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Novel mechanism of cardiac protection by valsartan: synergetic roles of TGF-β1 and HIF-1α in Ang II-mediated fibrosis after myocardial infarction.

Sui X, Wei H, Wang D - J. Cell. Mol. Med. (2015)

Bottom Line: By blocking with valsartan, a blocker of Ang II type I (AT1) receptor, we confirmed that the up-regulation of TGF-β/Smad and Hif-1α was through the Ang II-mediated pathway.By administering TGF-β or dimethyloxalylglycine, we determined that both TGF-β/Smad and Hif-1α contributed to Ang II-mediated collagen accumulation and a synergetic effect between them was observed.Heart function, infarcted size, wall thickness as well as myocardial vascularization of ischaemic hearts were also significantly improved by valsartan compared with saline and hydralazine.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiothoracic Surgery, The Civil Aviation General Hospital, Chaoyang District, Beijing, China.

No MeSH data available.


Related in: MedlinePlus

Evaluation of infarct size, wall thickness, myocardial fibrosis and vascular densities. (A) Viable myocardium was stained red and infarct area was stained green by Masson’s trichrome staining. Quantitative analysis showed that both infarct size and myocardial fibrosis in valsartan-treated group were significantly smaller than that in control and hydralazine groups, while wall thickness of infarct zone was significantly larger in the valsartan-treated group compared with that in control and hydralazine groups. (B) Immunostaining against v-WF demonstrated that significantly more tubular structures could be observed in heart sections from valsartan-treated animals than that from saline- and hydralazine-treated groups. Vessel perimeters were also significantly higher in the valsartan-treated group (n = 10, **P < 0.01 compared with saline group, ##P < 0.01 compared with hydralazine group, bar = 100 μm).
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fig06: Evaluation of infarct size, wall thickness, myocardial fibrosis and vascular densities. (A) Viable myocardium was stained red and infarct area was stained green by Masson’s trichrome staining. Quantitative analysis showed that both infarct size and myocardial fibrosis in valsartan-treated group were significantly smaller than that in control and hydralazine groups, while wall thickness of infarct zone was significantly larger in the valsartan-treated group compared with that in control and hydralazine groups. (B) Immunostaining against v-WF demonstrated that significantly more tubular structures could be observed in heart sections from valsartan-treated animals than that from saline- and hydralazine-treated groups. Vessel perimeters were also significantly higher in the valsartan-treated group (n = 10, **P < 0.01 compared with saline group, ##P < 0.01 compared with hydralazine group, bar = 100 μm).

Mentions: Masson’s trichrome staining of cardiac tissue slices at 4 weeks was performed to evaluate the potential effect of valsartan on infarct size, infarct wall thickness and myocardial fibrosis. As shown in Figure6A, fibroblasts and collagen were largely accumulated in the infarct area after MI. Compared with the saline-treated control group, valsartan treatment significantly prevented the enlargement of infarct size and increased the wall thickness of the infarct zone (P < 0.01). In addition, more viable myocardium could be detected in the valsartan-treated group than that in the saline-treated group, indicating that myocardial fibrosis was inhibited by valsartan after MI. Compared with the saline-treated group, hydralazine treatment did not produce significant effects on infarct size, wall thickness and myocardial fibrosis.


Novel mechanism of cardiac protection by valsartan: synergetic roles of TGF-β1 and HIF-1α in Ang II-mediated fibrosis after myocardial infarction.

Sui X, Wei H, Wang D - J. Cell. Mol. Med. (2015)

Evaluation of infarct size, wall thickness, myocardial fibrosis and vascular densities. (A) Viable myocardium was stained red and infarct area was stained green by Masson’s trichrome staining. Quantitative analysis showed that both infarct size and myocardial fibrosis in valsartan-treated group were significantly smaller than that in control and hydralazine groups, while wall thickness of infarct zone was significantly larger in the valsartan-treated group compared with that in control and hydralazine groups. (B) Immunostaining against v-WF demonstrated that significantly more tubular structures could be observed in heart sections from valsartan-treated animals than that from saline- and hydralazine-treated groups. Vessel perimeters were also significantly higher in the valsartan-treated group (n = 10, **P < 0.01 compared with saline group, ##P < 0.01 compared with hydralazine group, bar = 100 μm).
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4549028&req=5

fig06: Evaluation of infarct size, wall thickness, myocardial fibrosis and vascular densities. (A) Viable myocardium was stained red and infarct area was stained green by Masson’s trichrome staining. Quantitative analysis showed that both infarct size and myocardial fibrosis in valsartan-treated group were significantly smaller than that in control and hydralazine groups, while wall thickness of infarct zone was significantly larger in the valsartan-treated group compared with that in control and hydralazine groups. (B) Immunostaining against v-WF demonstrated that significantly more tubular structures could be observed in heart sections from valsartan-treated animals than that from saline- and hydralazine-treated groups. Vessel perimeters were also significantly higher in the valsartan-treated group (n = 10, **P < 0.01 compared with saline group, ##P < 0.01 compared with hydralazine group, bar = 100 μm).
Mentions: Masson’s trichrome staining of cardiac tissue slices at 4 weeks was performed to evaluate the potential effect of valsartan on infarct size, infarct wall thickness and myocardial fibrosis. As shown in Figure6A, fibroblasts and collagen were largely accumulated in the infarct area after MI. Compared with the saline-treated control group, valsartan treatment significantly prevented the enlargement of infarct size and increased the wall thickness of the infarct zone (P < 0.01). In addition, more viable myocardium could be detected in the valsartan-treated group than that in the saline-treated group, indicating that myocardial fibrosis was inhibited by valsartan after MI. Compared with the saline-treated group, hydralazine treatment did not produce significant effects on infarct size, wall thickness and myocardial fibrosis.

Bottom Line: By blocking with valsartan, a blocker of Ang II type I (AT1) receptor, we confirmed that the up-regulation of TGF-β/Smad and Hif-1α was through the Ang II-mediated pathway.By administering TGF-β or dimethyloxalylglycine, we determined that both TGF-β/Smad and Hif-1α contributed to Ang II-mediated collagen accumulation and a synergetic effect between them was observed.Heart function, infarcted size, wall thickness as well as myocardial vascularization of ischaemic hearts were also significantly improved by valsartan compared with saline and hydralazine.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiothoracic Surgery, The Civil Aviation General Hospital, Chaoyang District, Beijing, China.

No MeSH data available.


Related in: MedlinePlus