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Cited by 192Cellular Mechanics and InteractionsProtease and Inhibitor MechanismsRenin-Angiotensin System Studies

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Extracellular matrix alterations in hypertensive vascular remodeling

Lemarié, Catherine A., Tharaux, Pierre-Louis, Lehoux, Stéphanie·2010·Journal of Molecular and Cellular Cardiology
DOI 10.1016/j.yjmcc.2009.09.018
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Abstract

Vascular cells are very sensitive to their hemodynamic environment. Any change in blood pressure or blood flow can be sensed by endothelial and vascular smooth muscle cells and ultimately results in structural modifications within the vascular wall that accommodate the new conditions. In the case of hypertension, the increase in arterial stretch stimulates vessel thickening to normalize the tensile forces. This process requires modification of the extracellular matrix and of cell-matrix interactions, which mainly involves extracellular proteases. In hypertension, chronic exposure of the arterial wall to stretch leads to vascular remodeling, arterial stiffness and calcification, which finally affect target organ function. This review surveys how mechanical stretch regulates extracellular proteases, considering the signaling pathways involved and the consequences on the cardiovascular system.

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  • Mechanical properties of the ECM, particularly stiffness, can mediate cell signaling and regulate physiological processes such as angiogenesis, organogenesis, immune response, and wound healing.

    “mechanical properties of the ECMs, particularly rigidity or stiffness, can mediate cell signal and regulate the physiological processes, such as angiogenesis, organogenesis, immune response, and wound healing [4,5].”

    From Substrate stiffness modulates bone marrow-derived macrophage polarization through NF-κB signaling pathway (2020) · cites this paper as [4]

