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Rapamycin Improves Palmitate-Induced ER StressNFκB Pathways Associated with Stimulating Autophagy in Adipocytes
المؤلفون المشاركون
Yin, Jiajing
Gu, Liping
Wang, Yufan
Fan, Nengguang
Ma, Yuhang
Peng, Yongde
المصدر
العدد
المجلد 2015، العدد 2015 (31 ديسمبر/كانون الأول 2015)، ص ص. 1-12، 12ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2015-01-14
دولة النشر
مصر
عدد الصفحات
12
التخصصات الرئيسية
الملخص EN
Obesity-induced endoplasmic reticulum (ER) stress and inflammation lead to adipocytes dysfunction.
Autophagy helps to adapt to cellular stress and involves in regulating innate inflammatory response.
In present study, we examined the activity of rapamycin, a mTOR kinase inhibitor, against endoplasmic reticulum stress and inflammation in adipocytes.
An in vitro model was used in which 3T3-L1 adipocytes were preloaded with palmitate (PA) to generate artificial hypertrophy mature adipocytes.
Elevated autophagy flux and increased number of autophagosomes were observed in response to PA and rapamycin treatment.
Rapamycin attenuated PA-induced PERK and IRE1-associated UPR pathways, evidenced by decreased protein levels of eIF2α phosphorylation, ATF4, CHOP, and JNK phosphorylation.
Inhibiting autophagy with chloroquine (CQ) exacerbated these ER stress markers, indicating the role of autophagy in ameliorating ER stress.
In addition, cotreatment of CQ abolished the anti-ER stress effects of rapamycin, which confirms the effect of rapamycin on ERs is autophagy-dependent.
Furthermore, rapamycin decreased PA-induced nuclear translocation of NFκB P65 subunit, thereby NFκB-dependent inflammatory cytokines MCP-1 and IL-6 expression and secretion.
In conclusion, rapamycin attenuated PA-induced ER stress/NFκB pathways to counterbalance adipocytes stress and inflammation.
The beneficial of rapamycin in this context partly depends on autophagy.
Stimulating autophagy may become a way to attenuate adipocytes dysfunction.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Yin, Jiajing& Gu, Liping& Wang, Yufan& Fan, Nengguang& Ma, Yuhang& Peng, Yongde. 2015. Rapamycin Improves Palmitate-Induced ER StressNFκB Pathways Associated with Stimulating Autophagy in Adipocytes. Mediators of Inflammation،Vol. 2015, no. 2015, pp.1-12.
https://search.emarefa.net/detail/BIM-1072220
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Yin, Jiajing…[et al.]. Rapamycin Improves Palmitate-Induced ER StressNFκB Pathways Associated with Stimulating Autophagy in Adipocytes. Mediators of Inflammation No. 2015 (2015), pp.1-12.
https://search.emarefa.net/detail/BIM-1072220
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Yin, Jiajing& Gu, Liping& Wang, Yufan& Fan, Nengguang& Ma, Yuhang& Peng, Yongde. Rapamycin Improves Palmitate-Induced ER StressNFκB Pathways Associated with Stimulating Autophagy in Adipocytes. Mediators of Inflammation. 2015. Vol. 2015, no. 2015, pp.1-12.
https://search.emarefa.net/detail/BIM-1072220
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1072220
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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تقوم هذه الخدمة بالتحقق من التشابه أو الانتحال في الأبحاث والمقالات العلمية والأطروحات الجامعية والكتب والأبحاث باللغة العربية، وتحديد درجة التشابه أو أصالة الأعمال البحثية وحماية ملكيتها الفكرية. تعرف اكثر
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