Titre
Improved cutaneous healing in diabetic mice exposed to healthy peripheral circulation.
Type
article
Institution
Externe
Périodique
Auteur(s)
Pietramaggiori, G.
Auteure/Auteur
Scherer, S.S.
Auteure/Auteur
Alperovich, M.
Auteure/Auteur
Chen, B.
Auteure/Auteur
Orgill, D.P.
Auteure/Auteur
Wagers, A.J.
Auteure/Auteur
Liens vers les personnes
ISSN
1523-1747
Statut éditorial
Publié
Date de publication
2009-09
Volume
129
Numéro
9
Première page
2265
Dernière page/numéro d’article
2274
Peer-reviewed
Oui
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Publication Status: ppublish
Résumé
Impaired repair of skin defects is a major complication of diabetes; yet, the pathophysiology of diabetic (db) wound healing remains largely opaque. Here, we investigate the role of humoral factors in modulating db wound repair by generating chimeric animals through parabiotic joining of wild-type (wt) and diabetic (db/db) mice. This strategy allows wounds on healing-deficient db/db mice to be exposed to factors derived from the wt circulation at physiologically appropriate concentrations. When compared with db controls, chimeric db/db animals showed significantly improved healing of full-thickness, cutaneous wounds, with enhanced granulation tissue formation, angiogenesis, cell proliferation, and collagen deposition. Glycemic control was unaffected by parabiosis; however, the distribution of circulating leukocytes, altered in db controls, normalized in db-chimeras. Both wt and db cells were recruited from circulation into db wounds, but wt cells never exceeded 20% of total cells. Improved angiogenesis persisted in db-chimeras separated 24 hours after wounding, suggesting the existence of long-term normalizing factors. This study establishes a new model for studying db wound healing, and shows a key role for circulating factors in normalizing wound repair in diabetes.
PID Serval
serval:BIB_C4124A52393A
PMID
Open Access
Oui
Date de création
2018-01-16T13:57:16.166Z
Date de création dans IRIS
2025-05-20T23:46:23Z