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International Journal Of Bilogical Sciences

.: Home > International Journal Of Bilogical Sciences > 2015 > Volume 11 Number 8 > Junjun Yang, 1, Huan Sun, 1, Jihang Zhang2, Mingdong Hu1, Jianchun Wang1, Guangyu Wu3, Guansong Wang1

Regulation of β-Adrenergic Receptor Trafficking and Lung Microvascular Endothelial Cell Permeability by Rab5 GTPase

Junjun Yang, 1, Huan Sun, 1, Jihang Zhang2, Mingdong Hu1, Jianchun Wang1, Guangyu Wu3, Guansong Wang1
1. Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China 2. Department of Cardiology, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China 3. Department of Pharmacology and Toxicology, Medical College of Georgia, Georgia Regents University, Augusta 30912, USA These authors contributed equally to this work. Current address: Intensive Care Unit, Mianyang Central Hospital, Mianyang 621000, China Corresponding author: Dr. Guansong Wang, Professor of Medicine, Institute of Respiratory Diseases and Critical Care, Xinqiao Hospital of Third Military Medical University, 183 Xinqiao Street, Chongqing 400037, China, Email: wanggs2003@hotmail.com, wanggs@tmmu.edu.cn; Tel: +8623 6545 9972; Fax: +8623 6521 1653
Abstract :

Rab5 GTPase modulates the trafficking of the cell surface receptors, including G protein-coupled β-adrenergic receptors (β-ARs). Here, we have determined the role of Rab5 in regulating the internalization of β-ARs in lung microvascular endothelial cells (LMECs) and in maintaining the integrity and permeability of endothelial cell barrier. Our data demonstrate that lipopolysaccharide (LPS) treatment disrupts LMEC barrier function and reduces the cell surface expression of β-ARs. Furthermore, the activation of β-ARs, particularly β2-AR, is able to protect the LMEC permeability from LPS injury. Moreover, siRNA-mediated knockdown of Rab5 inhibits both the basal and agonist-provoked internalization of β-ARs, therefore, enhancing the cell surface expression of the receptors and receptor-mediated ERK1/2 activation. Importantly, knockdown of Rab5 not only inhibits the LPS-induced effects on β-ARs but also protects the LMEC monolayer permeability. All together, these data provide strong evidence indicating a crucial role of Rab5-mediated internalization of β-ARs in functional regulation of LMECs.

Keywords :
lung; microvascular endothelial cell; Rab5; β-adrenergic receptor; internalization; trafficking; permeability; lipopolysaccharide; small interfering RNA

Date Deposited : 01 Mar 2016 10:42

Last Modified : 01 Mar 2016 10:42

Official URL: http://www.ijbs.com/v11i8

Volume 11, Number 8, - 2015 , ISSN 1449-2288

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