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• W3115013227 abstract "HomeStrokeVol. 52, No. 1Response by Mechtouff and Nighoghossian to Letter Regarding Article “Matrix Metalloproteinase-9 and Monocyte Chemoattractant Protein-1 Are Associated With Collateral Status in Acute Ischemic Stroke With Large Vessel Occlusion” Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toFree AccessLetterPDF/EPUBResponse by Mechtouff and Nighoghossian to Letter Regarding Article “Matrix Metalloproteinase-9 and Monocyte Chemoattractant Protein-1 Are Associated With Collateral Status in Acute Ischemic Stroke With Large Vessel Occlusion” Laura Mechtouff, MD, PhD and Norbert Nighoghossian, MD, PhD Laura MechtouffLaura Mechtouff https://orcid.org/0000-0001-9165-5763 Stroke Department, Hospices Civils de Lyon, France (L.M., N.N.). INSERM U1060, CarMeN laboratory, University Lyon 1, France (L.M., N.N.). Search for more papers by this author and Norbert NighoghossianNorbert Nighoghossian https://orcid.org/0000-0003-0594-4409 Stroke Department, Hospices Civils de Lyon, France (L.M., N.N.). INSERM U1060, CarMeN laboratory, University Lyon 1, France (L.M., N.N.). Search for more papers by this author Originally published28 Dec 2020https://doi.org/10.1161/STROKEAHA.120.032518Stroke. 2021;52:e16In Response:We are grateful to Dr Della Schiava et al for their attention and their critical approach about our study. They stressed the link between angiogenesis, which corresponds to the formation of new capillary networks through sprouting of endothelial cells from preexisting vessels promoted by hypoxia, and MMP-9 (matrix metalloproteinase-9). Indeed, the HIF-1 (hypoxia inducible factor-1) is involved in upregulation of MMP-9.1 This pathway promotes neurogenesis in animal models. Therefore, they would have expected that our study reveals a positive relationship between MMP-9 level and good collateral status. However, these phenomena may occur likely during the stroke recovery. Experimental evidence argues that this process takes place 24 hours and 3 days from stroke onset for the proliferation of endothelial cells and the increase in the number of vessels, respectively.2 Accordingly, the added value of VEGF (vascular endothelial growth factor) assay may be relevant to assess angiogenesis process within this time window.In our study, early MMP-9 increase was likely related to reperfusion injury. Its proteolytic action on the extracellular matrix and the subsequent blood-brain barrier leakage and vasogenic edema may account for an increase in interstitial pressure that precipitates collateral failure.3 This latter may explain why low MMP-9 level at admission was associated with good collateral status.By contrast, MCP-1 (monocyte chemoattractant protein-1) level despite its contribution to ischemia-reperfusion injury was associated with good collateral status. This discrepancy may be explained by its early role in arteriogenesis, which refers to the proliferation of preexisting arteriolar connections into functional collateral arteries.4 Indeed, MCP-1 seems to be early expressed by activated endothelial cells in response to fluid shear stress, to recruit monocytes, a key step toward proliferation of vascular wall cells and remodeling processes.5 This hypothesis, arising from experimental cardiology, may be advanced here as an explanation of our results.Sources of FundingThis work was supported by the Recherche Hospitalo-Universitaire (RHU) MARVELOUS (Agence Nationale de la Recherche (ANR)-16-RHUS-0009) of Université de Lyon, within the program “Investissements d’Avenir” operated by the French National Research Agency and the Caisse d’Aide Sociale De l’Education Nationale (CASDEN) prize from CASDEN/Fondation de l’Avenir.DisclosuresProfessor Nighoghossian reports grants from French National Research agency during the conduct of the study; personal fees from Bohringer Ingelheim; and grants from French National research agency outside the submitted work.FootnotesFor Sources of Funding and Disclosures, see page e16.References1. Tsai SH, Huang PH, Hsu YJ, Peng YJ, Lee CH, Wang JC, Chen JW, Lin SJ. Inhibition of hypoxia inducible factor-1α attenuates abdominal aortic aneurysm progression through the down-regulation of matrix metalloproteinases.Sci Rep. 2016; 6:28612. doi: 10.1038/srep28612CrossrefMedlineGoogle Scholar2. Hayashi T, Noshita N, Sugawara T, Chan PH. Temporal profile of angiogenesis and expression of related genes in the brain after ischemia.J Cereb Blood Flow Metab. 2003; 23:166–180. doi: 10.1097/01.WCB.0000041283.53351.CBCrossrefMedlineGoogle Scholar3. Rocha M, Jovin TG. Fast versus slow progressors of infarct growth in large vessel occlusion stroke: clinical and research implications.Stroke. 2017; 48:2621–2627. doi: 10.1161/STROKEAHA.117.017673LinkGoogle Scholar4. Heil M, Schaper W. Influence of mechanical, cellular, and molecular factors on collateral artery growth (arteriogenesis).Circ Res. 2004; 95:449–458. doi: 10.1161/01.RES.0000141145.78900.44LinkGoogle Scholar5. Shyy YJ, Hsieh HJ, Usami S, Chien S. Fluid shear stress induces a biphasic response of human monocyte chemotactic protein 1 gene expression in vascular endothelium.Proc Natl Acad Sci U S A. 1994; 91:4678–4682. doi: 10.1073/pnas.91.11.4678CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetails January 2021Vol 52, Issue 1Article InformationMetrics © 2020 American Heart Association, Inc.https://doi.org/10.1161/STROKEAHA.120.032518PMID: 33370182 Originally publishedDecember 28, 2020 PDF download Advertisement SubjectsIschemic Stroke" @default.
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