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TRPA1 Promotes Cardiac Myofibroblast Transdifferentiation after Myocardial Infarction Injury via the Calcineurin-NFAT-DYRK1A Signaling Pathway
المؤلفون المشاركون
Chen, Jiangwei
Yang, Dachun
Li, De
Yang, Yongjian
Wang, Xin.
Wu, Hao
Gao, Erhe
Li, Shuang
Sun, Xiongshan
Yu, Peng
Jiang, Zhenhua
Qiu, Chenming
Song, Baomei
Chen, Ken
He, Kecheng
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2019، العدد 2019 (31 ديسمبر/كانون الأول 2019)، ص ص. 1-17، 17ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2019-05-14
دولة النشر
مصر
عدد الصفحات
17
التخصصات الرئيسية
الملخص EN
Cardiac fibroblasts (CFs) are a critical cell population responsible for myocardial extracellular matrix homeostasis.
After stimulation by myocardial infarction (MI), CFs transdifferentiate into cardiac myofibroblasts (CMFs) and play a fundamental role in the fibrotic healing response.
Transient receptor potential ankyrin 1 (TRPA1) channels are cationic ion channels with a high fractional Ca2+ current, and they are known to influence cardiac function after MI injury; however, the molecular mechanisms regulating CMF transdifferentiation remain poorly understood.
TRPA1 knockout mice, their wild-type littermates, and mice pretreated with the TRPA1 agonist cinnamaldehyde (CA) were subjected to MI injury and monitored for survival, cardiac function, and fibrotic remodeling.
TRPA1 can drive myofibroblast transdifferentiation initiated 1 week after MI injury.
In addition, we explored the underlying mechanisms via in vitro experiments through gene transfection alone or in combination with inhibitor treatment.
TRPA1 overexpression fully activated CMF transformation, while CFs lacking TRPA1 were refractory to transforming growth factor β- (TGF-β-) induced transdifferentiation.
TGF-β enhanced TRPA1 expression, which promoted the Ca2+-responsive activation of calcineurin (CaN).
Moreover, dual-specificity tyrosine-regulated kinase-1a (DYRK1A) regulated CaN-mediated NFAT nuclear translocation and TRPA1-dependent transdifferentiation.
These findings suggest a potential therapeutic role for TRPA1 in the regulation of CMF transdifferentiation in response to MI injury and indicate a comprehensive pathway driving CMF formation in conjunction with TGF-β, Ca2+ influx, CaN, NFATc3, and DYRK1A.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Li, Shuang& Sun, Xiongshan& Wu, Hao& Yu, Peng& Wang, Xin.& Jiang, Zhenhua…[et al.]. 2019. TRPA1 Promotes Cardiac Myofibroblast Transdifferentiation after Myocardial Infarction Injury via the Calcineurin-NFAT-DYRK1A Signaling Pathway. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-17.
https://search.emarefa.net/detail/BIM-1204610
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Li, Shuang…[et al.]. TRPA1 Promotes Cardiac Myofibroblast Transdifferentiation after Myocardial Infarction Injury via the Calcineurin-NFAT-DYRK1A Signaling Pathway. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-17.
https://search.emarefa.net/detail/BIM-1204610
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Li, Shuang& Sun, Xiongshan& Wu, Hao& Yu, Peng& Wang, Xin.& Jiang, Zhenhua…[et al.]. TRPA1 Promotes Cardiac Myofibroblast Transdifferentiation after Myocardial Infarction Injury via the Calcineurin-NFAT-DYRK1A Signaling Pathway. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-17.
https://search.emarefa.net/detail/BIM-1204610
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1204610
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
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