Department of Cardiology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, China.
J Cell Biochem. 2018 Feb;119(2):1511-1520. doi: 10.1002/jcb.26311. Epub 2017 Sep 7.
In response to assorted stimuli, the heart will develop into cardiomyocyte hypertrophy, but sustained cardiomyocyte hypertrophy will finally lead to heart failure. This research is aimed to examine the effect of VEGFB on cardiomyocyte hypertrophy by using the cardiomyocyte-derived cell line H9C2 of cultured rates. It turns out that VEGFB can positively prevent the Ang II-induced rising in the size of cardiomyocyte as well as reduce Ang II-induced mRNA and protein levels of β-MHC (β-myosin heavy chain), BNP (brain natriuretic peptide), and ANP (atrial natriuretic peptide). Moreover, VEGFB can regulate the decline of the Ang II-induced rising in Ca . After VEGFR1 knockdown, these effects of VEGFB were partially reversed. Moreover, VEGFB attenuated the suppression of PKG I, p-VASP, and RGS2 caused by Ang II; whereas VEGFR1 knockdown partially abolished the indicated effect of VEGFB. In a word, the effect of VEGFB on relevant downstream targets and the pathways of PKG I by VEGFR1 may explain its efficacy on cardiomyocyte hypertrophy. Thus, it can be suggested that it is feasible to apply VEGFB-VEGFR1 for reducing the symptoms of cardiomyocyte hypertrophy.
在各种刺激下，心脏会发生心肌细胞肥大，但持续的心肌细胞肥大最终会导致心力衰竭。本研究旨在通过培养的大鼠心肌细胞系 H9C2 来研究 VEGFB 对心肌细胞肥大的影响。结果表明，VEGFB 可积极预防 Ang II 诱导的心肌细胞大小增加，并降低 Ang II 诱导的 β-MHC（β-肌球蛋白重链）、BNP（脑利钠肽）和 ANP（心钠肽）的 mRNA 和蛋白水平。此外，VEGFB 可调节 Ang II 诱导的 Ca 增加的下降。在 VEGFR1 敲低后，VEGFB 的这些作用部分逆转。此外，VEGFB 减弱了 Ang II 引起的 PKG I、p-VASP 和 RGS2 抑制；而 VEGFR1 敲低部分消除了 VEGFB 的上述作用。总之，VEGFB 对相关下游靶点和 VEGFR1 的 PKG I 通路的作用可能解释了其对心肌细胞肥大的疗效。因此，应用 VEGFB-VEGFR1 减轻心肌细胞肥大症状是可行的。
