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• W2169046108 abstract "HomeCirculation ResearchVol. 104, No. 5Intracellular Signaling of LOX-1 in Endothelial Cell Apoptosis Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBIntracellular Signaling of LOX-1 in Endothelial Cell Apoptosis Dayuan Li and Jawahar L. Mehta Dayuan LiDayuan Li From the Division of Cardiovascular Medicine (D.L.), University of Virginia, Charlottesville, Va; and the Division of Cardiovascular Medicine (J.L.M.), University of Arkansas for Medical Sciences and the Central Arkansas Veterans Healthcare System, Little Rock. Search for more papers by this author and Jawahar L. MehtaJawahar L. Mehta From the Division of Cardiovascular Medicine (D.L.), University of Virginia, Charlottesville, Va; and the Division of Cardiovascular Medicine (J.L.M.), University of Arkansas for Medical Sciences and the Central Arkansas Veterans Healthcare System, Little Rock. Search for more papers by this author Originally published13 Mar 2009https://doi.org/10.1161/CIRCRESAHA.109.194209Circulation Research. 2009;104:566–568Atherosclerosis in the coronary artery is a major culprit in unstable coronary syndromes and sudden cardiac death. Rupture of the cap covering the atherosclerotic plaque is thought to lead to platelet deposition and formation of an occlusive thrombus resulting in cessation of blood flow. Oxidatively modified LDL (ox-LDL) has been implicated in the pathogenesis of atherosclerosis and plaque rupture by promoting lipid accumulation, proinflammatory response, release of metalloproteinases, and apoptotic cell death.1,2 Ox-LDL leads to endothelial activation, characterized by expression of adhesion molecules, contributing to adherence and migration of inflammatory cells across the endothelial barrier. Endothelial activation is followed by endothelial dysfunction and injury characterized by loss of expression and activity of constitutive endothelial nitric oxide synthase and a state of oxidative stress. Ox-LDL, particularly in large concentrations, induces apoptosis in endothelial cells, macrophages, and smooth muscle cells.3–5Ox-LDL is taken up by monocytes/macrophages and smooth muscle cells through a variety of scavenger receptors (SRs), such as SR-AI/II, CD36, SR-BI, macrosialin/CD68, SREC, and LOX-1, and exerts its proatherogenic effects on the vessel wall.1,6,7 Several studies have demonstrated that SRs other than LOX-1 are absent or expressed in minimal amounts in endothelial cells.6–8 LOX-1 plays a crucial role in ox-LDL–induced pathological transformation of the vessel wall components. The importance of LOX-1 became evident in studies that showed significant limitation of atherosclerotic lesion formation in the LDL receptor knockout mice with LOX-1 deletion.9 In these studies, there was clear evidence of preservation of endothelial function and reduction in oxidative stress and inflammatory response.Regulation of LOX-1LOX-1 is a type II membrane protein ox-LDL receptor with a C-type lectin-like extracellular domain and a short cytoplasmic tail.7,10 LOX-1 is minimally expressed in endothelial cells, monocytes, platelets, and smooth muscle cells under physiological conditions but highly induced under pathological conditions, such as diabetes, hypertension, myocardial ischemia, and atherosclerosis.10 LOX-1 can be induced by ox-LDL, shear, stress, cytokines, free radicals, angiotensin II, and advanced glycation end products.10–14 It is interesting that ox-LDL can upregulate its own receptor at transcriptional level in human coronary artery endothelial cells in a time- and concentration-dependent fashion. The upregulation of LOX-1 in