Silencing LncRNA AK139328 protects vascular endothelial cells from ischemia-reperfusion injury by increasing PI3K/Akt signaling

Zeng-Yang Pei; Sheng-Hao Wang; Yan Mao; Qi Li; Zi-Heng Wu; Xiang-Tao Zheng

doi:10.18632/oncotarget.22453

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Research Papers:

Silencing LncRNA AK139328 protects vascular endothelial cells from ischemia-reperfusion injury by increasing PI3K/Akt signaling

Zeng-Yang Pei _, Sheng-Hao Wang, Yan Mao, Qi Li, Zi-Heng Wu and Xiang-Tao Zheng

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Abstract

Zeng-Yang Pei1, Sheng-Hao Wang1, Yan Mao2, Qi Li1, Zi-Heng Wu3 and Xiang-Tao Zheng3

1Department of Veterinary Medicine, College of Animal Sciences, Zhejiang University, Hangzhou 310058, P.R. China

2Pet Shield Animal Hospital, Xihu District, Hangzhou 310000, P.R. China

3Department of Vascular Surgery, The First Affiliated Hospital of Medical School of Zhejiang University, Hangzhou 310003, P.R. China

Correspondence to:

Zeng-Yang Pei, email: [email protected]

Keywords: LncRNA AK139328; vascular endothelial cells; ischemia-reperfusion; PI3K/Akt signaling pathway; rat model

Received: July 12, 2016 Accepted: October 17, 2017 Published: January 02, 2018

ABSTRACT

We investigated the effects of lncRNA AK139328 and PI3K/Akt signaling during rat hindlimb ischemia-reperfusion (I/R) injury. Rat vascular endothelial cells (VECs) subjected to oxygen-glucose deprivation showed high lncRNA AK139328 expression and decreased PI3K/Akt signaling, whereas lncRNA AK139328 knockdown increased PI3K/Akt signaling in VECs. Correspondingly, gastrocnemius muscles from rats subjected to hindlimb I/R showed high levels of lncRNA AK139328 and low PI3K/Akt/eNOS signaling. I/R also increased serum levels of TNF-α, VCAM-1 and malondialdehyde, serum creatine kinase activity and the number of circulating endothelial cells (CECs). Gastrocnemius tissue from rats subjected to I/R exhibited inflammation, apoptosis and trauma with loosely attached, swollen VECs associated with inflammatory immune cells. LncRNA AK139328 knockdown increased PI3K/Akt/eNOS signaling in gastrocnemius muscles subjected to I/R, and decreased serum levels of TNF-α, VCAM-1 and malondialdehyde, serum creatine kinase activity and numbers of CECs. LncRNA AK139328 knockdown also decreased inflammation, apoptosis and trauma in gastrocnemius muscles, which showed tightly attached VECs that were not associated with inflammatory immune cells. Inhibition of PI3K/Akt signaling by wortmannin or LY294002 reversed the effects of lncRNA AK139328 knockdown. In conclusion, I/R induces expression of lncRNA AK139328, which suppresses PI3K/Akt signaling required to prevent I/R-related pathology in VECs.

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Research Papers:

Silencing LncRNA AK139328 protects vascular endothelial cells from ischemia-reperfusion injury by increasing PI3K/Akt signaling

Abstract