کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10759313 | 1050420 | 2013 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Arginase inhibition reduces interleukin-1β-stimulated vascular smooth muscle cell proliferation by increasing nitric oxide synthase-dependent nitric oxide production
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کلمات کلیدی
DMEMdiethylenetriamine NONOateDETA NONOateRASMCODQVSMC8-Br-cGMPS-nitrosoglutathioneGSNOnNOSIL-1βeNOSBECcGMPRT-PCRiNOS1400W - 1400 واتDulbecco’s modified Eagle medium - Modified Eagle اصلاح شده DulbeccoArginase - آرژینازAntisense - آنتیسنسInterleukin-1β - اینترلوکین-1βProliferation - ترویجRat aortic smooth muscle cell - سلول عضله صاف آئورت موشVascular smooth muscle cells - سلول های عضلانی صاف عروقیinducible nitric oxide synthase - سنتاز اکسید نیتریک القاییendothelial nitric oxide synthase - سنتاز اکسید نیتریک اندوتلیالneuronal nitric oxide synthase - سنتاز اکسید نیتریک عصبیcyclic guanosine monophosphate - مونوفسفات گوانوزین چرخه ایreverse transcription polymerase chain reaction - واکنش زنجیره ای پلیمراز رونویسی معکوس
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
We investigated whether arginase inhibition suppressed interleukin (IL)-1β-stimulated proliferation in vascular smooth muscle cells (VSMCs) and the possible mechanisms involved. IL-1β stimulation increased VSMC proliferation, while the arginase inhibitor BEC and transfection of the antisense (AS) oligonucleotide against arginase I decreased VSMC proliferation and was associated with increased protein content of the cell cycle regulator p21Waf1/Cip1. IL-1β incubation induced inducible nitric oxide synthase (iNOS) mRNA expression and protein levels in a dose-dependent manner, but did not affect arginase I and II expression. Consistent with this data, IL-1β stimulation resulted in increase in NO production that was significantly augmented by arginase inhibition. The specific iNOS inhibitor 1400W abolished IL-1β-mediated NO production and further accentuated IL-1β-stimulated cell proliferation. Incubation with NO donors GSNO and DETA/NO in the presence of IL-1β abolished VSMCs proliferation and increased p21Waf1/Cip1 protein content. Furthermore, incubation with the cGMP analogue 8-Br-cGMP prevented IL-1β-induced VSMCs proliferation. In conclusion, arginase inhibition augmented iNOS-dependent NO production that resulted in suppression of IL-1β-induced VSMCs proliferation in a cGMP-dependent manner.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 435, Issue 3, 7 June 2013, Pages 428-433
Journal: Biochemical and Biophysical Research Communications - Volume 435, Issue 3, 7 June 2013, Pages 428-433
نویسندگان
Jeongyeon Yoon, Sungwoo Ryoo,