Hdac8 Inhibitor Alleviates Transverse Aortic Constriction-Induced Heart Failure in Mice by Downregulating Ace1

Figure 6

PCI34051 or Hdac8 knockdown mitigates TGF-β1-induced fibrosis in rat cardiac fibroblasts. (a–e) Rat cardiac fibroblasts were pre-treated with TGF–β1 (10 ng/mL) for 1 h and cultured in the presence of vehicle or PCI34051 (10 μM) for 8 h. mRNA levels of Hdac8, Col1a1, Fn1, Acta2, and Tgfb1 were evaluated using quantitative real-time polymerase chain reaction (qRT-PCR) (–6 per group). (f–k) Representative immunoblots and quantification of Hdac8, Fn1, Acta2, Tgfb1, p-Smad2/3, and Smad2/3 levels in rat cardiac fibroblasts ( per group). Actb was used as a loading control. (l–p) Rat cardiac fibroblasts were transfected with control or short-interfering RNA against Hdac8 and treated with TGF-β1 (10 ng/mL) for 9 h. The mRNA levels of Hdac8, Fn1, Acta2, Tgfb1, and Ace1 were determined using qRT-PCR ( per group). (q–w) Representative immunoblots and quantification of Hdac8, Ace1, Fn1, Acta2, Tgfb1, p-Smad2/3, and Smad2/3 levels in rat cardiac fibroblasts ( per group). Actb was used as a loading control.

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