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2018 ; 19
(3
): ä Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Endostatin Stimulates Proliferation and Migration of Myofibroblasts Isolated from
Myocardial Infarction Model Rats
#MMPMID29509663
Sugiyama A
; Hirano Y
; Okada M
; Yamawaki H
Int J Mol Sci
2018[Mar]; 19
(3
): ä PMID29509663
show ga
Myofibroblasts contribute to the healing of infarcted areas after myocardial
infarction through proliferation, migration, and production of extracellular
matrix (ECM). Expression of endostatin, a cleaved fragment of type XVIII
collagen, increases in the heart tissue of an experimental myocardial infarction
model. In the present study, we examined the effect of endostatin on the function
of myofibroblasts derived from an infarcted area. The myocardial infarction model
was created by ligating the left anterior descending artery in rats. Two weeks
after the operation, ?-smooth muscle actin (?-SMA)-positive myofibroblasts were
isolated from the infarcted area. Endostatin significantly increased the
proliferation and migration of myofibroblasts in vitro. On the other hand,
endostatin had no effect on the production of type I collagen, a major ECM
protein produced by myofibroblasts. Endostatin activated Akt and extracellular
signal-regulated kinase (ERK), and the pharmacological inhibition of these
signaling pathways suppressed the endostatin-induced proliferation and migration.
A knockdown of the COL18A1 gene in the myocardial infarction model rats using
small interference RNA (siRNA) worsened the cardiac function concomitant with
wall thinning and decreased the ?-SMA-positive myofibroblasts and scar formation
compared with that of control siRNA-injected rats. In summary, we demonstrated
for the first time that endostatin might be an important factor in the healing
process after myocardial infarction through the activation of myofibroblasts.