Hypoxia- and mechanical stress–induced upregulation of mitochondrial HSP60 is associated with phenotypic switching of pulmonary arterial smooth muscle cells

Liu, Geng

doi:https://doi.org/10.1016/j.cstres.2025.100089

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Hypoxia- and mechanical stress–induced upregulation of mitochondrial HSP60 is associated with phenotypic switching of pulmonary arterial smooth muscle cells

http://hdl.handle.net/10069/0002003420

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KISYK56_Liu.pdf (2 MB)

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学位論文 / Thesis or Dissertation(1)

公開日

2025-11-18

タイトル

Hypoxia- and mechanical stress–induced upregulation of mitochondrial HSP60 is associated with phenotypic switching of pulmonary arterial smooth muscle cells

言語

eng

キーワード

言語

主題Scheme

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主題

Pulmonary arterial hypertension

キーワード

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主題

Smooth muscle cells

キーワード

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主題

Hypoxia

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Mechanical stress

キーワード

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主題

HSP60

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資源タイプ識別子

http://purl.org/coar/resource_type/c_db06

資源タイプ

doctoral thesis

アクセス権

open access

アクセス権URI

http://purl.org/coar/access_right/c_abf2

著者

Liu, Geng

抄録

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Abstract

内容記述

Background: Switching from a contractile to a synthetic phenotype of pulmonary arterial smooth muscle cells (PASMCs) is known to play a crucial role in pulmonary arterial hypertension (PAH). We investigated how hypoxia and mechanical stress mediate the phenotypic switching of PASMCs. Methods: Human PASMCs were used for experiments. Hypoxia treatment was done by culturing cells under 1% O₂. Mechanical stress was induced by loading cells to 50 mmHg hydrostatic pressure. We analyzed cell morphology, cell proliferation, phenotypic marker protein expression, cytokine release, and the activation of stress-related pathways at 24 h after treatment. Bulk and single-cell RNA-sequencing datasets were used to analyze heat shock protein family D member 1 (HSPD1) expression in PAH lungs and PASMCs. Heat shock protein 60 (HSP60) was knocked down in PASMCs by transfection of HSPD1-siRNA. Results: Either hypoxia or mechanical stress alone induced the morphology change, increased cell proliferation, and promoted the phenotypic switching and inflammatory cytokines release of PASMCs. Interestingly, all those were dramatically enhanced under the combination of hypoxia and mechanical stress. Mechanistically, we found that the combination of hypoxia and mechanical stress not only significantly enhanced the mitochondrial HSP60 expression but also induced its partial redistribution to the cytosol. Bioinformatic analyses also confirmed the elevated HSPD1 expression in PAH lungs and PASMCs. HSP60 knockdown effectively attenuated the phenotypic switching of PASMCs induced by hypoxia and mechanical stress. Conclusion: Hypoxia- and mechanical stress-induced upregulation of mitochondrial HSP60 is associated with phenotypic switching of PASMCs.

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長崎大学学位論文学位記番号:共博(医歯薬)甲第56号学位授与年月日:令和7年9月19日

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Author: Geng Liu, Han Nie, Xu Zhang, Zi-Sheng Huang, Koh-Ichiro Yoshiura, Ke-Xiang Liu, Yi Liu, Tao-Sheng Li

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Citation: Cell Stress and Chaperones, 30(4), art. no. 100089; 2025

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書誌情報

en : Cell Stress and Chaperones

巻 30, 号 4, p. art. no. 100089, 発行日 2025-09-19

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収録物識別子

1466-1268

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Ver.1

2025-11-18 00:36:48.129319

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Hypoxia- and mechanical stress–induced upregulation of mitochondrial HSP60 is associated with phenotypic switching of pulmonary arterial smooth muscle cells

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Hypoxia- and mechanical stress–induced upregulation of mitochondrial HSP60 is associated with phenotypic switching of pulmonary arterial smooth muscle cells

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