國家衛生研究院 NHRI:Item 3990099045/16123
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    题名: Role of hIF-1alpha-activated IL-22/IL-22R1/Bmi1 signaling modulates the self-renewal of cardiac stem cells in acute myocardial ischemia
    其它题名: Role of HIF-1α-activated IL-22/IL-22R1/Bmi1 signaling modulates the self-renewal of cardiac stem cells in acute myocardial ischemia
    作者: Lee, W;Lin, SL;Chiang, CS;Chen, JY;Chieng, WW;Huang, SR;Chang, TY;Yen, BL;Hung, MC;Chang, KC;Lee, HT;Jeng, LB;Shyu, WC
    贡献者: Institute of Cellular and Systems Medicine
    摘要: Impaired tissue regeneration negatively impacts on left ventricular (LV) function and remodeling after acute myocardial infarction (AMI). Little is known about the intrinsic regulatory machinery of ischemia-induced endogenous cardiac stem cells (eCSCs) self-renewing divisions after AMI. The interleukin 22 (IL-22)/IL-22 receptor 1 (IL-22R1) pathway has emerged as an important regulator of several cellular processes, including the self-renewal and proliferation of stem cells. However, whether the hypoxic environment could trigger the self-renewal of eCSCs via IL-22/IL-22R1 activation remains unknown. In this study, the upregulation of IL-22R1 occurred due to activation of hypoxia-inducible factor-1 alpha (HIF-1 alpha) under hypoxic and ischemic conditions. Systemic IL-22 administration not only attenuated cardiac remodeling, inflammatory responses, but also promoted eCSC-mediated cardiac repair after AMI. Unbiased RNA microarray analysis showed that the downstream mediator Bmi1 regulated the activation of CSCs. Therefore, the HIF-1 alpha-induced IL-22/IL-22R1/Bmi1 cascade can modulate the proliferation and activation of eCSCs in vitro and in vivo. Collectively, investigating the HIF-1 alpha-activated IL-22/IL-22R1/Bmi1 signaling pathway might offer a new therapeutic strategy for AMI via eCSC-induced cardiac repair.
    日期: 2024-09-12
    關聯: Stem Cell Reviews and Reports. 2024 Sep 12;Article in Press.
    Link to: http://dx.doi.org/10.1007/s12015-024-10774-8
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=2629-3269&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:001310642500001
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85203718524
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