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  1. Hu, 2008, Time courses of growth and remodeling of porcine aortic media during hypertension: a quantitative immunohistochemical examination, J. Histochem. Cytochem., 56, 359, 10.1369/jhc.7A7324.2007 · DOI
  2. O'Rourke, 2007, Arterial aging: pathophysiological principles, Vasc. Med., 12, 329, 10.1177/1358863X07083392 · DOI
  3. Baker, 2002, Metalloproteinase inhibitors: biological actions and therapeutic opportunities, J. Cell. Sci., 115, 3719, 10.1242/jcs.00063 · DOI
  4. Brew, 2000, Tissue inhibitors of metalloproteinases: evolution, structure and function, Biochim. Biophys. Acta, 1477, 267, 10.1016/S0167-4838(99)00279-4 · DOI
  5. Dollery, 1995, Matrix metalloproteinases and cardiovascular disease, Circ. Res., 77, 863, 10.1161/01.RES.77.5.863 · DOI
  6. Galis, 2002, Matrix metalloproteinases in vascular remodeling and atherogenesis: the good, the bad, and the ugly, Circ. Res., 90, 251, 10.1161/res.90.3.251 · DOI
  7. Newby, 2005, Dual role of matrix metalloproteinases (matrixins) in intimal thickening and atherosclerotic plaque rupture, Physiol. Rev., 85, 1, 10.1152/physrev.00048.2003 · DOI · Paper page
  8. Zempo, 1996, Regulation of vascular smooth muscle cell migration and proliferation in vitro and in injured rat arteries by a synthetic matrix metalloproteinase inhibitor, Arterioscler. Thromb. Vasc. Biol., 16, 28, 10.1161/01.ATV.16.1.28 · DOI
  9. Cho, 2002, Matrix metalloproteinase-9 is necessary for the regulation of smooth muscle cell replication and migration after arterial injury, Circ. Res., 91, 845, 10.1161/01.RES.0000040420.17366.2E · DOI
  10. Thyberg, 1997, Phenotypic modulation of smooth muscle cells after arterial injury is associated with changes in the distribution of laminin and fibronectin, J. Histochem. Cytochem., 45, 837, 10.1177/002215549704500608 · DOI
  11. Lehoux, 2004, Pressure-induced matrix metalloproteinase-9 contributes to early hypertensive remodeling, Circulation, 109, 1041, 10.1161/01.CIR.0000115521.95662.7A · DOI
  12. Jackson, 2002, Wall tissue remodeling regulates longitudinal tension in arteries, Circ. Res., 90, 918, 10.1161/01.RES.0000016481.87703.CC · DOI
  13. Flamant, 2007, Role of matrix metalloproteinases in early hypertensive vascular remodeling, Hypertension, 50, 212, 10.1161/HYPERTENSIONAHA.107.089631 · DOI
  14. Watts, 2007, Morphological and biochemical characterization of remodeling in aorta and vena cava of DOCA-salt hypertensive rats, Am. J. Physiol. Heart Circ. Physiol., 292, H2438, 10.1152/ajpheart.00900.2006 · DOI
  15. Derosa, 2006, Matrix metalloproteinase-2, -9, and tissue inhibitor of metalloproteinase-1 in patients with hypertension, Endothelium, 13, 227, 10.1080/10623320600780942 · DOI
  16. Zervoudaki, 2003, Plasma levels of active extracellular matrix metalloproteinases 2 and 9 in patients with essential hypertension before and after antihypertensive treatment, J. Hum. Hypertens., 17, 119, 10.1038/sj.jhh.1001518 · DOI
  17. Laviades, 1998, Abnormalities of the extracellular degradation of collagen type I in essential hypertension, Circulation, 98, 535, 10.1161/01.CIR.98.6.535 · DOI
  18. Seals, 2003, The ADAMs family of metalloproteases: multidomain proteins with multiple functions, Genes Dev., 17, 7, 10.1101/gad.1039703 · DOI
  19. Lautrette, 2005, Angiotensin II and EGF receptor cross-talk in chronic kidney diseases: a new therapeutic approach, Nat. Med., 11, 867, 10.1038/nm1275 · DOI
  20. Lemarie, 2006, Transforming growth factor-alpha mediates nuclear factor kappaB activation in strained arteries, Circ. Res., 99, 434, 10.1161/01.RES.0000237388.89261.47 · DOI
  21. Lijnen, 1999, Temporal and topographic matrix metalloproteinase expression after vascular injury in mice, Thromb. Haemost., 81, 799, 10.1055/s-0037-1614573 · DOI
  22. Kaikita, 2002, Potential roles of plasminogen activator system in coronary vascular remodeling induced by long-term nitric oxide synthase inhibition, J. Mol. Cell. Cardiol., 34, 617, 10.1006/jmcc.2002.2001 · DOI
  23. Furumoto, 2004, Maladaptive arterial remodeling with systemic hypertension associated with increased concentrations in blood of plasminogen activator inhibitor type-1 (PAI-1), Am. J. Cardiol., 93, 997, 10.1016/j.amjcard.2003.12.053 · DOI
  24. Lutgens, 2007, Cathepsin cysteine proteases in cardiovascular disease, Faseb J., 21, 3029, 10.1096/fj.06-7924com · DOI
  25. Fukuda, 1999, Contribution of synthetic phenotype on the enhanced angiotensin II-generating system in vascular smooth muscle cells from spontaneously hypertensive rats, J. Hypertens., 17, 1099, 10.1097/00004872-199917080-00009 · DOI
  26. Galewska, 2005, Preeclampsia-associated reduction of cathepsin D activity in the umbilical cord, Clin. Chim. Acta, 351, 177, 10.1016/j.cccn.2004.09.007 · DOI
  27. Platt, 2007, Expression of cathepsin K is regulated by shear stress in cultured endothelial cells and is increased in endothelium in human atherosclerosis, Am. J. Physiol. Heart Circ. Physiol., 292, H1479, 10.1152/ajpheart.00954.2006 · DOI
  28. Aikawa, 2009, Arterial and aortic valve calcification abolished by elastolytic cathepsin S deficiency in chronic renal disease, Circulation, 119, 1785, 10.1161/CIRCULATIONAHA.108.827972 · DOI
  29. Lehoux, 1998, Signal transduction of mechanical stresses in the vascular wall, Hypertension, 32, 338, 10.1161/01.HYP.32.2.338 · DOI
  30. Kyriakis, 2001, Mammalian mitogen-activated protein kinase signal transduction pathways activated by stress and inflammation, Physiol. Rev., 81, 807, 10.1152/physrev.2001.81.2.807 · DOI
  31. Reusch, 1997, Activation of JNK/SAPK and ERK by mechanical strain in vascular smooth muscle cells depends on extracellular matrix composition., Biochem. Biophys. Res. Commun., 237, 239, 10.1006/bbrc.1997.7121 · DOI
  32. Xu, 1996, Acute hypertension activates mitogen-activated protein kinases in arterial wall, J. Clin. Invest., 97, 508, 10.1172/JCI118442 · DOI
  33. Birukov, 1997, Increased pressure induces sustained PKC-independent herbimycin A-sensitive activation of extracellular signal-regulated kinase 1/2 in the rabbit aorta in organ culture, Circ. Res., 81, 895, 10.1161/01.RES.81.6.895 · DOI
  34. Schlaepfer, 1997, Focal adhesion kinase overexpression enhances Ras-dependent integrin signaling to ERK2/mitogen-activated protein kinase through interactions with and activation of c-Src, J. Biol. Chem., 272, 13189, 10.1074/jbc.272.20.13189 · DOI
