph nodes.J Cell Biol. 1988; 107: 1853-1862Crossref PubMed Google Scholar). MECA 79 antigens (one of which is a specialized glycoform of CD34 with restricted endothelial distribution) are sulfated carbohydrates that are constitutively expressed on peripheral lymph node HEV, but can also be found at sites of inflammation including skin (Sackstein, 1993Sackstein R. Physiologic migration of lymphocytes to lymph nodes following bone marrow transplantation: Role in immune recovery.Semin Oncol. 1993; 20: 34-39PubMed Google Scholar;Lechleitner et al., 1999Lechleitner S. Kunstfeld R. Messeritsch-Fanta C. Wolff K. Petzelbauer P. Peripheral lymph node addressins are expressed on skin endothelial cells.J Invest Dermatol. 1999; 113: 410-444Abstract Full Text Full Text PDF PubMed Scopus (22) Google Scholar;Mikulowska-Mennis et al., 2001Mikulowska-Mennis A. Xu B. Berberian J.M. Michie S.A. Lymphocyte migration to inflamed lacrimal glands is mediated by vascular cell adhesion molecule-1/alpha(4)beta(1) integrin, peripheral node addressin/L-selectin, and lymphocyte function-associated antigen-1 adhesion pathways.Am J Pathol. 2001; 159: 671-681Abstract Full Text Full Text PDF PubMed Google Scholar;Renkonen et al., 2002Renkonen J. Tynninen O. Hayry P. Paavonen T. Renkonen R. Glycosylation might provide endothelial zip codes for organ-specific leukocyte traffic into inflammatory sites.Am J Pathol. 2002; 161: 543-550Abstract Full Text Full Text PDF PubMed Google Scholar). The principal leukocyte counter-receptor for the vascular selectins is the glycoprotein known as P-selectin glycoprotein ligand-1 (PSGL-1). PSGL-1 is a cell surface mucin-like glycoprotein which can serve as a ligand for all three selectins (Sako et al., 1993Sako D. Chang X.J. Barone K.M. et al.Expression cloning of a functional glycoprotein ligand for P-selectin.Cell. 1993; 75: 1179-1186Abstract Full Text PDF PubMed Scopus (537) Google Scholar;Asa et al., 1995Asa D. Raycroft L. Ma L. Aeed P.A. Kaytes P.S. Elhammer A.P. Geng J.G. The P-selectin glycoprotein ligand functions as a common human leukocyte ligand for P- and E-selectins.J Biol Chem. 1995; 270: 11662-11670Crossref PubMed Scopus (152) Google Scholar;Guyer et al., 1996Guyer D.A. Moore K.L. Lynam E.B. Schammel C.M. Rogelj S. McEver R.P. Sklar L.A. P-selectin glycoprotein ligand-1 (PSGL-1) is a ligand for L-selectin in neutrophil aggregation.Blood. 1996; 88: 2415-2421Crossref PubMed Google Scholar;Spertini et al., 1996Spertini O. Cordey A.S. Monai N. Giuffre L. Schapira M. P-selectin glycoprotein ligand 1 is a ligand for L-selectin on neutrophils, monocytes, and CD34+ hematopoietic progenitor cells.J Cell Biol. 1996; 135: 523-531Crossref PubMed Scopus (160) Google Scholar;Walcheck et al., 1996Walcheck B. Moore K.L. McEver R.P. Kishimoto T.K. Neutrophil–neutrophil interactions under hydrodynamic shear stress involve L-selectin and PSGL-1. A mechanism that amplifies initial leukocyte accumulation of P-selectin in vitro.J Clin Invest. 1996; 98: 1081-1087Crossref PubMed Google Scholar), however, specialized post-translational modifications on the core PSGL-1 protein backbone are necessary for ligand activity for each of the selectins. In particular, the binding determinants on PSGL-1 for both L- and P-selectin are" @default.
• W2022242531 created "2016-06-24" @default.
• W2022242531 creator A5064373888 @default.
• W2022242531 date "2004-09-01" @default.
• W2022242531 modified "2023-10-01" @default.
• W2022242531 title "The Bone Marrow Is Akin to Skin: HCELL and the Biology of Hematopoietic Stem Cell Homing11Reprinted from J Invest Dermatol 122:1061-1069, 2004" @default.
• W2022242531 cites W117181554 @default.
