کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5860323 | 1133178 | 2014 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
SIRT4 inhibits cigarette smoke extracts-induced mononuclear cell adhesion to human pulmonary microvascular endothelial cells via regulating NF-κB activity
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
IL-1βSIRT4HEK-293VCAM-1NF-κBDAPICSERT-PCRFBSIL-64′,6-diamidino-2-phenylindole - 4 '، 6-دیامیدینو-2-فنیلینولinterleukin 6 - اینترلوکین 6interleukin-1b - اینترلوکین-1bCOPD - بیماری مزمن انسدادی ریهChronic obstructive pulmonary disease - بیماری مزمن انسدادی ریهfetal bovine serum - سرم جنین گاوHuman pulmonary microvascular endothelial cells - سلولهای اندوتلیال میکروواسکولار ریه انسانtumor necrosis factor-a - عامل نکروز تومور- acigarette smoke extract - عصاره سیگار سیگارTNF-α - فاکتور نکروز توموری آلفاcigarette smoking - مصرف سیگارvascular cell adhesion molecule-1 - مولکول چسبندگی سلولی عروقی-1Real time polymerase chain reaction - واکنش زنجیره ای پلیمراز واقعی در زمان واقعیMonocyte adhesion - چسبندگی مونوسیتhuman embryonic kidney 293 - کلیه جنینی انسان 293
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Cigarette smoking is an important risk factor for chronic obstructive pulmonary disease (COPD), yet its pathogenic mechanisms are not yet fully understood. Endothelial dysfunction is known to be involved in the pathogenesis of COPD. A detailed understanding of the mechanism involved in its progression would have a substantial impact on the optimization and development of treatment strategies. Here, we report that the expression of SIRT4, a mitochondrial sirtuin, is markedly down-regulated in cigarette smoke extract (CSE)-treated human pulmonary microvascular endothelial cells (HPMECs). Overexpression of SIRT4 significantly inhibits CSE-induced mononuclear cell adhesion to HPMECs. Consistently, we found that overexpression of SIRT4 attenuates the induction of vascular cell adhesion molecule 1 (VCAM-1) and E-selectin. Importantly, SIRT4 was found to negatively regulate CSE-induced NF-κB activation via inhibiting the degradation of IκBα. Moreover, we also found that proinflammatory cytokines interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and IL-6, the downstream target genes of NF-κB, are also inhibited by overexpression of SIRT4. These results suggest that SIRT4 protects HPMECs exposed to CSE stress via a mechanism that may involve the NF-κB pathway. Strategies based on the enhancement of SIRT4 may prove to be beneficial in the treatment of cigarette smoking caused COPD.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology Letters - Volume 226, Issue 3, 2 May 2014, Pages 320-327
Journal: Toxicology Letters - Volume 226, Issue 3, 2 May 2014, Pages 320-327
نویسندگان
Yongfeng Chen, Haijing Wang, Guangming Luo, Xiaotian Dai,