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2017 ; 7
(ä): 44473
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Overexpression of decorin promoted angiogenesis in diabetic cardiomyopathy via
IGF1R-AKT-VEGF signaling
#MMPMID28290552
Lai J
; Chen F
; Chen J
; Ruan G
; He M
; Chen C
; Tang J
; Wang DW
Sci Rep
2017[Mar]; 7
(ä): 44473
PMID28290552
show ga
Microcirculatory dysfunction is believed to play an important role in diabetic
cardiomyopathy. The small leucine-rich proteoglycan decorin is generally
considered a pro-angiogenic factor. Here, we investigate whether overexpression
of decorin ameliorates diabetic cardiomyopathy and its effects on angiogenesis in
vivo and in vitro. Diabetes was induced through intraperitoneal injection with
streptozotocin combined with a high-fat diet, and decorin was overexpressed via
recombinant adeno-associated virus in Wistar rats. Six months later, cardiac
function was determined using an echocardiography and cardiac catheter system.
The results showed that cardiac function was decreased in diabetic rats and
restored by overexpression of decorin. In addition, overexpression of decorin
upregulated the expression of VEGF and attenuated the reduction in the cardiac
capillary density. In the in vitro study, high glucose induced apoptosis and
inhibited the capabilities of tube formation, migration and proliferation, which
were all ameliorated by decorin overexpression. Meanwhile, decorin overexpression
increased the expression of VEGF and IGF1R, as well as the phosphorylation level
of AKT and AP-1. Nonetheless, all of these effects were abolished by pretreatment
with the IGF1R antibody or AKT inhibitor. In conclusion, overexpression of
decorin ameliorated diabetic cardiomyopathy and promoted angiogenesis through the
IGF1R-AKT-VEGF signaling pathway in vivo and in vitro.
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