Platelet-derived growth factor blockade on cardiac remodeling following infarction

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• 作者：Chang Liu (2)
  Wenyuan Zhao (1)
  Weixin Meng (2)
  Tieqiang Zhao (1)
  Yuanjian Chen (1)
  Robert A. Ahokas (1)
  Hongyu Liu (2)
  Yao Sun (1)
  
• 关键词：PDGF ; Myocardial infarction ; Interstitial fibrosis ; Angiogenesis ; Ventricular function
• 刊名：Molecular and Cellular Biochemistry
• 出版年：2014
• 出版时间：December 2014
• 年：2014
• 卷：397
• 期：1-2
• 页码：295-304
• 全文大小：1,287 KB
• 参考文献：1. Yu CM, Tipoe GL, Wing-Hon Lai K, Lau CP (2001) Effects of combination of angiotensin-converting enzyme inhibitor and angiotensin receptor antagonist on inflammatory cellular infiltration and myocardial interstitial fibrosis after acute myocardial infarction. J Am Coll Cardiol 38:1207-215 CrossRef
  2. Yang F, Yang XP, Liu YH, Xu J, Cingolani O, Rhaleb NE, Carretero OA (2004) Ac-SDKP reverses inflammation and fibrosis in rats with heart failure after myocardial infarction. Hypertension 43:229-36. doi:10.1161/01.HYP.0000107777.91185.89 CrossRef
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  5. Dean RG, Balding LC, Candido R, Burns WC, Cao Z, Twigg SM, Burrell LM (2005) Connective tissue growth factor and cardiac fibrosis after myocardial infarction. J Histochem Cytochem 53:1245-256. doi:10.1369/jhc.4A6560.2005 CrossRef
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  7. Ellmers LJ, Scott NJ, Medicherla S, Pilbrow AP, Bridgman PG, Yandle TG, Richards AM, Protter AA, Cameron VA (2008) Transforming growth factor-beta blockade down-regulates the renin-angiotensin system and modifies cardiac remodeling after myocardial infarction. Endocrinology 149:5828-834. doi:10.1210/en.2008-0165 CrossRef
  8. Zhao T, Zhao W, Chen Y, Ahokas RA, Sun Y (2011) Acidic and basic fibroblast growth factors involved in cardiac angiogenesis following infarction. Int J Cardiol 152:307-13. doi:10.1016/j.ijcard.2010.07.024 CrossRef
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  11. Deuel TF, Pierce GF, Yeh HJ, Shawver LK, Milner PG, Kimura A (1987) Platelet-derived growth factor/sis in normal and neoplastic cell growth. J Cell Physiol Suppl Suppl 5:95-9 CrossRef
  12. Borkham-Kamphorst E, van Roeyen CR, Ostendorf T, Floege J, Gressner AM, Weiskirchen R (2007) Pro-fibrogenic potential of PDGF-D in liver fibrosis. J Hepatol 46:1064-074. doi:10.1016/j.jhep.2007.01.029 CrossRef
  13. Czochra P, Klopcic B, Meyer E, Herkel J, Garcia-Lazaro JF, Thieringer F, Schirmacher P, Biesterfeld S, Galle PR, Lohse AW, Kanzler S (2006) Liver fibrosis induced by hepatic overexpression of PDGF-B in transgenic mice. J Hepatol 45:419-28. doi:10.1016/j.jhep.2006.04.010 CrossRef
  14. Floege J, Eitner F, Alpers CE (2008) A new look at platelet-derived growth factor in renal disease. J Am Soc Nephrol 19:12
• 作者单位：Chang Liu (2)
  Wenyuan Zhao (1)
  Weixin Meng (2)
  Tieqiang Zhao (1)
  Yuanjian Chen (1)
  Robert A. Ahokas (1)
  Hongyu Liu (2)
  Yao Sun (1)
  
  2. Division of Cardiac Surgery, Department of Surgery, The First Affiliate Hospital of Harbin Medical University, Harbin, China
  1. Division of Cardiovascular Diseases, Department of Medicine, University of Tennessee Health Science Center, 956 Court Ave, Room B324, Memphis, TN, 38163, USA
  
• ISSN：1573-4919

文摘

Cardiac repair and remodeling occur following myocardial infarction (MI). Our previous study demonstrated that?platelet-derived growth factor (PDGF)-A/-D and PDGF receptors (PDGFR) are increased in the infarcted heart, with cells expressing PDGFR primarily endothelial and fibroblast-like cells. In the present study, we tested the hypothesis that PDGF contributes to cardiac angiogenesis and fibrogenesis post-MI. Rats with experimental MI were treated with either a PDGFR antagonist (Imatinib, 40?mg/kg/day) or vehicle by gavage, and sham-operated rats served as the controls. Cardiac fibrogenesis, angiogenesis, and ventricular function were detected at weeks 1 and 4 post-MI. We found that (1) transforming growth factor (TGF)-β1, tissue inhibitors of metalloproteinases (TIMP)-1/-2, and type I collagen mRNA were all significantly increased in the infarcted heart at week 1 post-MI, while PDGFR blockade significantly reduced these fibrogenic mediators in the noninfarcted myocardium as compared to controls; (2) fibrosis developed in both the infarcted and noninfarcted myocardium at week 4 with PDGFR blockade significantly suppressing collagen volume in the noninfarcted myocardium; (3) angiogenesis was activated in the infarcted myocardium, particularly at week 1, and was not altered by treatment with imatinib; and (4) ventricular dysfunction was evident in MI rats at week 4, and mildly improved with imatinib treatment. These observations indicated that PDGF can contribute to the development of cardiac interstitial fibrosis in the noninfarcted myocardium, but does not alter scar formation in the infarcted myocardium. Further, this study suggests the potential therapeutic effects of PDGFR blockade on interstitial fibrosis of the infarcted heart.