• W2022242531 cites W1484660189 @default.
• W2022242531 cites W1489241767 @default.
• W2022242531 cites W1494355500 @default.
• W2022242531 cites W1510568385 @default.
• W2022242531 cites W1510898037 @default.
• W2022242531 cites W1537022860 @default.
• W2022242531 cites W1537188001 @default.
• W2022242531 cites W1538469124 @default.
• W2022242531 cites W1542326554 @default.
• W2022242531 cites W1552224341 @default.
• W2022242531 cites W1573893253 @default.
• W2022242531 cites W1586392520 @default.
• W2022242531 cites W1631250427 @default.
• W2022242531 cites W1632181686 @default.
• W2022242531 cites W1646966930 @default.
• W2022242531 cites W1661591147 @default.
• W2022242531 cites W1926140429 @default.
• W2022242531 cites W1963528166 @default.
• W2022242531 cites W1964092383 @default.
• W2022242531 cites W1965147661 @default.
• W2022242531 cites W1965357348 @default.
• W2022242531 cites W1973278012 @default.
• W2022242531 cites W1973312218 @default.
• W2022242531 cites W1975475795 @default.
• W2022242531 cites W1982022033 @default.
• W2022242531 cites W1983264988 @default.
• W2022242531 cites W1991374176 @default.
• W2022242531 cites W1993902386 @default.
• W2022242531 cites W1997196395 @default.
• W2022242531 cites W1999023229 @default.
• W2022242531 cites W1999569383 @default.
• W2022242531 cites W2001523744 @default.
• W2022242531 cites W2004721490 @default.
• W2022242531 cites W2004872316 @default.
• W2022242531 cites W2004977670 @default.
• W2022242531 cites W2006499389 @default.
• W2022242531 cites W2006608487 @default.
• W2022242531 cites W2012275753 @default.
• W2022242531 cites W2015201031 @default.
• W2022242531 cites W2017372035 @default.
• W2022242531 cites W2020617877 @default.
• W2022242531 cites W2025019998 @default.
• W2022242531 cites W2032494769 @default.
• W2022242531 cites W2033430917 @default.
• W2022242531 cites W2035525109 @default.
• W2022242531 cites W2043842162 @default.
• W2022242531 cites W2047916715 @default.
• W2022242531 cites W2052276868 @default.
• W2022242531 cites W2052838075 @default.
• W2022242531 cites W2053542946 @default.
• W2022242531 cites W2054322335 @default.
• W2022242531 cites W2055543949 @default.
• W2022242531 cites W2057177567 @default.
• W2022242531 cites W2058844396 @default.
• W2022242531 cites W2059207468 @default.
• W2022242531 cites W2060602170 @default.
• W2022242531 cites W2061140050 @default.
• W2022242531 cites W2062290953 @default.
• W2022242531 cites W2072424205 @default.
• W2022242531 cites W2075344844 @default.
• W2022242531 cites W2076603801 @default.
• W2022242531 cites W2076675912 @default.
• W2022242531 cites W2077261345 @default.
• W2022242531 cites W2079101601 @default.
• W2022242531 cites W2081769332 @default.
• W2022242531 cites W2082317171 @default.
• W2022242531 cites W2084345254 @default.
• W2022242531 cites W2085875957 @default.
• W2022242531 cites W2091395040 @default.
• W2022242531 cites W2094273511 @default.
• W2022242531 cites W2095257528 @default.
• W2022242531 cites W2095703958 @default.
• W2022242531 cites W2098234683 @default.
• W2022242531 cites W2098509726 @default.
• W2022242531 cites W2099545837 @default.
• W2022242531 cites W2099675490 @default.
• W2022242531 cites W2102862146 @default.
• W2022242531 cites W2104050261 @default.
• W2022242531 cites W2107259575 @default.
• W2022242531 cites W2114342114 @default.
• W2022242531 cites W2114988174 @default.
• W2022242531 cites W2115286309 @default.
• W2022242531 cites W2116348485 @default.
• W2022242531 cites W2123563395 @default.
• W2022242531 cites W2123774138 @default.
• W2022242531 cites W2124537587 @default.
• W2022242531 cites W2126278579 @default.
• W2022242531 cites W2126680127 @default.
• W2022242531 cites W2126757120 @default.
• W2022242531 cites W2136813292 @default.
• W2022242531 cites W2141593635 @default.

• next