Dysregulation of ghrelin in diabetes impairs the vascular reparative response to hindlimb ischemia in a mouse model; clinical relevance to peripheral artery disease.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
12 08 2020
Historique:
received: 24 04 2020
accepted: 21 07 2020
entrez: 14 8 2020
pubmed: 14 8 2020
medline: 12 1 2021
Statut: epublish

Résumé

Type 2 diabetes is a prominent risk factor for peripheral artery disease (PAD). Yet, the mechanistic link between diabetes and PAD remains unclear. This study proposes that dysregulation of the endogenous hormone ghrelin, a potent modulator of vascular function, underpins the causal link between diabetes and PAD. Moreover, this study aimed to demonstrate the therapeutic potential of exogenous ghrelin in a diabetic mouse model of PAD. Standard ELISA analysis was used to quantify and compare circulating levels of ghrelin between (i) human diabetic patients with or without PAD (clinic) and (ii) db/db diabetic and non-diabetic mice (lab). Db/db mice underwent unilateral hindlimb ischaemia (HLI) for 14 days and treated with or without exogenous ghrelin (150 µg/kg/day.) Subsequently vascular reparation, angiogenesis, hindlimb perfusion, structure and function were assessed using laser Doppler imaging, micro-CT, microangiography, and protein and micro-RNA (miRNA) analysis. We further examined hindlimb perfusion recovery of ghrelin KO mice to determine whether an impaired vascular response to HLI is linked to ghrelin dysregulation in diabetes. Patients with PAD, with or without diabetes, had significantly lower circulating levels of endogenous ghrelin, compared to healthy individuals. Diabetic db/db mice had ghrelin levels that were only 7% of non-diabetic mice. The vascular reparative capacity of diabetic db/db mice in response to HLI was impaired compared to non-diabetic mice and, importantly, comparable to ghrelin KO mice. Daily therapeutic treatment of db/db mice with ghrelin for 14 days post HLI, stimulated angiogenesis, and improved skeletal muscle architecture and cell survival, which was associated with an increase in pro-angiogenic miRNAs-126 and -132. These findings unmask an important role for endogenous ghrelin in vascular repair following limb ischemia, which appears to be downregulated in diabetic patients. Moreover, these results implicate exogenous ghrelin as a potential novel therapy to enhance perfusion in patients with lower limb PAD, especially in diabetics.

Identifiants

pubmed: 32788622
doi: 10.1038/s41598-020-70391-6
pii: 10.1038/s41598-020-70391-6
pmc: PMC7423620
doi:

Substances chimiques

Ghrelin 0
MicroRNAs 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

13651

Commentaires et corrections

Type : ErratumIn

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Auteurs

Joshua P H Neale (JPH)

Department of Physiology, School of Biomedical Sciences and HeartOtago, University of Otago, 270 Great King Street, Dunedin, 9018, New Zealand.

James T Pearson (JT)

Department of Cardiac Physiology, National Cerebral and Cardiovascular Center Research Institute, Suita, Osaka, Japan.
Biomedicine Discovery Institute and Department of Physiology, Monash University, Clayton, Australia.

Kate N Thomas (KN)

Department of Surgical Sciences, University of Otago, Dunedin, New Zealand.

Hirotsugu Tsuchimochi (H)

Department of Cardiac Physiology, National Cerebral and Cardiovascular Center Research Institute, Suita, Osaka, Japan.

Hiroshi Hosoda (H)

Department of Regenerative Medicine, National Cerebral and Cardiovascular Center Research Institute, Suita, Osaka, Japan.

Masayasu Kojima (M)

Molecular Genetics, Institute of Life Science, Kurume University, Kurume, Japan.

Takahiro Sato (T)

Molecular Genetics, Institute of Life Science, Kurume University, Kurume, Japan.

Gregory T Jones (GT)

Department of Surgical Sciences, University of Otago, Dunedin, New Zealand.

Adam P Denny (AP)

Department of Physiology, School of Biomedical Sciences and HeartOtago, University of Otago, 270 Great King Street, Dunedin, 9018, New Zealand.

Lorna J Daniels (LJ)

Department of Physiology, School of Biomedical Sciences and HeartOtago, University of Otago, 270 Great King Street, Dunedin, 9018, New Zealand.

Dhananjie Chandrasekera (D)

Department of Physiology, School of Biomedical Sciences and HeartOtago, University of Otago, 270 Great King Street, Dunedin, 9018, New Zealand.

Ping Liu (P)

Department of Anatomy, School of Biomedical Sciences, University of Otago, Dunedin, New Zealand.

Andre M van Rij (AM)

Department of Surgical Sciences, University of Otago, Dunedin, New Zealand.

Rajesh Katare (R)

Department of Physiology, School of Biomedical Sciences and HeartOtago, University of Otago, 270 Great King Street, Dunedin, 9018, New Zealand. rajesh.katare@otago.ac.nz.

Daryl O Schwenke (DO)

Department of Physiology, School of Biomedical Sciences and HeartOtago, University of Otago, 270 Great King Street, Dunedin, 9018, New Zealand. daryl.schwenke@otago.ac.nz.

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