![](/images/graphics-bg.png)
Plin5p-Plin5 Guards Diabetic CMECs by Regulating FFAs Metabolism Bidirectionally
Joint Authors
Pei, Haifeng
Zhao, Heng
Yang, Dachun
Li, De
Yang, Yongjian
Du, Jin
Hou, Juanni
Feng, Juan
Zhou, Hong
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2019, Issue 2019 (31 Dec. 2019), pp.1-15, 15 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2019-10-17
Country of Publication
Egypt
No. of Pages
15
Main Subjects
Abstract EN
Background.
Hyper-free fatty acidemia (HFFA) impairs cardiac capillaries, as well as type 2 diabetes mellitus (T2DM).
Perilipin 5 (Plin5) maintains metabolic balance of free fatty acids (FFAs) in high oxidative tissues via the states of nonphosphorylation and phosphorylation.
However, when facing to T2DM-HFFA, Plin5’s role in cardiac microvascular endothelial cells (CMECs) is not defined.
Methods.
In mice of WT or Plin5-/-, T2DM models were rendered by high-fat diet combined with intraperitoneal injection of streptozocin.
CMECs isolated from left ventricles were incubated with high glucose (HG) and high FFAs (HFFAs).
Plin5 phosphorylation was stimulated by isoproterenol.
Plin5 expression was knocked down by small interfering RNA (siRNA).
We determined cardiac function by small animal ultrasound, apoptotic rate by flow cytometry, microvessel quantity by immunohistochemistry, microvascular integrity by scanning electron microscopy, intracellular FFAs by spectrophotometry, lipid droplets (LDs) by Nile red staining, mRNAs by quantitative real-time polymerase chain reaction, proteins by western blots, nitric oxide (NO) and reactive oxygen species (ROS) by fluorescent dye staining and enzyme-linked immunosorbent assay kits.
Results.
In CMECs, HFFAs aggravated cell injury induced by HG and activated Plin5 expression.
In mice with T2DM-HFFA, Plin5 deficiency reduced number of cardiac capillaries, worsened structural incompleteness, and enhanced diastolic dysfunction.
Moreover, in CMECs treated with HG-HFFAs, both ablation and phosphorylation of Plin5 reduced LDs content, increased intracellular FFAs, stimulated mitochondrial β-oxidation, added ROS generation, and reduced the expression and activity of endothelial nitric oxide synthase (eNOS), eventually leading to increased apoptotic rate and decreased NO content, all of which were reversed by N-acetyl-L-cysteine.
Conclusion.
Plin5 preserves lipid balance and cell survival in diabetic CMECs by regulating FFAs metabolism bidirectionally via the states of nonphosphorylation and phosphorylation.
American Psychological Association (APA)
Du, Jin& Hou, Juanni& Feng, Juan& Zhou, Hong& Zhao, Heng& Yang, Dachun…[et al.]. 2019. Plin5p-Plin5 Guards Diabetic CMECs by Regulating FFAs Metabolism Bidirectionally. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-15.
https://search.emarefa.net/detail/BIM-1205849
Modern Language Association (MLA)
Du, Jin…[et al.]. Plin5p-Plin5 Guards Diabetic CMECs by Regulating FFAs Metabolism Bidirectionally. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-15.
https://search.emarefa.net/detail/BIM-1205849
American Medical Association (AMA)
Du, Jin& Hou, Juanni& Feng, Juan& Zhou, Hong& Zhao, Heng& Yang, Dachun…[et al.]. Plin5p-Plin5 Guards Diabetic CMECs by Regulating FFAs Metabolism Bidirectionally. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-15.
https://search.emarefa.net/detail/BIM-1205849
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1205849