response to ox-LDL can be blocked by a specific antibody or antisense to LOX-1 mRNA. Lysophosphotidylcholine, which has been implicated in atherogenesis, also induces mRNA and protein expression of LOX-1.11 The cytokine tumor necrosis factor (TNF)-α, a proinflammatory cytokine increases cell-surface expression of LOX-1 in a concentration-dependent manner, with a peak time to expression of 8 to 12 hours.12 TNF-α also activates the transcription of LOX-1, as measured by nuclear run-off assay. Shear stress in the physiological range (1 to 15 dynes/cm2) has also been shown to upregulate LOX-1 in a time-dependent fashion.13 Chelation of intracellular Ca2+ reduces shear stress-induced LOX-1 expression, and the Ca2+ ionophore ionomycin enhances LOX-1 expression. The upregulation of LOX-1 in response to shear stress may be important in endothelial cell activation and injury. Furthermore, angiotensin II, a critical player in atherogenesis, also upregulates the expression of LOX-1.14 Interestingly, angiotensin II and ox-LDL synergistically interact to induce ox-LDL uptake and endothelial injury.In this issue of Circulation Research, Lu et al15 examined whether LOX-1 mediates endothelial cell uptake of L5, an electronegative component of LDL abundant in dyslipidemic but not in normolipidemic human plasma. In cultured bovine aortic endothelial cells, L5 upregulated the expression of LOX-1 and induced apoptosis. Transfection of bovine aortic endothelial cells with LOX-1–specific small interfering RNAs (siLOX-1) minimized baseline LOX-1 production and inhibited L5-induced LOX-1 upregulation. Internalization of labeled L1–L5 was monitored in endothelial cells by fluorescence microscopy. LOX-1 knockdown with siLOX-1 impeded the endocytosis of L5, but not the L1–L4, component. In contrast, blocking LDL receptor stopped the internalization of L1–L4, but not of L5 component. It is important to recognize that although L5 and ox-LDL are chemically different, they competed for endothelial cell entry through LOX-1.Signaling of LOX-1 ActionsOx-LDL induces expression of genes for cell injury through several intracellular signaling pathways. The lectin-like domain of LOX-1 seems to be essential for ligand binding.16 In particular, the large loop between the third and fourth cysteine of the lectin-like domain plays a crucial role for ox-LDL binding, as well as C-terminal end residues. Alanine-directed mutagenesis of the basic amino acid residues around this region revealed that all of the basic residues are involved in ox-LDL binding. Simultaneous mutations of these basic residues almost abolished the ox-LDL–binding activity of LOX-1. An electrostatic interaction between basic residues in the lectin-like domain of LOX-1 and negatively charged ox-LDL is critical for the binding activity of LOX-1.Our group17 reported that protein kinase C plays an important role in LOX-1 induced intracellular signaling. LOX-1 via downstream signaling pathway of protein kinase C mediates the expression of CD40 and CD40 ligand in endothelial cells in response to ox-LDL. Inhibition of protein kinase C prevents LOX-1–mediated the expression of CD40 and CD40 ligand.17 These findings indicate that ox-LDL through LOX-1 triggers CD40 signaling pathway that activates inflammatory response in endothelial cells. Other intracellular protein kinases, such as p42/44 mitogen-activated protein kinase (MAPK) play a critical signaling pathway in LOX-1–mediated gene expression.18 The activation of p42/44 MAPK also plays a critical role in ox-LDL–mediated expression of monocyte chemoattractant protein-1 and adhesion molecules that subsequently lead to enhanced monocyte adhesion