Upregulation of T-type Ca<sup>2+</sup> channels expression following phenotype switch of mouse hepatic stellate cells.
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- Kawata Naoki
- Dept. Mol. Cell. Pharmacol., Grad. Sch. Pharmaceut. Sci., Nagoya City Univ.
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- Kondo Rubii
- Dept. Mol. Cell. Pharmacol., Grad. Sch. Pharmaceut. Sci., Nagoya City Univ.
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- Suzuki Yoshiaki
- Dept. Mol. Cell. Pharmacol., Grad. Sch. Pharmaceut. Sci., Nagoya City Univ.
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- Yamamura Hisao
- Dept. Mol. Cell. Pharmacol., Grad. Sch. Pharmaceut. Sci., Nagoya City Univ.
Bibliographic Information
- Other Title
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- マウス肝星細胞の形質転換に伴うT型Ca<sup>2+</sup>チャネルの発現増加
Abstract
<p>Hepatic stellate cells (HSCs) are largely involved in hepatic fibrosis associated with liver diseases such as non-alcoholic steatohepatitis. An increase in cytosolic [Ca2+] in HSCs facilitates hepatic fibrosis, however, the regulatory mechanism is unclear. T-type voltage-dependent Ca2+ channels (T-VDCCs) contribute to neuronal transmission and cardiac rhythm in excitable cells. Recently, the pathophysiological roles of T-VDCCs in non-excitable cells such as cancer cells and immune cells have been focused. Under whole-cell patch-clamp configurations, transient inward currents were observed in mouse activated HSCs, but not in quiescent HSCs. Quantitative real-time PCR analysis revealed that the mRNA expression of T-VDCCs was significantly higher in activated HSCs than in quiescent HSCs. The viability of activated HSCs was significantly reduced by the treatment with T-VDCC inhibitors. These results suggest that the upregulation of T-VDCC expression in activated HSCs contributes to the regulation of Ca2+ signaling and cell proliferation. This study may contribute to the comprehensive understanding of HSC functions in hepatic fibrosis.</p>
Journal
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- Proceedings for Annual Meeting of The Japanese Pharmacological Society
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Proceedings for Annual Meeting of The Japanese Pharmacological Society 97 (0), 1-B-SS03-3-, 2023
Japanese Pharmacological Society
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Keywords
Details 詳細情報について
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- CRID
- 1390861692692344064
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- ISSN
- 24354953
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- Text Lang
- ja
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- Data Source
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- JaLC
- Crossref
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- Abstract License Flag
- Disallowed