eprintid: 10091532
rev_number: 14
eprint_status: archive
userid: 608
dir: disk0/10/09/15/32
datestamp: 2020-02-20 17:01:22
lastmod: 2021-09-30 22:47:08
status_changed: 2020-02-20 17:01:22
type: article
metadata_visibility: show
creators_name: Jiang, X-S
creators_name: Chen, X-M
creators_name: Wan, J-M
creators_name: Gui, H-B
creators_name: Ruan, X-Z
creators_name: Du, X-G
title: Autophagy Protects against Palmitic Acid-Induced Apoptosis in Podocytes in vitro
ispublished: pub
divisions: UCL
divisions: B02
divisions: C10
divisions: D17
divisions: G93
note: This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
abstract: Autophagy is a highly conserved degradation process that is involved in the clearance of proteins and damaged organelles to maintain intracellular homeostasis and cell integrity. Type 2 diabetes is often accompanied by dyslipidemia with elevated levels of free fatty acids (FFAs). Podocytes, as an important component of the filtration barrier, are susceptible to lipid disorders. The loss of podocytes causes proteinuria, which is involved in the pathogenesis of diabetic nephropathy. In the present study, we demonstrated that palmitic acid (PA) promoted autophagy in podocytes. We further found that PA increased the production of reactive oxygen species (ROS) in podocytes and that NAC (N-acetyl-cysteine), a potent antioxidant, significantly eliminated the excessive ROS and suppressed autophagy, indicating that the increased generation of ROS was associated with the palmitic acid-induced autophagy in podocytes. Moreover, we also found that PA stimulation decreased the mitochondrial membrane potential in podocytes and induced podocyte apoptosis, while the inhibition of autophagy by chloroquine (CQ) enhanced palmitic acid-induced apoptosis accompanied by increased ROS generation, and the stimulation of autophagy by rapamycin (Rap) remarkably suppressed palmitic acid-induced ROS generation and apoptosis. Taken together, these in vitro findings suggest that PA-induced autophagy in podocytes is mediated by ROS production and that autophagy plays a protective role against PA-induced podocyte apoptosis.
date: 2017-02-22
date_type: published
official_url: https://doi.org/10.1038/srep42764
oa_status: green
full_text_type: pub
pmcid: PMC5320537
language: eng
primo: open
primo_central: open_green
verified: verified_manual
elements_id: 1699740
doi: 10.1038/srep42764
pii: srep42764
lyricists_name: Ruan, Xiong-Zhong
lyricists_id: XZRUA13
actors_name: Bracey, Alan
actors_id: ABBRA90
actors_role: owner
full_text_status: public
publication: Scientific Reports
volume: 7
article_number: 42764
event_location: England
citation:        Jiang, X-S;    Chen, X-M;    Wan, J-M;    Gui, H-B;    Ruan, X-Z;    Du, X-G;      (2017)    Autophagy Protects against Palmitic Acid-Induced Apoptosis in Podocytes in vitro.                   Scientific Reports , 7     , Article 42764.  10.1038/srep42764 <https://doi.org/10.1038/srep42764>.       Green open access   
 
document_url: https://discovery.ucl.ac.uk/id/eprint/10091532/1/srep42764.pdf