Mistletoe alkaloid fractions alleviates carbon tetrachloride-induced liver fibrosis through inhibition of hepatic stellate cell activation via TGF-β/Smad interference

Jiang, Ying; Wang, Chi; Li, Ying-Ying; Wang, Xuecong; An, Jian-Duo; Wang, Yunjiao; Wang, Xuejiang

doi:10.1016/j.jep.2014.10.028

Cited by 36 publications

(22 citation statements)

References 59 publications

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“…Multiple comparisons for different groups were carried out using unpaired t-test or one-way analysis of variance ( ANOVA ) followed by S.N.K. test as post-hoc analysis with SPSS 18.0 software, and p < 0.05 was considered statistically significant37.…”

Section: Methodsmentioning

confidence: 99%

MircoRNA-145 promotes activation of hepatic stellate cells via targeting krüppel-like factor 4

Men

Wen

Zhao

et al. 2017

Sci Rep

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Krüppel-like Factor 4 (KLF4), a target gene of miR-145, can negatively regulate lung fibrosis. However, the potential role of KLF4 and miR-145 in hepatic stellate cells (HSCs) activation or in hepatic fibrosis keeps unclear. This study aims to characterize miR-145 and KLF4 in activated HSCs and liver cirrhotic, and the underlying molecular basis. miR-145 was significantly up-regulated, while KLF4 was dramatically down-regulated during the activation of rat primary HSCs and TGF-βtreated HSCs. Furthermore, miR-145 mimics induced and inhibition of miR-145 reduced α-SMA and COL-I expression in primary HSCs. Additionally, the mRNA and protein levels of KLF4 in the liver of cirrhotic patients and rats were significantly down-regulated. α-SMA and COL-I were increased after inhibition of KLF4 by specific shRNA in primary HSCs. Forced KLF4 expression led to a reduction of α-SMA and COL-I expression in HSCs. miR-145 promotes HSC activation and liver fibrosis by targeting KLF4.

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Section: Methodsmentioning

confidence: 99%

MircoRNA-145 promotes activation of hepatic stellate cells via targeting krüppel-like factor 4

Men

Wen

Zhao

et al. 2017

Sci Rep

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show abstract

“…A previous study, demonstrated that the expression of Smad-7 protein in HCC tissue was markedly higher than that in carcinoma-adjacent and normal tissues, the anticancer effect of TGF-β/Smad signaling was suppressed and the development of liver cancer was promoted (25). In another study, following the transfection of mouse hepatic cells with a Smad-7-containing adenovirus, Smad-7 was observed to decrease the intranuclear accumulation of Smads, including Smad3 induced by activin A, promote DNA synthesis stimulated by epithelial growth factor and alleviate the growth-inhibitory effect of activin A on hepatic cells (26). Furthermore, a study by Liu et al (27) revealed that, after an exogenous Smad-7 gene was transferred into L-02 hepatic cells, Smad-7 rescued the TGF-β-induced inhibition of L-02 hepatocellular proliferation and its apoptosis-inducing effect (27).…”

Section: Discussionmentioning

confidence: 99%

The inhibition of microRNA-15a suppresses hepatitis B virus-associated liver cancer cell growth through the Smad/TGF-β pathway

Wang

2017

Oncology Reports

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In the present study, the role of microRNA‑15a (miR‑15a) was investigated in hepatitis B virus (HBV)‑associated liver cancer. The results revealed that the expression levels of miR-15a were increased in HBV-associated liver cancer tissues compared with the levels in normal tumor‑adjacent tissues. Moreover, Smad-7 protein expression in patients with HBV-associated liver cancer was higher than that in normal tumor-adjacent tissues. In addition, miR-15a expression and Smad-7 protein expression were increased in HepG2 hepatocellular carcinoma cells compared with that noted in L-02 normal hepatocytes. In HepG2 cells, miR-15a inhibition suppressed cell proliferation and increased Smad-7 protein expression. The inhibition of miR-15a was also demonstrated to decrease transforming growth factor (TGF)-β1 protein expression and Smad-2, p-Smad-2 and Smad-4 expression levels in HepG2 cells. Furthermore, FSP1 protein expression and caspase-3/-7 activities were enhanced by miR-15a inhibition in HepG2 cells compared with the control group. Treatment with recombinant TGF-β1 was demonstrated to activate Smad‑2/-4 and FSP1 protein expression and increase caspase-3/-7 activity in HepG2 cells. Collectively, these findings demonstrate that the miR-15a/Smad-7/TGF-β pathway is important in HBV-associated liver cancer.

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“…It has been largely demonstrated that disruption of TGF-b/Smad signaling shows a protective effect on tissue fibrosis. Jiang et al reported that mistletoe alkaloid fractions alleviates carbon tetrachloride-induced liver fibrosis through inhibition of hepatic stellate cell activation via TGF-b/Smad interference [34]. EW-7197, a molecule inhibitor of the TGF-b type I receptor kinase, inhibits hepatic, renal, and pulmonary fibrosis by blocking TGF-b/Smad and ROS signaling [35].…”

Section: Discussionmentioning

confidence: 99%

Activation of imidazoline I1 receptor by moxonidine regulates the progression of liver fibrosis in the Nrf2-dependent pathway

Zhang

Liu

et al. 2017

Biomedicine & Pharmacotherapy

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Mistletoe alkaloid fractions alleviates carbon tetrachloride-induced liver fibrosis through inhibition of hepatic stellate cell activation via TGF-β/Smad interference

Cited by 36 publications

References 59 publications

MircoRNA-145 promotes activation of hepatic stellate cells via targeting krüppel-like factor 4

MircoRNA-145 promotes activation of hepatic stellate cells via targeting krüppel-like factor 4

The inhibition of microRNA-15a suppresses hepatitis B virus-associated liver cancer cell growth through the Smad/TGF-β pathway

Activation of imidazoline I1 receptor by moxonidine regulates the progression of liver fibrosis in the Nrf2-dependent pathway

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