Abnormal Cell Responses and Role of TNF-<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:mrow><mml:mi mathvariant="bold-italic">α</mml:mi></mml:mrow></mml:math>in Impaired Diabetic Wound Healing

Xu, Fanxing; Zhang, Chenying; Graves, Dana T.

doi:10.1155/2013/754802

Cited by 177 publications

(145 citation statements)

References 104 publications

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“…The systemic condition of diabetes mellitus can affect the healing process. 30 Traumatic ulcers in cases of diabetes mellitus can precipitate a delayed healing process due to a prolonged inflammatory process marked by an increased pro-inflammatory cytokine, TNF-α.…”

Section: Discussionmentioning

confidence: 99%

“…34,38 The proliferative stage of the healing process is, moreover, characterized by the proliferation of fibroblast and collagen synthesis. 30 The formation of granulation tissue at the proliferative stage of the wound healing process triggers fibroblasts to reduce collagenase so that the degradation process decreases. Furthermore, at this stage, the fibroblasts also undergo apoptosis resulting in the granulation tissue being replaced by collagen.…”

Section: Discussionmentioning

confidence: 99%

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Increase of collagen in diabetes-related traumatic ulcers after the application of liquid smoke coconut shell

Surboyo

Arundina

Rahayu

2017

Dent. J. (Maj. Ked. Gigi)

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Increase of collagen in diabetes-related traumatic ulcers after the application of liquid smoke coconut shell

Surboyo

Arundina

Rahayu

2017

Dent. J. (Maj. Ked. Gigi)

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“…Navarro & Mora-Fernández (2006), Roszer (2011) and Xu et al (2013)). In addition to TNFa, AGE-BSA increased the mRNA levels of other apoptogenic ligands, such as lymphotoxin alpha (Etemadi et al 2013) and TRAIL (Falschlehner et al 2007).…”

Section: Discussionmentioning

confidence: 99%

AGEs induce caspase-mediated apoptosis of rat BMSCs via TNFα production and oxidative stress

Weinberg¹,

Maymon²,

Weinreb³

2013

Journal of Molecular Endocrinology

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Diabetic humans and animals exhibit lower bone mass and healing, resulting from diminished bone formation. We have recently reported that type 1 diabetic rats have fewer bone marrow osteoprogenitor cells, and since the formation of advanced glycation end products (AGEs) in bone increases in diabetes, we explored possible mechanisms involved in AGE-induced apoptosis of rat bone marrow stromal cells (BMSCs). BMSCs isolated from 4-month-old rats were exposed to 10-400 mg/ml AGE-BSA for 16 h and apoptosis was quantified with PI/annexin V staining and flow cytometry. Signaling mechanisms were evaluated by preincubating the cells with appropriate inhibitors. The formation of reactive oxygen species (ROS) was quantified by flow cytometric analysis of DCFDA fluorescence and the expression of genes by RT-PCR analysis. AGE-BSA at a concentration of 400 mg/ml increased the apoptosis of BMSCs two-to threefold, an effect completely blocked by a pan-caspase inhibitor. BSA or high concentrations of glucose had no effect. AGE-BSA-induced BMSC apoptosis was attenuated by a p38 inhibitor but not by an NF-kB inhibitor. Treatment with AGE-BSA induced the expression of several pro-apoptotic ligands and receptors, most notably tumor necrosis factor a (TNFa), TRAIL, lymphotoxin alpha, CD40, and TNFR2. Furthermore, AGE-BSA-induced apoptosis was completely blocked by pirfenidone, an inhibitor of TNFa production/secretion. Finally, AGE-BSA increased the production of ROS in BMSCs, and its apoptogenic effect was blocked by the antioxidant N-acetylcysteine (N-acetyl-L-cysteine). Thus, AGE-BSA increases the apoptosis of rat BMSCs via the activation of caspases, involving TNFa production/ secretion, p38 MAPK signaling, and oxidative stress. We propose that increased protein glycation, such as that occurring under hyperglycemia, causes the apoptosis of BMSCs, which might significantly contribute to the development of osteopenia in diabetic animals.

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“…The proliferation phase is also compromised in diabetic wounds; 34 however, re-epithelialization scoring and epithelial thicknesses results in this study indicate that tissue proliferation was promoted in heparin mimetic hydrogel treated wounds.…”

Section: Acs Biomaterials Science and Engineeringmentioning

confidence: 51%

Angiogenic Peptide Nanofibers Improve Wound Healing in STZ-Induced Diabetic Rats

Şentürk

Mercan²,

Delibaşı

et al. 2016

ACS Biomater. Sci. Eng.

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Low expressions of angiogenic growth factors delay the healing of diabetic wounds by interfering with the process of blood vessel formation. Heparin mimetic peptide nanofibers can bind to and enhance production and activity of major angiogenic growth factors, including VEGF. In this study, we showed that heparin mimetic peptide nanofibers can serve as angiogenic scaffolds that allow slow release of growth factors and protect them from degradation, providing a new therapeutic way to accelerate healing of diabetic wounds. We treated wounds in STZ-induced diabetic rats with heparin mimetic peptide nanofibers and studied repair of full-thickness diabetic skin wounds. Wound recovery was quantified by analyses of reepithelialization, granulation tissue formation and blood vessel density, as well as VEGF and inflammatory response measurements. Wound closure and granulation tissue formation were found to be significantly accelerated in heparin mimetic gel treated groups. In addition, blood vessel counts and the expressions of alpha smooth muscle actin and VEGF were significantly higher in bioactive gel treated animals. These results strongly suggest that angiogenic heparin mimetic nanofiber therapy can be used to support the impaired healing process in diabetic wounds.

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Abnormal Cell Responses and Role of TNF-αin Impaired Diabetic Wound Healing

Cited by 177 publications

References 104 publications

Increase of collagen in diabetes-related traumatic ulcers after the application of liquid smoke coconut shell

Increase of collagen in diabetes-related traumatic ulcers after the application of liquid smoke coconut shell

AGEs induce caspase-mediated apoptosis of rat BMSCs via TNFα production and oxidative stress

Angiogenic Peptide Nanofibers Improve Wound Healing in STZ-Induced Diabetic Rats

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