抑制脑周细胞中转化生长因子-β 的产生会导致环孢素 A 诱导的血脑屏障功能障碍。
Inhibition of transforming growth factor-beta production in brain pericytes contributes to cyclosporin A-induced dysfunction of the blood-brain barrier.
作者信息
Takata Fuyuko, Dohgu Shinya, Yamauchi Atsushi, Sumi Noriko, Nakagawa Shinsuke, Naito Mikihiko, Tsuruo Takashi, Shuto Hideki, Kataoka Yasufumi
机构信息
Department of Pharmaceutical Care and Health Sciences, Faculty of Pharmaceutical Sciences, Fukuoka University, Jonan-ku, Fukuoka 814-0180, Japan.
出版信息
Cell Mol Neurobiol. 2007 May;27(3):317-28. doi: 10.1007/s10571-006-9125-x. Epub 2006 Dec 28.
Abstract
: 1. The present study was designed to clarify whether brain pericytes and pericyte-derived transforming growth factor-beta1 (TGF-beta1) participate in cyclosporin A (CsA)-induced dysfunction of the blood-brain barrier (BBB).2. The presence of brain pericytes markedly aggravated CsA-increased permeability of MBEC4 cells to sodium fluorescein and accumulation of rhodamine 123 in MBEC4 cells.3. Exposure to CsA significantly decreased the levels of TGF-beta1 mRNA in brain pericytes in pericyte co-cultures. Treatment with TGF-beta1 dose-dependently inhibited CsA-induced hyperpermeability and P-glycoprotein dysfunction of MBEC4 cells in pericyte co-cultures.4. These findings suggest that an inhibition of brain pericyte-derived TGF-beta1 contributes to the occurrence of CsA-induced dysfunction of the BBB.
摘要
本研究旨在阐明脑周细胞和周细胞源性转化生长因子-β1（TGF-β1）是否参与环孢素A（CsA）诱导的血脑屏障（BBB）功能障碍。
脑周细胞的存在显著加重了CsA增加MBEC4细胞对荧光素钠的通透性以及罗丹明123在MBEC4细胞中的蓄积。
暴露于CsA可显著降低周细胞共培养体系中脑周细胞TGF-β1 mRNA的水平。用TGF-β1处理可剂量依赖性地抑制周细胞共培养体系中CsA诱导的MBEC4细胞高通透性和P-糖蛋白功能障碍。
这些发现表明，抑制脑周细胞源性TGF-β1有助于CsA诱导的BBB功能障碍的发生。
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