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• W2117715744 abstract "HomeCirculation ResearchVol. 97, No. 7A New Perspective on the Biology of C-Reactive Protein Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBA New Perspective on the Biology of C-Reactive Protein Edward T.H. Yeh Edward T.H. YehEdward T.H. Yeh From the Department of Cardiology, The University of Texas M.D. Anderson Cancer Center, Research Center for Cardiovascular Diseases at The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, The University of Texas Health Science Center at Houston, and Texas Heart Institute, St Luke’s Episcopal Hospital, Houston, Texas. Search for more papers by this author Originally published30 Sep 2005https://doi.org/10.1161/01.RES.0000186188.38344.13Circulation Research. 2005;97:609–611C-reactive protein (CRP), composed of 5 23-kDa subunits, was traditionally viewed as one of the acute phase reactants.1 More recently, CRP has risen in statue to subsume the role of the “best” marker of inflammation useful in the prediction of future cardiovascular risks.2 However, the clinical utility of CRP measurement in cardiovascular risk prediction is still not well defined. Furthermore, there is an intense debate on whether CRP is merely a marker of inflammation or a direct participant.1 The finding reported by Dr Janos Filep’s group in this issue of Circulation Research provides additional insights into the current CRP debate.3 In this editorial, I will focus my discussion on 2 main issues. Where is CRP produced? And, is CRP biologically active?Where Is CRP Produced?CRP was traditionally thought to be produced by the liver in response to inflammatory cytokines. Several recent studies, however, clearly showed that CRP can be produced by nonhepatic tissues. Two studies have shown that both epithelial cells of the respiratory tract and renal epithelium can produce CRP under certain circumstances.4,5 Moreover, neuronal cells also seem to be capable of synthesizing acute phase reactants involved in the pathogenesis of neurodegenerative disease such as Alzheimer disease.6 These new sources of CRP production pointed to a more systemic generation of CRP in our body. However, these new sources provided only tenuous link to atherosclerosis. CRP has been shown to colocalize with the terminal complement complex in atherosclerotic plaques.7 Furthermore, Yasojima et al reported that mRNAs for CRP and the classical complement components C1 to C9 could be detected in both normal artery and plaque tissue.8 We recently showed that human coronary artery smooth muscle cells, but not human umbilical vein endothelial cells, could synthesize CRP after stimulation by inflammatory cytokines.9 This locally produced CRP may directly participate in the pathogenesis of atherosclerosis. Moreover, we have also shown that human adipocytes could produce CRP after stimulation by inflammatory cytokines and by a specific adipokine, resistin.10 Production of CRP by adipocytes may partially explain why CRP levels are elevated in patients with metabolic syndrome (Figure). Download figureDownload PowerPointCRP is produced by the liver, adipocytes, and vascular smooth muscle cells. Native CRP exists as a pentamer, which could dissociate to form a monomeric CRP (mCRP). Native CRP binds to CD32, whereas mCRP binds to CD16. There are also other CRP binding proteins.Does CRP Have Biological Activities?In recent years, there has been a proliferation of reports demonstrating direct biological activity of CRP on vascular cells and monocytes/macrophages. For example, several laboratories reported CRP could directly activate endothelial cells to express adhesion molecules, chemokines, and cytokines.11 CRP was also shown to inhibit nitric oxide (NO) production and stimulation of NO release via downregulation of endothelial NO synthase. CRP unregulated angiotesin receptor-1 (AT1-R) protein expression, increased AT1-R number on vascular smooth muscle cells, and promoted vascular smooth muscle migration and proliferation in vitro. CRP functioned as a chemotattractant for monocytes and was able to induce tissue factor expression in macrophages. Furthermore, soluble CRP and immobilized CRP have been demonstrated to mediate uptake of native LDL into macrophages. Many of the studies cited above used recombinant CRP obtained from commercial sources that are contaminated by lipopolysaccharides (LPS) or by sodium azide. Thus, many of the reported biological effects could be due to either LPS or sodium azide contamination.12,13To avoid the potential artifact caused by LPS or sodium azide contamination, we have to turn to the results of in vivo animal models. Because mouse CRP is not an acute phase reactant, a model using expression of a human CRP-transgene has been employed. Two of these studies support the theory that CRP is proatherogenic and prothrombotic, but the other 3 studies reported negative results. First, human