Báo cáo y học: "Inorganic pyrophosphate generation by transforming growth factor-beta-1 is mainly dependent on ANK induction by Ras/Raf-1/extracellular signal-regulated kinase pathways in chondrocytes"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: Inorganic pyrophosphate generation by transforming growth factor-beta-1 is mainly dependent on ANK induction by Ras/Raf-1/extracellular signal-regulated kinase pathways in chondrocytes. | Available online http content 9 6 R1 22 Research article Inorganic pyrophosphate generation by transforming growth factor-beta-1 is mainly dependent on ANK induction by Ras Raf-1 extracellular signal-regulated kinase pathways in chondrocytes Frederic Cailotto Arnaud Bianchi Sylvie Sebillaud Narayanan Venkatesan David Moulin Jean-Yves Jouzeau and Patrick Netter Open Access UMR 7561 CNRS-Nancy-Université Laboratoire de Physiopathologie et Pharmacologie Articulaires LPPA and Faculte de Médecine Avenue de la forêt de Haye BP184 54505 Vandreuvre-Lès-Nancy France Corresponding author Arnaud Bianchi Received 21 Sep 2007 Revisions requested 22 Oct 2007 Revisions received 12 Nov 2007 Accepted 22 Nov 2007 Published 22 Nov 2007 Arthritis Research Therapy 2007 9 R122 doi ar2330 This article is online at http content 9 6 R1 22 2007 Cailotto et al. licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract ANK is a multipass transmembrane protein transporter thought to play a role in the export of intracellular inorganic pyrophosphate and so to contribute to the pathophysiology of chondrocalcinosis. As transforming growth factor-beta-1 TGF-P1 was shown to favor calcium pyrophosphate dihydrate deposition we investigated the contribution of ANK to the production of extracellular inorganic pyrophosphate ePPi by chondrocytes and the signaling pathways involved in the regulation of Ank expression by TGF-P1. Chondrocytes were exposed to 10 ng mL of TGF-P1 and Ank expression was measured by quantitative polymerase chain reaction and Western blot. ePPi was quantified in cell supernatants. RNA silencing was used to define the respective roles of Ank and PC-1

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