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Overexpression of collagen type III in injured myocardium prevents cardiac systolic dysfunction by changing the balance of collagen distribution.

J. Thorac. Cardiovasc. Surg.. 2018-07; 
UchinakaAyako,YoshidaMaho,TanakaKiyoka,HamadaYoshinosuke,MoriSeiji,MaenoYoshitaka,MiyagawaShigeru,SawaYoshiki,NagataKohzo,YamamotoHirofumi,KawaguchiNao
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Gene Synthesis … A fragment of human Col3 α1 chain (COL3a1) cDNA including a HindIII site and secretory signal sequence at the 5′ end and XbaI sites at the 3′ end (Figure 1, A and Figure E1) was synthesized by GenScript (Piscataway, NJ) … Get A Quote

摘要

Left ventricular (LV) remodeling alters the contractile and relaxation properties and induces myocardial stiffness. As LV remodeling progresses, the amount of collagen type III (Col3) is gradually decreased, being replaced by collagen type I (Col1). We evaluated whether Col3 overexpression improved cardiac function and remodeling in a rat with ischemic cardiomyopathy (ICM). We also investigated the functional motif and mechanism of thrombin-cleaved N-terminal osteopontin (N-OPN) on cardiac remodeling.

关键词

collagen type III,ischemic cardiomyopathy,remode