CRP created a prothrombotic phenotype as evidenced by higher rates of thrombotic occlusion after arterial injury.14 Second, by crossing CRP-tg mice with ApoE−/− mice, CRP increased atherogenesis in vivo.15 These CRP-tg/ApoE−/− mice displayed accelerated aortic atherosclerosis, which was associated with increased complement deposition and elevated expression of angiotensin type 1 receptor, vascular cell adhesion molecule-1, and collagen within the lesions.15 Crossing the human CRP transgenic mice with the apolipoprotein E*3-Leiden transgenic mice, however, failed to show a role of CRP to the development of early atherosclerosis lesions. The CRP level in the apolipoprotein E*3-Leiden mice is lower than those in the ApoE−/− mice.16 Another study crossing rabbit CRP transgenic mice into apoE knockout mice also did not augment atherogenesis at 20 weeks and at 52 weeks.17 Hirschfield et al also showed that transgenic expression of human CRP had no effect on development, progression, or severity of spontaneous atherosclerosis, or on morbidity or mortality, in male apolipoprotein E (ApoE)-deficient C57BL/6 mice up to 56 weeks, despite deposition of human CRP and mouse complement component 3 in the plaques.18 However, among human CRP transgenic mice, the circulating CRP concentration was higher in ApoE knockouts than in wild-type controls. The higher CRP values were associated with substantially lower estradiol concentrations in the apoE-deficient animals. Thus, the in vivo animal models also provide conflicting data regarding the role of CRP in atherogenesis.Another explanation of the conflicting results of CRP biology came from the observation made with modified CRP. Khreiss et al provided evidence suggesting that native pentameric CRP must undergo structural modification, forming monomeric subunits (mCRP), before being able to promote a proinflammatory response.19 They showed that mCRP was able to induce endothelial activation within 4 hours, whereas with native CRP could only exert a proinflammatory effect in 24 hours. This could be attributable to the conversion of native CRP to mCRP after 24 hour incubation. This in vitro observation, however, was contradicted by an in vivo animal experiment. Schwedler et al showed that native CRP increases whereas mCRP reduces atherosclerosis in the ApoE-deficient mice after 8 weeks of injection.20 VCAM, ICAM, and CD154 expression were higher in the native CRP-treated mice than in those treated with mCRP. On the other hand, mCRP-treated ApoE−/− mice exhibited higher serum level of the antiinflammatory cytokine interleukin-10. Thus, the studies using mCRP also provide contradictory results that are difficult to reconcile.Perhaps the best evidence to support a biological activity for CRP comes from studies on CRP receptors and CRP signaling. In this issue of Circulation Research, Kreiss et al showed that mCRP induced interleukin-8 secretion through peroxynitrite signaling in human neutrophils.3 These authors have previously shown that native CRP binds to CD32, one of the Fc receptors, whereas mCRP binds to CD16, another Fc receptor isoform, on human neutrophils and exerting opposite function. Conformational alterations of CRP could provide additional insights into its biological activity, but also raise additional questions. For example, we do not know how mCRP is generated in vivo. It was suggested that native CRP dissociated into monomeric unit after binding to plasma membrane or in denaturing or oxidative environment.3 Identification of suitable assays that allow for direct testing of mCRP versus native CRP in serum or tissue will further clarify the biological significance of mCRP.The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.This work was supported in part by the DREAM project sponsored by the U.S. Army.FootnotesCorrespondence to Dr Edward T.H. Yeh, Department of Cardiology, Unit 449, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd, Houston, TX 77030. E-mail [email protected] References 1 Pepys MB, Hirschfield GM. C-reactive protein: a critical update. J Clin Invest. 2003; 111: 1805–1812.CrossrefMedlineGoogle Scholar2 Yeh ET, Willerson JT. Coming of age of C-reactive protein: using inflammation markers in cardiology. Circulation. 2003; 107: 370–371.LinkGoogle Scholar3 Khreiss T, Jozsef L, Potempa LA, Filep JG. Loss of Pentameric Symmetry in C-reactive protein induces interleukin-8 secretion through peroxynitrite signaling in human neutrophils. Circ Res. 2005; 97: 690–697.LinkGoogle Scholar4 Gould JM, Weiser JN. Expression of C-reactive protein in the human respiratory tract. Infect Immun. 2001; 69: 1747–1754.CrossrefMedlineGoogle Scholar5 Jabs WJ, Logering BA, Gerke P, Kreft B, Wolber EM, Klinger MH, Fricke L, Steinhoff J. The kidney as a second site of human C-reactive protein formation in vivo. Eur J Immunol. 