ArticleThe Kaohsiung journal of medical sciences2020
Role of phosphatidylinositol 3-kinase signaling pathway in radiation-induced liver injury.
Article in The Kaohsiung journal of medical sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 6 citations in OpenAlex.
- Contribution of immune cells and cytokines to radiation-induced injury: the key roles and potential targets.Frontiers in immunology · 2026Review
- VIM model: a novel model to depict the spatial heterogeneity of the radiation microenvironment.International journal of medical sciences · 2025Review
- Radiation-Induced Liver Injury: An Overview.Journal of hepatocellular carcinoma · 2025Review
- Radiation-induced liver disease: beyond DNA damage.Cell cycle (Georgetown, Tex.) · 2023Review
- Radiation-induced liver injury and hepatocyte senescence.Cell death discovery · 2021Review
- Role of phosphatidylinositol 3-kinase signaling pathway in radiation-induced liver injury.The Kaohsiung journal of medical sciences · 2020Article
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8 authors at 1 institution in 1 country.
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Abstract
Transforming growth factor-β1 (TGF-β1) is one of critical cytokines in radiation-induced liver injury. Hepatic stellate cells (HSC) are activated in the early stage of radiation-induced liver injury. However, it is currently unclear whether phosphatidylinositol 3-kinase (PI3K/Akt) signal pathway is activated in radiation-induced liver injury. Herein, male Sprague-Dawley rats were irradiated with 6 MV X-rays (30 Gy) on the right liver. Next, Hematoxylin and eosin staining, Masson staining, and electron microscopy were performed to examine pathological changes. Immunohistochemistry was performed to assess the expression of TGF-β1, α-SMA, and p-Akt (S473) in liver tissues. In vitro, rat HSC cell line HSC-T6 cells were given different doses of 6 MV X-ray irradiation (10 and 20 Gy) and treated with LY294002. The expression of α-SMA and p-Akt in mRNA and protein levels were measured by reverse transcription-polymerase chain reactioin (RT-PCR) and Western blot. TGF-β1 expression was detected by enzyme-linked immuno sorbent assay (ELISA). After irradiation, the liver tissues showed obvious pathological changes, indicating the establishment of the radiation-induced liver injury. Expression levels of TGF-β1, α-SMA, and p-Akt (S473) protein in liver tissues were significantly increased after irradiation, and this increase was in a time-dependent manner, suggesting the activation of HSC and PI3K/Akt signal pathway. in vitro experiments showed that the TGF-β1 secreted by HSCs, and the expression of Akt and α-SMA at mRNA and protein levels were significantly increased in irradiation groups. However, the expression of TGF-β1, Akt, and α-SMA were significantly decreased in PI3K/Akt signal pathway inhibitor LY294002-treated group. Our results suggest that during radiation-induced liver injury, HSCs are activated by TGF-β1-mediated PI3K/Akt signal pathway.
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