Oxidative Stress-Induced Growth Inhibitor (OSGIN1), a Target of X-Box-Binding Protein 1, Protects Palmitic Acid-Induced Vascular Lipotoxicity through Maintaining Autophagy.
OSGIN1
XBP1s
autophagy
eNOS
endothelial cells
palmitic acid
unfolded protein response
Journal
Biomedicines
ISSN: 2227-9059
Titre abrégé: Biomedicines
Pays: Switzerland
ID NLM: 101691304
Informations de publication
Date de publication:
25 Apr 2022
25 Apr 2022
Historique:
received:
08
03
2022
revised:
18
04
2022
accepted:
19
04
2022
entrez:
28
5
2022
pubmed:
29
5
2022
medline:
29
5
2022
Statut:
epublish
Résumé
Saturated free fatty acids (FFAs) strongly correlate with metabolic syndromes and are well-known risk factors for cardiovascular diseases (CVDs). The mechanism of palmitic acid (PA)-induced vascular lipotoxicity under endoplasmic reticulum (ER) stress is unknown. In the present paper, we investigate the roles of spliced form of X-box-binding protein 1 (XBP1s) target gene oxidative stress-induced growth inhibitor 1 (OSGIN1) in PA-induced vascular dysfunction. PA inhibited the tube formation assay of primary human umbilical vein endothelial cells (HUVECs). Simultaneously, PA treatment induced the XBP1s expression in HUVECs. Attenuate the induction of XBP1s by silencing the XBP1s retarded cell migration and diminished endothelial nitric oxide synthase (eNOS) expression. OSGIN1 is a target gene of XBP1s under PA treatment. The silencing of OSGIN1 inhibits cell migration by decreasing phospho-eNOS expression. PA activated autophagy in endothelial cells, inhibiting autophagy by 3-methyladenine (3-MA) decreased endothelial cell migration. Silencing XBP1s and OSGIN1 would reduce the induction of LC3 II; therefore, OSGIN1 could maintain autophagy to preserve endothelial cell migration. In conclusion, PA treatment induced ER stress and activated the inositol-requiring enzyme 1 alpha-spliced XBP1 (IRE1α-XBP1s) pathway. OSGIN1, a target gene of XBP1s, could protect endothelial cells from vascular lipotoxicity by regulating autophagy.
Identifiants
pubmed: 35625730
pii: biomedicines10050992
doi: 10.3390/biomedicines10050992
pmc: PMC9138516
pii:
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : National Taiwan University Hospital
ID : NTUH-108-S4373 and NTUH-UN109
Organisme : NTUH-FEMH Joint Research Program
ID : 108-FTN-16 and 110-FTN-21
Organisme : Far Eastern Memorial hospital
ID : FEMH-2020-C-028 and FEMH-2021-C-030
Organisme : Ministry of Science and Technology, Taiwan
ID : MOST-107-2314-B-002-027-MY3 and MOST 110-2314-B-002-130
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