Display options
Cite
Zhu L, Cheng M, Liu Y, et al. Thymosin-β4 inhibits proliferation and induces apoptosis of hepatic stellate cells through PI3K/AKT pathway. Oncotarget. 2017;8(40):68847-68853doi: 10.18632/oncotarget.18748.
Zhu, L., Cheng, M., Liu, Y., Yao, Y., Zhu, Z., Zhang, B., Mou, Q., & Cheng, Y. (2017). Thymosin-β4 inhibits proliferation and induces apoptosis of hepatic stellate cells through PI3K/AKT pathway. Oncotarget, 8(40), 68847-68853. https://doi.org/10.18632/oncotarget.18748
Zhu, Lili, et al. "Thymosin-β4 inhibits proliferation and induces apoptosis of hepatic stellate cells through PI3K/AKT pathway." Oncotarget vol. 8,40 (2017): 68847-68853. doi: https://doi.org/10.18632/oncotarget.18748
Zhu L, Cheng M, Liu Y, Yao Y, Zhu Z, Zhang B, Mou Q, Cheng Y. Thymosin-β4 inhibits proliferation and induces apoptosis of hepatic stellate cells through PI3K/AKT pathway. Oncotarget. 2017 Jun 28;8(40):68847-68853. doi: 10.18632/oncotarget.18748. eCollection 2017 Sep 15. PMID: 28978161; PMCID: PMC5620301.
Copy Download .nbib Format: NLM
Share it on

Oncotarget. 2017 Jun 28;8(40):68847-68853. doi: 10.18632/oncotarget.18748. eCollection 2017 Sep 15.

Thymosin-β4 inhibits proliferation and induces apoptosis of hepatic stellate cells through PI3K/AKT pathway.

Oncotarget

Lili Zhu, Mingliang Cheng, Yongmei Liu, Yumei Yao, Zixin Zhu, Baofang Zhang, Qiuju Mou, Yiju Cheng

Affiliations

  1. Department of Infectious Diseases, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China.
  2. The Affliated Baiyun Hospital of Guizhou Medical University, Guiyang, Guizhou, China.
  3. Guizhou Medical University, Guiyang, Guizhou, China.

PMID: 28978161 PMCID: PMC5620301 DOI: 10.18632/oncotarget.18748

Abstract

Liver fibrosis is a necessary stage for chronic liver diseases, and serious threat to human health. Hepatic fibrosis is a necessary stage for chronic liver diseases. Hepatic stellate cells (HSCs) are the primary cell type responsible for fibrosis. Thymosin beta 4 (Tβ4) has a potential role in the pathogenesis of liver fibrosis and that it is especially associated with the activation of HSCs, however, the underlying mechanisms are not fully elucidated. Herein, we investigated the potential role of Tβ4 in liver fibrosis by describing the effects of Tβ4, and we discuss the possible signaling pathway regulated by Tβ4. The expression of Tβ4 was significantly decreased in human HSC cell line LX-2 and CCl4-treated mouse liver. The depletion of Tβ4 significantly associated with the activation of HSCs via the enhanced expression of α-SMA and vimentin. Tβ4 significantly suppressed the viability and migration of HSCs. Understanding the potential effects and regulatory mechanism of Tβ4 in liver fibrosis might help to provide a novel treatment for patients with liver fibrosis.

Keywords: AKT; Thymosin-β4; hepatic stellate cell; liver fibrosis

Conflict of interest statement

CONFLICTS OF INTEREST No potential conflicts of interest were disclosed.

References

  1. Oncogene. 2007 Apr 26;26(19):2781-90 - PubMed
  2. Dig Dis. 2017;35(4):310-313 - PubMed
  3. Kidney Int. 2013 Dec;84(6):1166-75 - PubMed
  4. J Clin Invest. 2005 Feb;115(2):209-18 - PubMed
  5. Gastroenterology. 2008 May;134(6):1655-69 - PubMed
  6. PLoS One. 2015 Mar 31;10 (3):e0122758 - PubMed
  7. Ann N Y Acad Sci. 2012 Oct;1269:61-8 - PubMed
  8. Lancet. 2008 Mar 8;371(9615):838-51 - PubMed
  9. Cell Physiol Biochem. 2014;34(2):356-67 - PubMed
  10. J Natl Cancer Inst. 2003 Nov 19;95(22):1674-80 - PubMed
  11. Trends Mol Med. 2005 Sep;11(9):421-9 - PubMed
  12. Physiol Rev. 2008 Jan;88(1):125-72 - PubMed
  13. Oncotarget. 2015 Mar 30;6(9):7325-38 - PubMed
  14. Hepatology. 2009 Oct;50(4):1294-306 - PubMed

Publication Types