to endothelial cells.Cominacini et al19 showed that it is the binding of ox-LDL to LOX-1 that initiates nuclear factor κB activation, as well as the increase in intracellular reactive oxygen species formation. These effects of ox-LDL were blocked by a monoclonal antibody to LOX-1. Direct evidence for ox-LDL–mediated intracellular reactive oxygen species formation in endothelial cells through activation of LOX-1 has also been demonstrated.20 As mentioned earlier, treatment of endothelial cells with ox-LDL results in the activation of p42/44 MAPK and nuclear factor κB and subsequent expression of several genes related to apoptosis.2,18Many studies have shown that LOX-1 mediates ox-LDL–induced apoptosis. Chen et al3 examined proapoptotic signaling in endothelial cells in response to ox-LDL. Ox-LDL decreased antiapoptotic proteins c-IAP-1 (inhibitory apoptotic protein-1) and Bcl-2 but did not significantly change FLIP (Fas-associated death domain-like interlukin-1-β–converting enzyme-inhibitory protein) and proapoptotic protein Fas. Furthermore, ox-LDL activated caspase-9 and caspase-3, which related to the degradation of c-IAP-1 and Bcl-2, and caspase-9 inhibitor blocked ox-LDL–induced activation of caspase-9 and -3 and apoptosis. In contrast, ox-LDL did not activate caspase-8 which related to induction of Fas and degradation of cFLIP, and caspase-8 inhibitor also did not inhibit ox-LDL–induced caspase-3 activity. Importantly, LOX-1 blockade with an antisense and caspase-9 inhibitor both inhibited ox-LDL–induced apoptosis of endothelial cells. These findings suggest that ox-LDL binding to LOX-1 subsequently decreases the expression of antiapoptotic proteins such as Bcl-2 and c-IAP-1 and then activates apoptotic signaling pathway caspase-9 and caspase-3 and finally results in apoptosis.In this issue of Circulation Research, Lu et al15 report that L5 via LOX-1 attenuated Akt phosphorylation and suppressed expression of Bcl-2. L5 also selectively inhibited Bcl-xL expression and endothelial nitric oxide synthase phosphorylation, but increased synthesis of Bax, Bad, and TNF-α. Blocking Akt phosphorylation increased LOX-1 expression, suggesting a modulatory role of Akt in LOX-1 synthesis. This finding provides new evidence that the L5 component of dyslipidemic plasma impairs Akt-mediated growth and survival signals via LOX-1. This study provides another link between L5, LOX-1, and endothelial cell apoptosis. This observation is consistent with previous finding21 that protein kinase B, the cellular homologue of v-Akt, is akey signaling component downstream of phosphatidylinositide-3 kinase. Activation of protein kinase B appears to be vitally important in the expression of endothelial nitric oxide synthase. These observations have obvious implications relative to an important role of LOX-1 in atherogenesis. The Figure incorporates results of many studies linking LOX-1, apoptosis, and atherosclerosis. Download figureDownload PowerPointFigure. Summary of many of the disease states and mediators leading to upregulation of LOX-1. The upregulation of LOX-1 induces endothelial apoptosis by a variety of pathways, which may be interrelated. Apoptosis and activation of redox-sensitive pathways are then associated with atherogenesis and destabilization of the atherosclerotic plaque.PerspectivesThe key pathological steps involved in the process of a stable atherosclerotic plaque changing into a ruptured plaque remain poorly understood. It is important to elucidate molecular, cellular, and signaling processes that modify plaque composition and lead to plaque destabilization. Identification of these key steps is of immense clinical