Vascular endothelial insulin/IGF-1 signaling controls skin wound vascularization

Aghdam, Saeed Yadranji; Eming, Sabine A.; Willenborg, Sebastian; Neuhaus, Brit; Niessen, Carien M.; Partridge, Linda; Krieg, Thomas

doi:10.1016/j.bbrc.2012.03.134

Cited by 38 publications

(25 citation statements)

References 29 publications

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“…Frozen sections (7 µm) were fixed with 2% paraformaldehyde and stained with haematoxylin and eosin (H/E) to determine the granulation tissue area and the distance between the ends of the panniculus carnosus as described [38] using the ImageJ software. Significance of differences was analyzed using the two-tailed t-test.…”

Section: Methodsmentioning

confidence: 99%

Col6a1 Null Mice as a Model to Study Skin Phenotypes in Patients with Collagen VI Related Myopathies: Expression of Classical and Novel Collagen VI Variants during Wound Healing

et al. 2014

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Patients suffering from collagen VI related myopathies caused by mutations in COL6A1, COL6A2 and COL6A3 often also display skin abnormalities, like formation of keloids or “cigarette paper” scars, dry skin, striae rubrae and keratosis pilaris (follicular keratosis). Here we evaluated if Col6a1 null mice, an established animal model for the muscle changes in collagen VI related myopathies, are also suitable for the study of mechanisms leading to the skin pathology. We performed a comprehensive study of the expression of all six collagen VI chains in unwounded and challenged skin of wild type and Col6a1 null mice. Expression of collagen VI chains is regulated in both skin wounds and bleomycin-induced fibrosis and the collagen VI α3 chain is proteolytically processed in both wild type and Col6a1 null mice. Interestingly, we detected a decreased tensile strength of the skin and an altered collagen fibril and basement membrane architecture in Col6a1 null mice, the latter being features that are also found in collagen VI myopathy patients. Although Col6a1 null mice do not display an overt wound healing defect, these mice are a relevant animal model to study the skin pathology in collagen VI related disease.

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Section: Methodsmentioning

confidence: 99%

Col6a1 Null Mice as a Model to Study Skin Phenotypes in Patients with Collagen VI Related Myopathies: Expression of Classical and Novel Collagen VI Variants during Wound Healing

et al. 2014

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“…Previous studies using cultured keratinocytes from insulin receptor knock out mice showed that absence of insulin signaling induces abnormal differentiation despite increased IGF-1 signaling (Wertheimer, Spravchikov et al 2001). In addition, recent studies using transgenic mice with an inducible Cre-LoxP deletion of both the insulin and IGF-1 receptors on vascular endothelial cells showed that deletion of insulin and IGF-1 receptors in endothelial cells had little effect on days to superficial wound closure but that the loss of insulin signaling resulted in a large reduction of wound vascularization and granulation tissue formation underscoring the need for insulin signaling in this aspect of wound healing (Aghdam, Eming et al 2012). …”

Section: Insulinmentioning

confidence: 99%

Diabetes medications: Impact on inflammation and wound healing

Salazar

Ennis

Koh

2016

Journal of Diabetes and its Complications

162

101

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Chronic wounds are a common complication in patients with diabetes that often lead to amputation. These non-healing wounds are described as being stuck in a persistent inflammatory state characterized by accumulation of pro-inflammatory macrophages, cytokines and proteases. Some medications approved for management of type 2 diabetes have demonstrated anti-inflammatory properties independent of their marketed insulinotropic effects and thus have underappreciated potential to promote wound healing. In this review, the potential for insulin, metformin, specific sulfonylureas, thiazolidinediones, and dipeptidyl peptidase-4 inhibitors to promote healing is evaluated by reviewing human and animal studies on inflammation and wound healing. The available evidence indicates that diabetic medications have potential to prevent wounds from becoming arrested in the inflammatory stage of healing and to promote wound healing by downregulating pro-inflammatory cytokines, upregulating growth factors, lowering matrix metalloproteinases, stimulating angiogenesis, and increasing epithelization. However, no clinical recommendations currently exist on the potential for specific diabetic medications to impact healing of chronic wounds. Thus, we encourage further research that may guide physicians on providing personalized diabetes treatments that achieve glycemic goals while promoting healing in patients with chronic wounds.

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“…The most prominent of these are the “diabetic foot ulcers” resulting from defective wound healing, in which impaired angiogenesis is considered as the main contributing factor [1]. Hyperglycemia is a well-recognized major causative factor in development of such complications, but growing evidence also points to inflammation as a significant factor [2].…”

Section: Introductionmentioning

confidence: 99%

Association of circulating sTRAIL and high-sensitivity CRP with type 2 diabetic nephropathy and foot ulcers

et al. 2013

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BackgroundHyperglycemia is among the potent factors that may induce or facilitate apoptosis. TNF-Related Apoptosis-Inducing Factor (TRAIL) is known for its apoptotic and immunomodulatory effects that have recently been correlated with diabetes. We examined serum-soluble TRAIL (sTRAIL) and high-sensitivity CRP (hs-CRP) levels and their association with various distinct parameters in type 2 diabetic nephropathy patients with diabetic foot disease.Material/MethodsTwenty-two diabetic nephropathy patients with foot ulcers were enrolled in our study. Patients had been diagnosed with diabetes at age 24±10.58 years. Circulating sTRAIL and Hs-CRP levels were compared with control values, and possible correlations were investigated with parameters such as age, Wagner’s Grade (WG), BMI, HbA1c, and creatinine.ResultsSerum sTRAIL levels were significantly reduced in the patient group, compared to healthy subjects. High HsCRP levels correlated with age, and WGS correlated with BMI and creatinine levels.ConclusionsSignificantly suppressed sTRAIL levels in diabetic nephropathy patients with foot ulcers compared to healthy controls suggest a protective role for TRAIL in the disease setting.

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Vascular endothelial insulin/IGF-1 signaling controls skin wound vascularization

Cited by 38 publications

References 29 publications

Col6a1 Null Mice as a Model to Study Skin Phenotypes in Patients with Collagen VI Related Myopathies: Expression of Classical and Novel Collagen VI Variants during Wound Healing

Col6a1 Null Mice as a Model to Study Skin Phenotypes in Patients with Collagen VI Related Myopathies: Expression of Classical and Novel Collagen VI Variants during Wound Healing

Diabetes medications: Impact on inflammation and wound healing

Association of circulating sTRAIL and high-sensitivity CRP with type 2 diabetic nephropathy and foot ulcers

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