2003; 33: 152–161.CrossrefMedlineGoogle Scholar6 Yasojima K, Schwab C, McGeer EG, McGeer PL. Human neurons generate C-reactive protein and amyloid P: upregulation in Alzheimer’s disease. Brain Res. 2000; 887: 80–89.CrossrefMedlineGoogle Scholar7 Torzewski M, Rist C, Mortensen RF, Zwaka TP, Bienek M, Waltenberger J, Koenig W, Schmitz G, Hombach V, Torzewski J. C-reactive protein in the arterial intima: role of C-reactive protein receptor-dependent monocyte recruitment in atherogenesis. Arterioscler Thromb Vasc Biol. 2000; 20: 2094–2099.CrossrefMedlineGoogle Scholar8 Yasojima K, Schwab C, McGeer EG, McGeer PL. Generation of C-reactive protein and complement components in atherosclerotic plaques. Am J Pathol. 2001; 158: 1039–1051.CrossrefMedlineGoogle Scholar9 Calabro P, Willerson JT, Yeh ET. Inflammatory cytokines stimulated C-reactive protein production by human coronary artery smooth muscle cells. Circulation. 2003; 108: 1930–1932.LinkGoogle Scholar10 Calabro P, Chang D, Willerson JT, Yeh ET. Release of C-reactive protein in response to inflammatory cytokines by human adipocytes. J Am Coll Cardiol. 2005; 46: 1112–1113.CrossrefMedlineGoogle Scholar11 Verma S, Yeh ET. C-reactive protein and atherothrombosis-beyond a biomarker: an actual partaker of lesion formation. Am J Physiol Regul Integr Comp Physiol. 2003; 285: R1253–R1256;discussion R1257–R1258.CrossrefMedlineGoogle Scholar12 van den Berg CW, Taylor KE, Lang D. C-reactive protein-induced in vitro vasorelaxation is an artefact caused by the presence of sodium azide in commercial preparations. Arterioscler Thromb Vasc Biol. 2004; 24: e168–e171.LinkGoogle Scholar13 Taylor KE, Giddings JC, van den Berg CW. C-reactive protein-induced in vitro endothelial cell activation is an artefact caused by azide and lipopolysaccharide. Arterioscler Thromb Vasc Biol. 2005; 25: 1225–1230.LinkGoogle Scholar14 Danenberg HD, Szalai AJ, Swaminathan RV, Peng L, Chen Z, Seifert P, Fay WP, Simon DI, Edelman ER. Increased thrombosis after arterial injury in human C-reactive protein-transgenic mice. Circulation. 2003; 108: 512–515.LinkGoogle Scholar15 Paul A, Ko KW, Li L, Yechoor V, McCrory MA, Szalai AJ, Chan L. C-reactive protein accelerates the progression of atherosclerosis in apolipoprotein E-deficient mice. Circulation. 2004; 109: 647–655.LinkGoogle Scholar16 Trion A, de Maat MP, Jukema JW, van der Laarse A, Maas MC, Offerman EH, Havekes LM, Szalai AJ, Princen HM, Emeis JJ. No effect of C-reactive protein on early atherosclerosis development in apolipoprotein E*3-leiden/human C-reactive protein transgenic mice. Arterioscler Thromb Vasc Biol. 2005; 25: 1635–1640.LinkGoogle Scholar17 Reifenberg K, Lehr HA, Baskal D, Wiese E, Schaefer SC, Black S, Samols D, Torzewski M, Lackner KJ, Husmann M, Blettner M, Bhakdi S. Role of C-reactive protein in atherogenesis: can the apolipoprotein E knockout mouse provide the answer? Arterioscler Thromb Vasc Biol. 2005; 25: 1641–1646.LinkGoogle Scholar18 Hirschfield GM, Gallimore JR, Kahan MC, Hutchinson WL, Sabin CA, Benson GM, Dhillon AP, Tennent GA, Pepys MB. Transgenic human C-reactive protein is not proatherogenic in apolipoprotein E-deficient mice. Proc Natl Acad Sci U S A. 2005; 102: 8309–8314.CrossrefMedlineGoogle Scholar19 Khreiss T, Jozsef L, Potempa LA, Filep JG. Conformational rearrangement in C-reactive protein is required for proinflammatory actions on human endothelial cells. Circulation. 2004; 109: 2016–2022.LinkGoogle Scholar20 Schwedler SB, Amann K, Wernicke K, Krebs A, Nauck M, Wanner C, Potempa LA, Galle J. Native C-reactive protein increases whereas modified C-reactive protein reduces atherosclerosis in apolipoprotein E-knockout mice. Circulation. 2005; 112: 1016–1023.LinkGoogle Scholar eLetters(0)eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Comments are reviewed for appropriate use of tone and language. Comments are not peer-reviewed. Acceptable comments are posted to the journal website only. Comments are not published in an issue and are not indexed in PubMed. Comments should be no longer than 500 words and will only be posted online. References are limited to 10. Authors of the article cited in the comment will be invited to reply, as appropriate.Comments and feedback on AHA/ASA Scientific Statements and Guidelines should be directed to the AHA/ASA Manuscript Oversight Committee via its Correspondence page.Sign In to Submit a Response to This Article Previous Back to top Next FiguresReferencesRelatedDetailsCited By Wu K, Liang Q, Huang B, Ding N, Li B and Hao J (2020) The plasma level of mCRP is linked to cardiovascular disease in antineutrophil cytoplasmic antibody-associated vasculitis, Arthritis Research & Therapy, 10.1186/s13075-020-02321-w, 22:1, Online publication date: 1-Dec-2020. Mehta A and Jana D (2020) CARDIOVASCULAR RISK IN PATIENTS WITH SUBCLINICAL HYPOTHYROIDISM, INTERNATIONAL JOURNAL OF SCIENTIFIC RESEARCH, 10.36106/ijsr/5126352, (56-57), Online publication date: 1-Nov-2020. 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