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Aquaporin 1 confers apoptosis resistance in pulmonary arterial smooth muscle cells from the SU5416 hypoxia rat model.

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  • معلومة اضافية
    • المصدر:
      Publisher: published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society Country of Publication: United States NLM ID: 101607800 Publication Model: Print Cited Medium: Internet ISSN: 2051-817X (Electronic) Linking ISSN: 2051817X NLM ISO Abbreviation: Physiol Rep Subsets: MEDLINE
    • بيانات النشر:
      Original Publication: [Malden MA] : published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society, 2013-
    • الموضوع:
    • نبذة مختصرة :
      Pulmonary hypertension (PH) arises from increased pulmonary vascular resistance due to contraction and remodeling of the pulmonary arteries. The structural changes include thickening of the smooth muscle layer from increased proliferation and resistance to apoptosis. The mechanisms underlying apoptosis resistance in PH are not fully understood. In cancer cells, high expression of aquaporin 1 (AQP1), a water channel, is associated with apoptosis resistance. We showed AQP1 protein was expressed in pulmonary arterial smooth muscle cells (PASMCs) and upregulated in preclinical PH models. In this study, we used PASMCs isolated from control male rats and the SU5416 plus hypoxia (SuHx) model to test the role of AQP1 in modulating susceptibility to apoptosis. We found the elevated level of AQP1 in PASMCs from SuHx rats was necessary for resistance to apoptosis and that apoptosis resistance could be conferred by increasing AQP1 in control PASMCs. In exploring the downstream pathways involved, we found AQP1 levels influence the expression of Bcl-2, with enhanced AQP1 levels corresponding to increased Bcl-2 expression, reducing the ratio of BAX to Bcl-2, consistent with apoptosis resistance. These results provide a mechanism by which AQP1 can regulate PASMC fate.
      (© 2024 The Author(s). Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.)
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    • Grant Information:
      HL126514 HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI); 23PRE1022720 American Heart Association (AHA); F32 HL165766 United States HL NHLBI NIH HHS; R01 HL159906 United States HL NHLBI NIH HHS; R01 HL073859 United States HL NHLBI NIH HHS; R01 HL126514 United States HL NHLBI NIH HHS; 18POST34030262 American Heart Association (AHA); T32 HL007534 United States HL NHLBI NIH HHS
    • Contributed Indexing:
      Keywords: cell death; lung; pulmonary hypertension; remodeling
    • الرقم المعرف:
      146410-94-8 (Aquaporin 1)
      0 (Aqp1 protein, rat)
      71IA9S35AJ (Semaxinib)
      0 (Pyrroles)
      0 (Indoles)
      0 (Proto-Oncogene Proteins c-bcl-2)
    • الموضوع:
      Date Created: 20240822 Date Completed: 20240822 Latest Revision: 20241003
    • الموضوع:
      20241003
    • الرقم المعرف:
      PMC11341275
    • الرقم المعرف:
      10.14814/phy2.16156
    • الرقم المعرف:
      39175041