  35. Lehoux, 2005, Differential regulation of vascular focal adhesion kinase by steady stretch and pulsatility, Circulation, 111, 643, 10.1161/01.CIR.0000154548.16191.2F · DOI
  36. Lehoux, 2000, Pulsatile stretch-induced extracellular signal-regulated kinase 1/2 activation in organ culture of rabbit aorta involves reactive oxygen species, Arterioscler. Thromb. Vasc. Biol., 20, 2366, 10.1161/01.ATV.20.11.2366 · DOI
  37. Lemarie, 2003, Pressure-induced vascular activation of nuclear factor-kappaB: role in cell survival, Circ. Res., 93, 207, 10.1161/01.RES.0000086942.13523.88 · DOI
  38. Wang, 2004, The upregulation of ICAM-1 and P-selectin requires high blood pressure but not circulating renin-angiotensin system in vivo, J. Hypertens., 22, 1323, 10.1097/01.hjh.0000125437.28861.40 · DOI
  39. Tschumperlin, 2004, Mechanotransduction through growth-factor shedding into the extracellular space, Nature, 429, 83, 10.1038/nature02543 · DOI
  40. Shiraya, 2006, Hypertension accelerated experimental abdominal aortic aneurysm through upregulation of nuclear factor kappaB and Ets, Hypertension, 48, 628, 10.1161/01.HYP.0000240266.26185.57 · DOI
  41. Meiners, 2004, Downregulation of matrix metalloproteinases and collagens and suppression of cardiac fibrosis by inhibition of the proteasome, Hypertension, 44, 471, 10.1161/01.HYP.0000142772.71367.65 · DOI
  42. Milkiewicz, 2007, Static strain stimulates expression of matrix metalloproteinase-2 and VEGF in microvascular endothelium via JNK- and ERK-dependent pathways, J. Cell. Biochem., 100, 750, 10.1002/jcb.21055 · DOI
  43. Castier, 2009, Role of NFkappaB in flow-induced vascular remodeling, Antioxid. Redox Signal., 11, 1641, 10.1089/ars.2008.2393 · DOI
  44. Wilkinson, 2004, Arterial stiffness, endothelial function and novel pharmacological approaches, Clin. Exp. Pharmacol. Physiol., 31, 795, 10.1111/j.1440-1681.2004.04074.x · DOI
  45. Lee, 2008, Vascular compliance in hypertension: therapeutic implications, Curr. Diabetes Rep., 8, 208, 10.1007/s11892-008-0036-8 · DOI
  46. Faury, 2003, Developmental adaptation of the mouse cardiovascular system to elastin haploinsufficiency, J. Clin. Invest., 112, 1419, 10.1172/JCI19028 · DOI
  47. Lakatta, 2003, Arterial and cardiac aging: major shareholders in cardiovascular disease enterprises. Part III: cellular and molecular clues to heart and arterial aging, Circulation, 107, 490, 10.1161/01.CIR.0000048894.99865.02 · DOI
  48. Zieman, 2005, Mechanisms, pathophysiology, and therapy of arterial stiffness, Arterioscler. Thromb. Vasc. Biol., 25, 932, 10.1161/01.ATV.0000160548.78317.29 · DOI · Paper page
  49. Long, 2003, Elastic fiber production in cardiovascular tissue-equivalents, Matrix Biol., 22, 339, 10.1016/S0945-053X(03)00052-0 · DOI
  50. Marque, 2001, Determination of aortic elastic modulus by pulse wave velocity and wall tracking in a rat model of aortic stiffness, J. Vasc. Res., 38, 546, 10.1159/000051090 · DOI
  51. Lorand, 2003, Transglutaminases: crosslinking enzymes with pleiotropic functions, Nat. Rev. Mol. Cell Biol., 4, 140, 10.1038/nrm1014 · DOI
  52. Haydar, 2004, Coronary artery calcification and aortic pulse wave velocity in chronic kidney disease patients, Kidney Int., 65, 1790, 10.1111/j.1523-1755.2004.00581.x · DOI
  53. Mourad, 2001, Conventional antihypertensive drug therapy does not prevent the increase of pulse pressure with age, Hypertension, 38, 958, 10.1161/hy1001.096362 · DOI
  54. Hruska, 2005, Bone morphogenetic proteins in vascular calcification, Circ. Res., 97, 105, 10.1161/01.RES.00000175571.53833.6c · DOI
  55. Demer, 1995, A skeleton in the atherosclerosis closet, Circulation, 92, 2029, 10.1161/01.CIR.92.8.2029 · DOI
  56. Csiszar, 2005, Regulation of bone morphogenetic protein-2 expression in endothelial cells: role of nuclear factor-kappaB activation by tumor necrosis factor-alpha, H2O2, and high intravascular pressure, Circulation, 111, 2364, 10.1161/01.CIR.0000164201.40634.1D · DOI
  57. Ungvari, 2004, Chronic high pressure-induced arterial oxidative stress: involvement of protein kinase C-dependent NAD(P)H oxidase and local renin-angiotensin system, Am. J. Pathol., 165, 219, 10.1016/S0002-9440(10)63290-7 · DOI
  58. Speer, 2002, Inactivation of the osteopontin gene enhances vascular calcification of matrix Gla protein-deficient mice: evidence for osteopontin as an inducible inhibitor of vascular calcification in vivo, J. Exp. Med., 196, 1047, 10.1084/jem.20020911 · DOI
  59. Bucay, 1998, Osteoprotegerin-deficient mice develop early onset osteoporosis and arterial calcification, Genes Dev., 12, 1260, 10.1101/gad.12.9.1260 · DOI · Paper page
  60. Johnson, 2008, Transglutaminase 2 is central to induction of the arterial calcification program by smooth muscle cells, Circ. Res., 102, 529, 10.1161/CIRCRESAHA.107.154260 · DOI
  61. Stork, 2004, Carotid artery plaque burden, stiffness, and mortality risk in elderly men: a prospective, population-based cohort study, Circulation, 110, 344, 10.1161/01.CIR.0000134966.10793.C9 · DOI
  62. Sutton-Tyrrell, 2005, Elevated aortic pulse wave velocity, a marker of arterial stiffness, predicts cardiovascular events in well-functioning older adults, Circulation, 111, 3384, 10.1161/CIRCULATIONAHA.104.483628 · DOI
  63. London, 1997, Large arteries haemodynamics: conduit versus cushioning function, Blood Press. Suppl., 2, 48
  64. Westerhof, 1995, Haemodynamic basis for the development of left ventricular failure in systolic hypertension and for its logical therapy, J. Hypertens., 13, 943, 10.1097/00004872-199509000-00002 · DOI
  65. Berk, 2007, ECM remodeling in hypertensive heart disease, J. Clin. Invest., 117, 568, 10.1172/JCI31044 · DOI
  66. Mourad, 2001, Creatinine clearance, pulse wave velocity, carotid compliance and essential hypertension, Kidney Int., 59, 1834, 10.1046/j.1523-1755.2001.0590051834.x · DOI
  67. Schillaci, 2006, Relation between renal function within the normal range and central and peripheral arterial stiffness in hypertension, Hypertension, 48, 616, 10.1161/01.HYP.0000240346.42873.f6 · DOI
  68. Hanon, 2005, Relationship between arterial stiffness and cognitive function in elderly subjects with complaints of memory loss, Stroke, 36, 2193, 10.1161/01.STR.0000181771.82518.1c · DOI · Paper page
  69. Matsumoto, 2007, Associations of brachial-ankle pulse wave velocity and carotid atherosclerotic lesions with silent cerebral lesions, Hypertens. Res., 30, 767, 10.1291/hypres.30.767 · DOI
  70. Levy, 2001, Microcirculation in hypertension: a new target for treatment?, Circulation, 104, 735, 10.1161/hc3101.091158 · DOI

