Pulmonary Vascular Disease: Pulmonary Vascular Disease: PAH |

Capping Protein Gelsolin-Like as a Therapeutic Target to Prevent Hypoxic Pulmonary Hypertension FREE TO VIEW

Xiaoling Xu, MD; Ruifeng Zhang, PhD; Kejing Ying, MD
Author and Funding Information

Department of Respiratory Medicine, Sir Run Run Shaw Hospital, Medicine School of Zhejiang University, Hangzhou, China

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;149(4_S):A511. doi:10.1016/j.chest.2016.02.533
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SESSION TITLE: Pulmonary Vascular Disease: PAH

SESSION TYPE: Original Investigation Poster

PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM

PURPOSE: We previously observed that capping protein gelsolin-like (CapG) was preferentially expressed in human pulmonary arterial smooth muscle cells (PAMSCs) under hypoxia compared with normoxia, and reduced CapG expression was accompanied by significantly impaired migration ability in vitro under hypoxia. This result indicates that CapG could play an important role in the pathogenesis of pulmonary vascular remodeling under hypoxia.

METHODS: In the present study, we observed that CapG was expressed in rat PASMCs under hypoxia. A lentiviral vector named as Lenti-CapG was constructed and used to inhibit CapG expression in vitro and in vivo.

RESULTS: CapG expression was diminished in Lenti-CapG treated cells at both the mRNA and protein levels under hypoxia. Inhibition of CapG expression by RNA interference resulted in impaired proliferation and migration ability in vitro under hypoxia. The rats models were intratracheally instilled with Lenti-CapG two weeks prior to hypoxia exposure, subsequent 28-day chronic hypoxia (10% O2) exposure was utilizes. Our findings indicated that inhibition of CapG expression locally could attenuate increased right ventricular systolic pressure and its associated cardiac and pulmonary vessel remodeling under hypoxia.

CONCLUSIONS: Inhibition of CapG expression could prevent hypoxic pulmonary hypertension and pulmonary vascular remodeling in vivo.

CLINICAL IMPLICATIONS: Inhibition of CapG expression resulted in impaired proliferation and migration ability under hypoxia in vitro and prevented hypoxic pulmonary hypertension and pulmonary vascular remodeling in vivo. Our data indicate that CapG might be a novel target to prevent hypoxic pulmonary hypertension.

DISCLOSURE: The following authors have nothing to disclose: Xiaoling Xu, Ruifeng Zhang, Kejing Ying

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