TY - JOUR
T1 - Hepatic fibrosis and angiogenesis after bile duct ligation are endogenously expressed vasohibin-1 independent
AU - Furutani, Yutaka
AU - Shiozaki-Sato, Yumi
AU - Hara, Mitsuko
AU - Sato, Yasufumi
AU - Kojima, Soichi
N1 - Funding Information:
We thank Yuta Yamazaki and Ikuyo Inoue for their advices and technical assistance to perform BDL and Sirius red staining, respectively. We also thank members of the Research Resource Center at RIKEN BSI for technical supports. This work was supported partly by JSPS KAKENHI Grant Number 26670390 to S.K. and the Cooperative Research Project Program of Joint Usage/Research Center at the Institute of Development, Aging, and Center, Tohoku University Grant Number 58 to Y.F.
Publisher Copyright:
© 2015 Elsevier Inc. All rights reserved.
Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 2015/6/14
Y1 - 2015/6/14
N2 - Liver fibrosis is linked to VEGF-induced angiogenesis. Overexpression of exogenous vasohibin-1, a feedback inhibitor of angiogenesis, has been reported to reduce liver fibrosis after bile duct ligation (BDL). To uncover the function of endogenous vasohibin-1, we performed BDL using vasohibin-1-deficient mice and analyzed liver fibrosis, injury, and angiogenesis. Liver fibrosis was induced by 14-days of BDL in both wild-type and vasohibin-1-deficient mice. The liver sections were stained with anti-CD31 to visualize endothelial cells and with Sirius red to observe fibrotic regions. Total RNAs were purified from the livers and expression of collagen I α1 mRNA was measured by quantitative PCR. Plasma ALT activity was determined to assess liver injury. Surprisingly, the same extents of increases were seen in anti-CD31 and Sirius red stainings, collagen I α1 mRNA expressions, hepatic hydroxyproline contents, and ALT activity after 14-days of BDL in both wild-type and vasohibin-1-deficient mice. There was unexpectedly no difference between these mice, suggesting that anti-fibrogenic and angiogenic activities of the endogenous vasohibin-1 might be masked in the normal liver at early stage of hepatic fibrosis in mice.
AB - Liver fibrosis is linked to VEGF-induced angiogenesis. Overexpression of exogenous vasohibin-1, a feedback inhibitor of angiogenesis, has been reported to reduce liver fibrosis after bile duct ligation (BDL). To uncover the function of endogenous vasohibin-1, we performed BDL using vasohibin-1-deficient mice and analyzed liver fibrosis, injury, and angiogenesis. Liver fibrosis was induced by 14-days of BDL in both wild-type and vasohibin-1-deficient mice. The liver sections were stained with anti-CD31 to visualize endothelial cells and with Sirius red to observe fibrotic regions. Total RNAs were purified from the livers and expression of collagen I α1 mRNA was measured by quantitative PCR. Plasma ALT activity was determined to assess liver injury. Surprisingly, the same extents of increases were seen in anti-CD31 and Sirius red stainings, collagen I α1 mRNA expressions, hepatic hydroxyproline contents, and ALT activity after 14-days of BDL in both wild-type and vasohibin-1-deficient mice. There was unexpectedly no difference between these mice, suggesting that anti-fibrogenic and angiogenic activities of the endogenous vasohibin-1 might be masked in the normal liver at early stage of hepatic fibrosis in mice.
KW - Angiogenesis
KW - Bile duct ligation
KW - Fibrosis
KW - Liver
KW - Vasohibin-1
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U2 - 10.1016/j.bbrc.2015.05.074
DO - 10.1016/j.bbrc.2015.05.074
M3 - Article
C2 - 26025651
AN - SCOPUS:84930924332
VL - 463
SP - 384
EP - 388
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 3
ER -