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2016 ; 65
(7
): 2006-19
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Mast Cells Regulate Wound Healing in Diabetes
#MMPMID27207516
Tellechea A
; Leal EC
; Kafanas A
; Auster ME
; Kuchibhotla S
; Ostrovsky Y
; Tecilazich F
; Baltzis D
; Zheng Y
; Carvalho E
; Zabolotny JM
; Weng Z
; Petra A
; Patel A
; Panagiotidou S
; Pradhan-Nabzdyk L
; Theoharides TC
; Veves A
Diabetes
2016[Jul]; 65
(7
): 2006-19
PMID27207516
show ga
Diabetic foot ulceration is a severe complication of diabetes that lacks
effective treatment. Mast cells (MCs) contribute to wound healing, but their role
in diabetes skin complications is poorly understood. Here we show that the number
of degranulated MCs is increased in unwounded forearm and foot skin of patients
with diabetes and in unwounded dorsal skin of diabetic mice (P < 0.05).
Conversely, postwounding MC degranulation increases in nondiabetic mice, but not
in diabetic mice. Pretreatment with the MC degranulation inhibitor disodium
cromoglycate rescues diabetes-associated wound-healing impairment in mice and
shifts macrophages to the regenerative M2 phenotype (P < 0.05). Nevertheless,
nondiabetic and diabetic mice deficient in MCs have delayed wound healing
compared with their wild-type (WT) controls, implying that some MC mediator is
needed for proper healing. MCs are a major source of vascular endothelial growth
factor (VEGF) in mouse skin, but the level of VEGF is reduced in diabetic mouse
skin, and its release from human MCs is reduced in hyperglycemic conditions.
Topical treatment with the MC trigger substance P does not affect wound healing
in MC-deficient mice, but improves it in WT mice. In conclusion, the presence of
nondegranulated MCs in unwounded skin is required for proper wound healing, and
therapies inhibiting MC degranulation could improve wound healing in diabetes.
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