significance. Understanding LOX-1 activation may also lead to the development of novel diagnostic techniques which will help in the detection of early changes in atherosclerotic plaque composition in vivo. Recent clinical studies have underscored the importance of multiple locations of vulnerable and ruptured atherosclerotic plaques and the diffuse inflammation of the arterial tree in patients with acute ischemic events.22 LOX-1 appears to be an excellent target to develop novel diagnostic strategy to assess atherosclerotic plaques, as well as therapeutic target to treat atherosclerosis-related disease states.The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.Sources of FundingSupported in part by funds from the Department of Veterans Affairs and the Arkansas Biosciences Institute.DisclosuresNone.FootnotesCorrespondence to J.L. Mehta, MD, PhD, Division of Cardiovascular Medicine, University of Arkansas for Medical Sciences, Little Rock, AR 72205. E-mail [email protected] References 1 Witztum JL, Steinberg D. Role of oxidized low density lipoprotein in atherogenesis. J Clin Invest. 1991; 88: 1785–1792.CrossrefMedlineGoogle Scholar2 Li D, Mehta JL. Antisense to LOX-1 inhibits oxidized LDL-mediated upregulation of monocyte chemoattractant protein-1 and monocyte adhesion to human coronary artery endothelial cells. Circulation. 2000; 101: 2889–2895.CrossrefMedlineGoogle Scholar3 Chen J, Mehta JL, Zhang X, Singh BK, Li D. Role of LOX-1 in expression of apoptotic proteins and activation of caspase pathways in human coronary artery endothelial cells. Circ Res. 2004; 94: 370–376.LinkGoogle Scholar4 Gerry AB, Leake DS. A moderate reduction in extracellular pH protects macrophages against apoptosis induced by oxidized low density lipoproteins. J Lipid Res. 2008; 49: 782–789.CrossrefMedlineGoogle Scholar5 Kashiwakura Y, Watanabe M, Kusumi N, Sumiyoshi K, Nasu Y, Yamada H, Sawamura T, Kumon H, Takei K, Daida H. Dynamin-2 regulates oxidized low-density lipoprotein-induced apoptosis of vascular smooth muscle cell. Circulation. 2004, 23;110: 3329–3334.Google Scholar6 Steinbrecher UP. Receptors for oxidized low density lipoprotein. Biochim Biophys Acta. 1999; 1436: 279–298.CrossrefMedlineGoogle Scholar7 Sawamura T, Kume N, Aoyama T, Moriwaki H, Hoshikawa H, Aiba Y, Tanaka T, Miwa S, Katsura Y, Kita T, Masaki T. An endothelial receptor for oxidized low-density lipoprotein. Nature. 1997; 386: 73–77.CrossrefMedlineGoogle Scholar8 Bickel PE, Freeman M. Rabbit aortic smooth muscle cells express inducible macrophage scavenger receptor messenger RNA that is absent from endothelial cells. J Clin Invest. 1992; 90: 1450–1457.CrossrefMedlineGoogle Scholar9 Mehta JL, Sanada N, Hu CP, Chen J, Dandapat A, Sugawara F, Takeya M, Inoue K, Kawase Y, Jishage K, Suzuki H, Satoh H, Schnackenberg L, Beger R, Hermonat PL, Thomas M, Sawamura T. Deletion of LOX-1 reduces atherogenesis in LDLR knockout mice fed high cholesterol diet. Circ Res. 2007; 100: 1634–1642.LinkGoogle Scholar10 Mehta JL, Chen J, Hermonat PL, Romeo F, Novelli G. Lectin-like, oxidized low-density lipoprotein receptor-1 (LOX-1): a critical player in the development of atherosclerosis and related disorders. Cardiovasc Res. 2006; 69: 36–45.CrossrefMedlineGoogle Scholar11 Aoyama T, Fujiwara H, Masaki T, Sawamura T. Induction of lectin-like oxidized LDL receptor by oxidized LDL and lysophosphatidylcholine in cultured endothelial cells. J Mol Cell Cardiol. 