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MiR-10a improves hepatic fibrosis by regulating the TGF β l/Smads signal transduction pathway

View Article: PubMed Central - PubMed

ABSTRACT

The aim of the present study was to examine the expression variation of the mouse hepatic fibrosis tissue transforming growth factor (TGF)-βl/Smads signal transduction pathway and its correlation with progression of hepatic fibrosis. The promotion effect of microRNA (miR)-10a on hepatic fibrosis and its possible mechanism was also assessed. Forty healthy female 8-week-old C57BL6/J mice were randomly divided into the control group (intraperitoneal injection of 5 µl/g normal saline, twice per week for 8 weeks) and the hepatic fibrosis group (intraperitoneal injection of 5 µl/g 10% CCI4 olive oil, twice per week for 8 weeks), with 20 mice per group. RT-PCR was used to test miR-10a expression in cells in the control and hepatic fibrosis groups. Cell culture and transfection of miR-10a mimics were conducted in the two groups and a Cell Counting Kit-8 was used to test the expression of TGF-β1 and Smad7 in hepatic fibroblasts. It was found that in comparison with the control group, miR-10a expression was significantly increased in the hepatic fibrosis group compared with the control group (P<0.05). The expression quantity of miR-10a was significantly increased in the transfection group compared with the control group (P<0.05). A high expression of miR-10a significantly improved TGF-β1 expression and reduced Smad7 expression in the hepatic fibrosis group (P<0.05). In conclusion, miR-10a expression was high in mouse hepatic tissues, transfection of miR-10a mimics significantly promoted the cell proliferation of hepatic fibrosis, and miR-10a improved hepatic fibrosis by regulating the TGF-βl/Smads signal transduction pathway.

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MicroRNA (miR)-10a low-expression significantly increased the expression of transforming growth factor (TGF)-βl (A) and decreased the expression of Smad7 (B) in hepatic fibroblasts.
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f3-etm-0-0-3542: MicroRNA (miR)-10a low-expression significantly increased the expression of transforming growth factor (TGF)-βl (A) and decreased the expression of Smad7 (B) in hepatic fibroblasts.

Mentions: To examine the molecular mechanism of miR-10a in the genesis and development of hepatic fibrosis, the protein expression of TGF-βl and Smad7 was determined in hepatic fibroblasts after miR-10a mimics were transfected. Compared to the control group, TGF-βl protein expression in the transfection group was significantly increased, indicating that miR-10a upregulated TGF-βl expression while Smad7 protein expression in the transfection group significantly was decreased, indicating that miR-10a downregulated Smad7 expression (Fig. 3).


MiR-10a improves hepatic fibrosis by regulating the TGF β l/Smads signal transduction pathway
MicroRNA (miR)-10a low-expression significantly increased the expression of transforming growth factor (TGF)-βl (A) and decreased the expression of Smad7 (B) in hepatic fibroblasts.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4998216&req=5

f3-etm-0-0-3542: MicroRNA (miR)-10a low-expression significantly increased the expression of transforming growth factor (TGF)-βl (A) and decreased the expression of Smad7 (B) in hepatic fibroblasts.
Mentions: To examine the molecular mechanism of miR-10a in the genesis and development of hepatic fibrosis, the protein expression of TGF-βl and Smad7 was determined in hepatic fibroblasts after miR-10a mimics were transfected. Compared to the control group, TGF-βl protein expression in the transfection group was significantly increased, indicating that miR-10a upregulated TGF-βl expression while Smad7 protein expression in the transfection group significantly was decreased, indicating that miR-10a downregulated Smad7 expression (Fig. 3).

View Article: PubMed Central - PubMed

ABSTRACT

The aim of the present study was to examine the expression variation of the mouse hepatic fibrosis tissue transforming growth factor (TGF)-βl/Smads signal transduction pathway and its correlation with progression of hepatic fibrosis. The promotion effect of microRNA (miR)-10a on hepatic fibrosis and its possible mechanism was also assessed. Forty healthy female 8-week-old C57BL6/J mice were randomly divided into the control group (intraperitoneal injection of 5 µl/g normal saline, twice per week for 8 weeks) and the hepatic fibrosis group (intraperitoneal injection of 5 µl/g 10% CCI4 olive oil, twice per week for 8 weeks), with 20 mice per group. RT-PCR was used to test miR-10a expression in cells in the control and hepatic fibrosis groups. Cell culture and transfection of miR-10a mimics were conducted in the two groups and a Cell Counting Kit-8 was used to test the expression of TGF-β1 and Smad7 in hepatic fibroblasts. It was found that in comparison with the control group, miR-10a expression was significantly increased in the hepatic fibrosis group compared with the control group (P<0.05). The expression quantity of miR-10a was significantly increased in the transfection group compared with the control group (P<0.05). A high expression of miR-10a significantly improved TGF-β1 expression and reduced Smad7 expression in the hepatic fibrosis group (P<0.05). In conclusion, miR-10a expression was high in mouse hepatic tissues, transfection of miR-10a mimics significantly promoted the cell proliferation of hepatic fibrosis, and miR-10a improved hepatic fibrosis by regulating the TGF-βl/Smads signal transduction pathway.

No MeSH data available.


Related in: MedlinePlus