کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5589661 | 1569809 | 2017 | 30 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
GATA4 and LMO3 balance angiocrine signaling and autocrine inflammatory activation by BMP2 in liver sinusoidal endothelial cells
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کلمات کلیدی
GATA4HUVECqRT-PCRkiloDaltonkDacDNA - cDNAComplementary DNA - DNA تکمیلیMouse hepatocytes - hepatocytes ماوسLSEC - lseceempty vector - بردار خالیfold change - تغییر در برابرGene regulation - تنظیم ژنMicroarray - ریزآرایهliver sinusoidal endothelial cell - سلول اندوتلیال سینوسی کبدیEndothelial cell - سلول های اندوتلیالHuman umbilical vein endothelial cells - سلول های اندوتلیالی ورید ناف انسانEndothelial cells - سلولهای اندوتلیالMHC - مجموعه سازگاری بافتی اصلیquantitative reverse-transcription polymerase chain reaction - واکنش زنجیره ای پلیمراز کمی معکوس رونویسیWestern blot - وسترن بلاتbone morphogenetic protein (BMP) - پروتئین مورفوژنیک استخوان (BMP)
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
ژنتیک
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Liver sinusoidal endothelial cells (LSEC) represent a unique, organ-specific type of discontinuous endothelial cells. LSEC instruct the hepatic vascular niche by paracrine-acting angiocrine factors. Recently, we have shown that LSEC-specific transcriptional regulator GATA4 induces expression of BMP2 in cultured endothelial cells (EC) in vitro. Furthermore, angiocrine Bmp2 signaling in the liver in vivo was demonstrated to control iron homeostasis. Here, we investigated GATA4-dependent autocrine BMP2 signaling in endothelial cells by gene expression profiling. GATA4 induced a large cluster of inflammatory endothelial response genes in cultured EC, which is similar to previously identified virus-induced and interferon-associated responses. Treating the cells with the BMP2 inhibitor Noggin counter-regulated the GATA4-dependent inflammatory phenotype of EC, indicating that BMP2 is indeed the major driver. In contrast to continuous EC, LSEC were less prone to activation by BMP2. Notably, GATA4-dependent induction of the inflammatory EC response gene cluster was attenuated by over-expression of the LSEC-specific transcriptional modifier LMO3 while hepatocyte activation was fully preserved, indicating conserved BMP2 synthesis. In summary, our data suggest that transcriptional counter-regulation by GATA4 and LMO3 in LSEC prevents autocrine induction of an inflammatory phenotype, while maintaining angiocrine BMP2-mediated cell-cell communication in the liver vascular niche.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gene - Volume 627, 5 September 2017, Pages 491-499
Journal: Gene - Volume 627, 5 September 2017, Pages 491-499
نویسندگان
Victor Olsavszky, Friederike Ulbrich, Sandhya Singh, Miriam Diett, Carsten Sticht, Christian David Schmid, Johanna Zierow, Sebastian A. Wohlfeil, Kai Schledzewski, Steven Dooley, Haristi Gaitantzi, Katja Breitkopf-Heinlein, Cyrill Géraud, Sergij Goerdt,