The value of α‐SMA in the evaluation of hepatic fibrosis severity in hepatitis B infection and cirrhosis development: a histopathological and immunohistochemical study

@article{Akpolat2005TheVO,
  title={The value of $\alpha$‐SMA in the evaluation of hepatic fibrosis severity in hepatitis B infection and cirrhosis development: a histopathological and immunohistochemical study},
  author={Nusret Akpolat and Seyfettin Yahşi and Ahmet Godekmerdan and Mehmet Yalnız and Kutbettin Demirbag},
  journal={Histopathology},
  year={2005},
  volume={47}
}
Aims : To investigate the value of α‐smooth muscle actin (α‐SMA), an indicator of stellate cell activation, in predicting fibrosis in chronic hepatitis B (CHB) patients. 

α-SMA and Ki-67 immunohistochemistry as indicators for the fibrotic remodeling process in the liver of dogs.

Investigating the expression of two immunohistochemical markers in liver diseases with and without fibrosis in dogs concluded that Ki-67 and a-SMA can be potentially used as markers for the fibrotic remodeling of the liver.

Value of α-smooth muscle actin and glial fibrillary acidic protein in predicting early hepatic fibrosis in chronic hepatitis C virus infection

Glial fibrillary acidic protein could represent a more useful marker than α-SMA of early activation of HSCs in CHC patients and seems to be an early indicator of hepatic fibrogenesis.

Bevacizumab as a potential anti‐angiogenic therapy in schistosomiasis: A double‐edged, but adjustable weapon

Investigating the anti‐angiogenic effect of bevacizumab on chronic schistosomiasis mansoni in a trial to hinder the Schistosome‐induced angiogenesis and porto‐systemic shunting complications.

Activated liver stellate cells in chronic viral C hepatitis: histopathological and immunohistochemical study.

An increased number of activated hepatic stellate cells within portal spaces and fibrous septa may be a useful prognostic marker for the development of advanced fibrosis and cirrhosis in chronic C hepatitis.

β-Actin: Not a Suitable Internal Control of Hepatic Fibrosis Caused by Schistosoma japonicum

It is found that the expressions of both β-actin mRNA and protein increased significantly with hepatic fibrosis formation after 6 weeks infection with Schistosoma japonicum and kept high level during the progression of hepatic Fibrosis, while the levels of β-Tubulin and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) remained stable.

[Immunohistochemical analysis of alpha-SMA and GFAP expression in liver stellate cells].

This study showed the existance of two different stellate cell subpopulations in liver tissue, and differentiation between them was possible on the basis of SMA/GFAP expression.

Therapeutic effects of vitamin A on experimental cholestatic rats with hepatic fibrosis

Although most of the data are qualitative observation, vitamin A may ameliorate hepatic fibrosis in the BDL model by restoring vitamin A in the HSCs.

The fibrosis progression, and treatment of the NCU-G1gt/gt mouse model

The fibrosis progression in the NCU-G1 mice is investigated with gene expression, protein and liver component analyses, and with treatment with the anti-fibrotic agent sodium hydrogen sulfide (NaHS) is attenuated.

Newcastle disease virus represses the activation of human hepatic stellate cells and reverses the development of hepatic fibrosis in mice

  • Ya-lin LiJiao Wu H. Bian
  • Medicine, Biology
    Liver international : official journal of the International Association for the Study of the Liver
  • 2009
Activated hepatic stellate cells are the crucial factor responsible for liver fibrosis and involved in development of hepatocellular carcinoma (HCC) by interaction with tumour cells.

Origin and function of myofibroblasts in the liver.

The hypothesis that each fibrogenic cell population in the liver exerts specific functions is discussed, and whether cell type-specific antifibrotic strategies are required or whether one therapeutic strategy fits all is discussed.

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