Bradykinin Protects Human Endothelial Progenitor Cells from High-Glucose-Induced Senescence through B2 Receptor-Mediated Activation of the Akt/eNOS Signalling Pathway.
Bradykinin
/ pharmacology
Case-Control Studies
Cells, Cultured
Cellular Senescence
/ drug effects
DNA, Mitochondrial
/ genetics
Diabetes, Gestational
Dinoprost
/ analogs & derivatives
Endothelial Progenitor Cells
/ cytology
Female
Fetal Blood
Gene Dosage
Glucose
/ pharmacology
Humans
Infant, Newborn
Nitric Oxide
/ blood
Nitric Oxide Synthase Type III
/ metabolism
Pregnancy
Proto-Oncogene Proteins c-akt
/ metabolism
Receptor, Bradykinin B2
/ metabolism
Signal Transduction
Telomerase
Telomere
Journal
Journal of diabetes research
ISSN: 2314-6753
Titre abrégé: J Diabetes Res
Pays: England
ID NLM: 101605237
Informations de publication
Date de publication:
2021
2021
Historique:
received:
16
10
2020
revised:
25
04
2021
accepted:
10
08
2021
entrez:
24
9
2021
pubmed:
25
9
2021
medline:
27
1
2022
Statut:
epublish
Résumé
Circulating endothelial progenitor cells (EPCs) play important roles in vascular repair. However, the mechanisms of high-glucose- (HG-) induced cord blood EPC senescence and the role of B2 receptor (B2R) remain unknown. Cord blood samples from 26 patients with gestational diabetes mellitus (GDM) and samples from 26 healthy controls were collected. B2R expression on circulating CD34 B2R expression on circulating CD34 BK, acting through PI3K-AKT-eNOS signalling pathways, reduced hTERT translocation, increased the relative length of telomeres while reducing mtDNA copy number, and finally protected against EPC senescence induced by HG.
Sections du résumé
BACKGROUND
BACKGROUND
Circulating endothelial progenitor cells (EPCs) play important roles in vascular repair. However, the mechanisms of high-glucose- (HG-) induced cord blood EPC senescence and the role of B2 receptor (B2R) remain unknown.
METHODS
METHODS
Cord blood samples from 26 patients with gestational diabetes mellitus (GDM) and samples from 26 healthy controls were collected. B2R expression on circulating CD34
RESULTS
RESULTS
B2R expression on circulating CD34
CONCLUSION
CONCLUSIONS
BK, acting through PI3K-AKT-eNOS signalling pathways, reduced hTERT translocation, increased the relative length of telomeres while reducing mtDNA copy number, and finally protected against EPC senescence induced by HG.
Identifiants
pubmed: 34557552
doi: 10.1155/2021/6626627
pmc: PMC8452971
doi:
Substances chimiques
DNA, Mitochondrial
0
Receptor, Bradykinin B2
0
8-epi-prostaglandin F2alpha
27415-26-5
Nitric Oxide
31C4KY9ESH
Dinoprost
B7IN85G1HY
NOS3 protein, human
EC 1.14.13.39
Nitric Oxide Synthase Type III
EC 1.14.13.39
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
TERT protein, human
EC 2.7.7.49
Telomerase
EC 2.7.7.49
Glucose
IY9XDZ35W2
Bradykinin
S8TIM42R2W
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
6626627Informations de copyright
Copyright © 2021 Yuehuan Wu et al.
Déclaration de conflit d'intérêts
The authors declare that there are no conflicts of interest.
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