1999; 31: 2101–2114.CrossrefMedlineGoogle Scholar12 Kume N, Murase T, Moriwaki H, Aoyama T, Sawamura T, Masaki T, Kita T. Inducible expression of lectin-like oxidized LDL receptor-1 in vascular endothelial cells. Circ Res. 1998; 83: 322–327.CrossrefMedlineGoogle Scholar13 Murase T, Kume N, Korenaga R, Ando J, Sawamura T, Masaki T, Kita T. Fluid shear stress transcriptionally induces lectin-like oxidized LDL receptor-1 in vascular endothelial cells. Circ Res. 1998; 83: 328–333.CrossrefMedlineGoogle Scholar14 Morawietz H, Rueckschloss U, Niemann B, Duerrschmidt N, Galle J, Hakim K, Zerkowski HR, Sawamura T, Holtz J. Angiotensin II induces LOX-1, the human endothelial receptor for oxidized low-density lipoprotein. Circulation. 1999; 100: 899–902.CrossrefMedlineGoogle Scholar15 Lu J, Yang J-H, Burns AR, Chen H-H, Tang D, Walterscheid JP, Suzuki S, Yang C-Y, Sawamura T, Chen C-H. Mediation of electronegative low-density lipoprotein signaling by LOX-1. A possible mechanism of endothelial apoptosis. Circ Res. 2009; 104: 619–627.LinkGoogle Scholar16 Chen M, Inoue K, Narumiya S, Masaki T, Sawamura T. Requirements of basic amino acid residues within the lectin-like domain of LOX-1 for the binding of oxidized low-density lipoprotein. FEBS Lett. 2001; 499: 215–219.CrossrefMedlineGoogle Scholar17 Li D, Liu L, Chen H, Sawamura T, Mehta JL. LOX-1, an oxidized LDL endothelial receptor, induces CD40/CD40L signaling in human coronary artery endothelial cells. Arterioscler Thromb Vasc Biol. 2003; 23: 816–821.LinkGoogle Scholar18 Li L, Sawamura T, Renier G. Glucose enhances endothelial LOX-1 expression: role for LOX-1 in glucose-induced human monocyte adhesion to endothelium. Diabetes. 2003; 52: 1843–1850.CrossrefMedlineGoogle Scholar19 Cominacini L, Pasini AF, Garbin U, Garbin U, Davoli A, Campagnola M, Pastorino AM, Lo Cascio V, Sawamura T. Oxidized low density lipoprotein (ox-LDL) binding to ox-LDL receptor-1 in endothelial cells induces the activation of NF-κB through an increased production of intracellular reactive oxygen species. J Biol Chem. 2000; 275: 12633–12638.CrossrefMedlineGoogle Scholar20 Cominacini L, Rigoni A, Pasini AF, Garbin U, Davoli A, Campagnola M, Pastorino AM, Lo Cascio V, Sawamura T. The binding of oxidized low density lipoprotein (ox-LDL) to ox-LDL receptor-1 reduces the intracellular concentration of nitric oxide in endothelial cells through an increased production of superoxide. J Biol Chem. 2001; 276: 13750–13755.CrossrefMedlineGoogle Scholar21 Du XL, Edelstein D, Dimmeler S, Ju Q, Sui C, Brownlee M. Hyperglycemia inhibits endothelial nitric oxide synthase activity by posttranslational modification at the Akt site. J Clin Invest. 2001; 108: 1341–1348.CrossrefMedlineGoogle Scholar22 Diethrich EB, Pauliina Margolis M, Reid DB, Burke A, Ramaiah V, Rodriguez-Lopez JA, Wheatley G, Olsen D, Virmani R. Virtual histology intravascular ultrasound assessment of carotid artery disease: the Carotid Artery Plaque Virtual Histology Evaluation (CAPITAL) study. J Endovasc Ther. 2007; 14: 676–686.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Yang T, Minami M, Yoshida K, Nagata M, Yamamoto Y, Takayama N, Suzuki K, Miyata T, Okawa M and Miyamoto S (2021) Niclosamide downregulates LOX-1 expression in mouse vascular smooth muscle cells and changes the composition of atherosclerotic plaques in ApoE−/− mice, Heart and Vessels, 10.1007/s00380-021-01983-z, 37:3, (517-527), Online publication date: 1-Mar-2022. Akamatsu T, Sugiyama T, Oshima T, Aoki Y, Mizukami A, Goishi K, Shichino H, Kato N, Takahashi N, Goto Y, Oka A and Itoh M (2021) Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1–Related Microglial Activation in Neonatal Hypoxic-Ischemic Encephalopathy, The American Journal of Pathology, 10.1016/j.ajpath.2021.04.009, 191:7, (1303-1313), Online publication date: 1-Jul-2021. 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