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Research Paper|Volume 12, Issue 12|pp 11485—11499

CTRP13 attenuates the expression of LN and CAV-1 Induced by high glucose via CaMKKβ/AMPK pathway in rLSECs

Qi Zhang1,2,4, Xiang’e Niu1,2,3, Limin Tian1,2, Jing Liu1,2, Ruilan Niu1,2, Jinxing Quan1,2, Jing Yu1,2, Wenyan Lin1,2, Zibing Qian1,2,3, Peiyun Zeng1,2,3
  • 1Department of Endocrinology, Gansu Provincial Hospital, Lanzhou 730000, Gansu Province, China
  • 2Clinical Research Center for Metabolic Disease, Lanzhou 730000, Gansu Province, China
  • 3School of Clinical Medicine, Gansu University of Chinese Medicine, Lanzhou 730000, Gansu Province, China
  • 4School of Life Sciences, Lanzhou University, Lanzhou 730000, Gansu Province, China
* Equal contribution
Received: December 3, 2019Accepted: March 30, 2020Published: June 17, 2020
https://doi.org/10.18632/aging.103234

Copyright © 2020 Zhang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Objective: To investigate the effect and mechanism of CTRP13 on hepatic sinusoidal capillarization induced by high glucose in rat liver sinusoidal endothelial cells (rLSECs).

Results: CTRP13 was reduced in high glucose-treated rLSECs. High glucose increased LN and CAV-1 expression and inhibited CaMKKβ and AMPK phosphorylation. CTRP13 overexpression protected rLSECs against high glucose-induced increase of LN and CAV-1 expression. Moreover, CTRP13 overexpression increased high glucose-induced inhibition of CaMKKβ and AMPK activation in CTRP13-overexpressing rLSECs. Inhibition of CaMKKβ and AMPK disturbed the protective effects of CTRP13 in high glucose-induced increase of LN and CAV-1. Hepatic steatosis was enhanced and basement membrane was thickened in liver of diabetic fatty liver rats.

Conclusions: Our data identified the protective role of CTRP13 in hepatic sinusoidal capillarization induced by high glucose via activating CAMKKβ/AMPK pathway. CTRP13 may be a potential target for screening and treating diabetic fatty liver.

Methods: Construct lentiviral CTRP13 overexpression vector and transfect rLSECs. Use STO-609 (a CaMKKβ inhibitor) or Compound C (an AMPK inhibitor) to treat rLSECs. CTRP13, CaMKKβ, AMPK, laminin (LN) and caveolin-1 (CAV-1) were detected by qRT-PCR and Western blotting. Establish rat model of diabetic fatty liver. Use immunohistochemistry, hematoxylin-eosin and silver staining to observe the histopathological features of liver.