title: Hydrogen sulfide suppresses the expression of MMP-8, MMP-13, and TIMP-1 in left ventricles of rats with cardiac volume overload.
abstract: OBJECTIVE
  To study the effects of hydrogen sulfide (H2S) on the left ventricular expression of MMP-8, MMP-13, and TIMP-1 in a rat model of congenital heart disease.
  
  
  METHODS
  Male SD rats underwent abdominal aorta-inferior vena cava shunt operation. H2S donor NaHS (56 μmol·kg(-1)·d(-1), ip) was injected from the next day for 8 weeks. At 8 weeks, the hemodynamic parameters, including the left ventricular systolic pressure (LVSP), the left ventricular peak rate of contraction and relaxation (LV ± dp/dtmax) and the left ventricular end diastolic pressure (LVEDP) were measured. The left ventricular tissues were dissected out, and hydroxyproline and collagen I contents were detected with ELISA. The expression of MMP-8, MMP-13, and a tissue inhibitor of metalloproteinase-1 (TIMP-1) in the tissues was measured using real-time PCR, Western blotting, and immunohistochemistry, respectively.
  
  
  RESULTS
  The shunt operation markedly reduced LVSP and LV ± dp/dtmax, increased LVEDP, hydroxyproline and collagen I contents, as well as the mRNA and protein levels of MMP-8, MMP-13, and TIMP-1 in the left ventricles. Chronic treatment of the shunt operation rats with NaHS effectively prevented the abnormalities in the hemodynamic parameters, hydroxyproline and collagen I contents, and the mRNA and protein levels of MMP-13 and TIMP-1 in the left ventricles. NaHS also prevented the increase of MMP-8 protein expression, but did not affect the increase of mRNA level of MMP-8 in the shunt operation rats.
  
  
  CONCLUSIONS
  H2S suppresses protein and mRNA expression of MMP-8, MMP-13, and TIMP-1 in rats with cardiac volume overload, which may be contributed to the amelioration of ventricular structural remodeling and cardiac function.
authors: Department of Cardiovascular Diseases, Children's Hospital Affiliated to Capital Institute of Pediatrics, Beijing 100020, China.
authors: Chao-Ying
authors: CY
authors: Zhang
authors: Xiao-Hui
authors: XH
authors: Li
authors: Ting
authors: T
authors: Zhang
authors: Jin
authors: J
authors: Fu
authors: Xiao-Dai
authors: XD
authors: Cui
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002306:Cardiac Volume; D004195:Disease Models, Animal; D005786:Gene Expression Regulation; D006330:Heart Defects, Congenital / Q000503:physiopathology*; D006352:Heart Ventricles / Q000378:metabolism / Q000503:physiopathology; D006862:Hydrogen Sulfide / Q000378:metabolism*; D008297:Male; D053509:Matrix Metalloproteinase 13 / Q000235:genetics*; D020784:Matrix Metalloproteinase 8 / Q000235:genetics*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D060888:Real-Time Polymerase Chain Reaction; D013440:Sulfides / Q000494:pharmacology; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000235:genetics*; D020257:Ventricular Remodeling
chemical_list: D012333:RNA, Messenger; D013440:Sulfides; C576839:TIMP1 protein, rat; D019715:Tissue Inhibitor of Metalloproteinase-1; D053509:Matrix Metalloproteinase 13; D020784:Matrix Metalloproteinase 8; C025451:sodium bisulfide; D006862:Hydrogen Sulfide
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