Adiponectin and leptin up‐regulate extracellular matrix production by dermal fibroblasts

Ezure, Tomonobu; Amano, Sadao

doi:10.1002/biof.5520310310

Cited by 73 publications

(69 citation statements)

References 26 publications

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“…On the other hand, our results showed no significant difference in the number of macrophages in subcutaneous adipose tissue between the control and obesity groups on the day before wounding. This result differed from previous and up-regulating collagen production by dermal fibroblasts [44]. In this study, we did not observe the blood leptin concentration on the day before wounding.…”

Section: Discussioncontrasting

confidence: 99%

Does Obesity without Hyperglycemia Delay Wound Healing in an Obese Mouse Model Induced by a High-Fat Diet?

Urai¹,

Nakajima²,

Mukai³

et al. 2017

Health

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It was unclear that wound healing was delayed in obesity without hyperglycemia. The purpose of this study was to compare the wound healing process between obese and non-obese mice without hyperglycemia by attaching a splint. Three-week-old male mice (C57BL/6N) were fed high-fat diets (60% of calories from fat) in the obesity group, and commercial diets in the control group for 15 weeks. Two circular (4 mm in diameter) full-thickness wounds were made on the dorsal skin. Body weights and serum leptin levels were significantly higher in the obesity group than in the control group until day 15 after wounding. Fasting blood glucose levels before wounding were lower in the obesity group than in a hyperglycemic rodent model. The macrophage infiltration into subcutaneous fat before wounding in the obesity group was negligible. The ratios of the wound area were not significantly different between the two groups. No significant differences were observed in the number of neutrophils or macrophages or new blood vessels and ratio of myofibroblasts or collagen fibers between the two groups. Our results demonstrated that cutaneous wound healing was not delayed in the obesity group without hyperglycemia and macrophage infiltration into the subcutaneous fat and with high serum leptin levels.

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Section: Discussioncontrasting

confidence: 99%

Does Obesity without Hyperglycemia Delay Wound Healing in an Obese Mouse Model Induced by a High-Fat Diet?

Urai¹,

Nakajima²,

Mukai³

et al. 2017

Health

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“…22 Moreover, adiponectin upregulates the ECM production by dermal fibroblasts. 23 All these findings suggest that adiponectin may affect collagen homeostasis via different mechanisms in the various tissues. Therefore, we were interested in the effect of adiponectin overexpression on the stability of preexisting plaques.…”

Section: Discussionmentioning

confidence: 99%

Effect of Adiponectin Overexpression on Stability of Preexisting Plaques by Inducing Prolyl-4-Hydroxylase Expression

Cai

Feng³

et al. 2010

Circ J

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“…Dermal fibroblasts are the dominant players in the process of granulation tissue formation during cutaneous wound healing. Recent reports have revealed that adiponectin induces proliferation of dermal fibroblasts and upregulation of collagen production (47,48). Furthermore, adiponectin induces proliferation of HUVECs and stimulates angiogenesis (10), indicating the positive contribution of adiponectin to optimal wound repair.…”

Section: Discussionmentioning

confidence: 99%

Adiponectin Regulates Cutaneous Wound Healing by Promoting Keratinocyte Proliferation and Migration via the ERK Signaling Pathway

Shibata

Tada

Asano

et al. 2012

The Journal of Immunology

135

109

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Diabetic patients are at high risk of developing delayed cutaneous wound healing. Adiponectin plays a pivotal role in the pathogenesis of diabetes and is considered to be involved in various pathological conditions associated with diabetes; however, its role in wound repair is unknown. In this study, we elucidated the involvement of adiponectin in cutaneous wound healing in vitro and in vivo. Normal human keratinocytes expressed adiponectin receptors, and adiponectin enhanced proliferation and migration of keratinocytes in vitro. This proliferative and migratory effect of adiponectin was mediated via AdipoR1/AdipoR2 and the ERK signaling pathway. Consistent with in vitro results, wound closure was significantly delayed in adiponectin-deficient mice compared with wild-type mice, and more importantly, keratinocyte proliferation and migration during wound repair were also impaired in adiponectin-deficient mice. Furthermore, both systemic and topical administration of adiponectin ameliorated impaired wound healing in adiponectin-deficient and diabetic db/db mice, respectively. Collectively, these results indicate that adiponectin is a potent mediator in the regulation of cutaneous wound healing. We propose that upregulation of systemic and/or local adiponectin levels is a potential and very promising therapeutic approach for dealing with diabetic wounds.

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Adiponectin and leptin up‐regulate extracellular matrix production by dermal fibroblasts

Cited by 73 publications

References 26 publications

Does Obesity without Hyperglycemia Delay Wound Healing in an Obese Mouse Model Induced by a High-Fat Diet?

Does Obesity without Hyperglycemia Delay Wound Healing in an Obese Mouse Model Induced by a High-Fat Diet?

Effect of Adiponectin Overexpression on Stability of Preexisting Plaques by Inducing Prolyl-4-Hydroxylase Expression

Adiponectin Regulates Cutaneous Wound Healing by Promoting Keratinocyte Proliferation and Migration via the ERK Signaling Pathway

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