Key result
VEGFB prevented Ang II-induced cardiomyocyte hypertrophy and reduced hypertrophy markers via the Ca2+-mediated PKG I pathway, effects partially reversed by VEGFR1 knockdown.
Identifies VEGFR1 signaling as a potential therapeutic target for pathological remodeling; leaves open whether these.
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 2+ . 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.
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Zhang et al. (2017) studied Cardiomyocyte hypertrophy. VEGFB vs. Ang II alone / VEGFR1 knockdown was evaluated on Cardiomyocyte size and mRNA/protein levels of β‐MHC, BNP, and ANP. VEGFB prevented Ang II-induced cardiomyocyte hypertrophy and reduced hypertrophy markers via the Ca2+-mediated PKG I pathway, effects partially reversed by VEGFR1 knockdown.
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