The authors used rat liver-derived hepatocytes injured by CCl4 treatment in co-culture system with Vitamin E pretreated-Wharton’s jelly-derived MSCs (WJMSCs) to evaluate the hepatoprotective effect of vitamin E-WJMSCs.
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Tayyab Baig, M., Ghufran, H., Mehmood, A., Azam, M., Humayun, S., & Riazuddin, S. (2021). Vitamin E pretreated Wharton’s jelly-derived mesenchymal stem cells attenuate CCl4-induced hepatocyte injury in vitro and liver fibrosis in vivo. Biochemical Pharmacology, 114480. https://doi.org/10.1016/j.bcp.2021.114480 Cite
Investigators discuss the role of platelets in liver fibrosis and accompanying hemostatic disorders. They present the results of animal and human studies on antiplatelet drugs in liver disorders and their potential therapeutic utility.
To mimic liver fibrosis in vitro, LX-2 cells were treated with TGF-β. Gene and protein expressions were detected by RT-qPCR and western blot, respectively.
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The authors summarize findings indicating that the dysregulation of stress kinases plays a fundamental role in the development of steatosis and are important players inducing liver fibrosis.
Investigators systematically analyzed proteomics of decellularized hepatic matrix and identified four unique clusters of ECM proteins at tissue damage/inflammation, transitional ECM remodeling or fibrogenesis stage in carbon tetrachloride-induced liver fibrosis.
[Cell Death & Disease]
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While hepatocyte-specific c-jun deletion led to increased fibrosis, the opposite outcome was observed when c-jun was deleted in both hepatocytes and Kupffer cells.
[Life Science Alliance]
Researchers showed that hepatic macrophages expressed the primary relaxin receptor, and that, on relaxin binding, they switch from the profibrogenic to the pro-resolution phenotype.
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The structural information of the insulin-like growth factor 2 receptor (IGF2R), an overexpressed protein on activated hepatic stellate cells, were used for an in silico screening of novel IGF2R-specific peptide ligands.
[Journal of Materials Chemistry B]
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Weber, F., Casalini, T., Valentino, G., Brülisauer, L., Andreas, N., Koeberle, A., Kamradt, T., Contini, A., & Luciani, P. (2021). Targeting transdifferentiated hepatic stellate cells and monitoring the hepatic fibrogenic process by means of IGF2R-specific peptides designed in silico. Journal of Materials Chemistry B. https://doi.org/10.1039/D0TB02372H Cite
Stem cells from human exfoliated deciduous teeth-derived hepatocytes were intrasplenically transplanted into chronically CCl4-treated liver fibrosis model mice, followed by the analysis of donor integration and hepatobiliary metabolism in vivo.
[Current Stem Cell Research & Therapy]
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Yuniartha, R., Yamaza, T., Sonoda, S., Yoshimaru, K., Matsuura, T., Yamaza, H., Oda, Y., Ohga, S., & Taguchi, T. (2021). Cholangiogenic potential of human deciduous pulp stem cell-converted hepatocyte-like cells. Stem Cell Research & Therapy, 12(1), 57. https://doi.org/10.1186/s13287-020-02113-8 Cite
Hepatic stellate cell (HSC)‐T6 cells were activated by interleukin-1 beta and then treated with helenalin. HSC‐T6 cells were transfected with miR-200a mimic or inhibitor, and the effect of helenalin on the miR-200a-mediated PI3K/Akt and NF-κB signaling pathways was investigated.
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Fang, B., Wen, S., Li, Y., Bai, F., Wei, Y., Xiong, Y., Huang, Q., & Lin, X. (2021). Prediction and verification of target of helenalin against hepatic stellate cell activation based on miR-200a-mediated PI3K/Akt and NF-κB pathways. International Immunopharmacology, 92, 107208. https://doi.org/10.1016/j.intimp.2020.107208 Cite
Integrin α‐subunits were investigated systematically for their expression over the course of hepatic stellate cells activation and their distribution on fibroblasts and other systemic primary cells.
[Journal of Pathology]
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Nishimichi, N., Tsujino, K., Kanno, K., Sentani, K., Kobayashi, T., Chayama, K., Sheppard, D., & Yokosaki, Y. (n.d.). Induced hepatic stellate cell integrin, α8β1, enhances cellular contractility and TGFβ activity in liver fibrosis. The Journal of Pathology, n/a(n/a). https://doi.org/https://doi.org/10.1002/path.5618 Cite