Abstract 2056 Insulin Receptor Regulates Cell Growth Rate and TGFβ-Induced Transcriptional Responsiveness and Kinase Activities in Human Hepatic Stellate Cells

The hepatic stellate cell (HSC) is the cell type that promotes liver fibrosis development. Insulin stimulation's role in regulating HSC fibrogenesis activity, and the insulin receptor (INSR) in HSC responsiveness to fibrotic environment is not completely understood. We hypothesized that INSR would be inhibitory to HSC activation during liver fibrosis. This was derived from the use of insulin-sensitizing medications that are used to treat liver fibrosis. To study this hypothesis, we removed a small portion of the INSR with CRISPR Cas9 technology, essential for insulin signaling in a human HSC LX2 cell line.

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Publication Details

Journal
Journal of Biological Chemistry
Published
2025-05-01
DOI
https://doi.org/10.1016/j.jbc.2025.109505
Primary Topic
Liver Disease Diagnosis and Treatment
Type
article
Field-Weighted Citation Impact
0.00
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Abstract 2056 Insulin Receptor Regulates Cell Growth Rate and TGFβ-Induced Transcriptional Responsiveness and Kinase Activities in Human Hepatic Stellate Cells

Genesee Martinez, Evelyn Bates, Terry D. Hinds, Wang‐Hsin Lee et al.
Journal of Biological Chemistry
Liver Disease Diagnosis and Treatment
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Abstract 2056 Insulin Receptor Regulates Cell Growth Rate and TGFβ-Induced Transcriptional Responsiveness and Kinase Activities in Human Hepatic Stellate Cells

Genesee Martinez, Evelyn Bates, Terry D. Hinds, Wang‐Hsin Lee, Zachary Kipp, Sally Pauss, Mei Xu
article en

Abstract

The hepatic stellate cell (HSC) is the cell type that promotes liver fibrosis development. Insulin stimulation's role in regulating HSC fibrogenesis activity, and the insulin receptor (INSR) in HSC responsiveness to fibrotic environment is not completely understood. We hypothesized that INSR would be inhibitory to HSC activation during liver fibrosis. This was derived from the use of insulin-sensitizing medications that are used to treat liver fibrosis. To study this hypothesis, we removed a small portion of the INSR with CRISPR Cas9 technology, essential for insulin signaling in a human HSC LX2 cell line.

Journal of Biological ChemistryVol. 301(5)
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Liver Disease Diagnosis and Treatment
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