Metadata

Authors
Lemarié, C. A., Tharaux, P.-L., & Lehoux, S.
Affiliations
  • Lady Davis Institute for Medical Research (CA)
  • Inserm (FR)
Corresponding author
Lehoux, Stéphanie
ORCID
Venue
Journal of Molecular and Cellular Cardiology
Publisher
Elsevier BV
Published
2010-03
Volume
48
Issue
3
Pages
433-439
ISSN
0022-2828 (ISSN-L)
DOI
10.1016/j.yjmcc.2009.09.018
OpenAlex
W2115236695
Cited by
192
References
73
Citations by year
2026: 8 · 2025: 5 · 2024: 14 · 2023: 12 · 2022: 5 · 2021: 6 · 2020: 12 · 2019: 12 · 2018: 17 · 2017: 14 · 2016: 14 · 2015: 17 · 2014: 11 · 2013: 17 · 2012: 12
FWCI
0.68
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Journal of Molecular and Cellular Cardiology (publishedVersion)
  • PubMed (publishedVersion)
Funders
Canadian Institutes of Health Research (89063_1)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Protease and Inhibitor Mechanisms
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
Keywords
hypertension, vascular remodeling, extracellular matrix, mechanical stretch, extracellular protease, cell-matrix interactions, arterial stiffness, vascular calcification, endothelial cells, vascular smooth muscle cells, signaling pathways
MeSH terms
Animals, Extracellular Matrix, Humans, Hypertension, Peptide Hydrolases, Signal Transduction, NF-kappa B

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