scholarly journals Quercetin Improves Inflammation, Oxidative Stress, and Impaired Wound Healing in Atopic Dermatitis Model of Human Keratinocytes

2020 ◽  
Vol 33 (2) ◽  
pp. 69-79
Author(s):  
Burcin Beken ◽  
Riza Serttas ◽  
Mehtap Yazicioglu ◽  
Kader Turkekul ◽  
Suat Erdogan
Keyword(s):  
Oxidative Stress ◽  
Wound Healing ◽  
Atopic Dermatitis ◽  
Human Keratinocytes ◽  
Impaired Wound Healing

Diabetic ferroptosis plays an important role in triggering on inflammation in diabetic wound

2021 ◽  
Author(s):  
Shuangwen Li ◽  
Yuan Li ◽  
Ziyu Wu ◽  
Zhongming Wu ◽  
Hongjuan Fang
Keyword(s):  
Oxidative Stress ◽  
Wound Healing ◽  
High Glucose ◽  
Vascular Endothelial Cells ◽  
Major Complication ◽  
Lipid Peroxides ◽  
Diabetic Wound ◽  
Impaired Wound Healing ◽  
Wound Site

Impaired wound healing is a major complication of diabetes and involves sustained inflammation and oxidative stress at the wound site. Here, we investigated the potential involvement of ferroptosis, a newly discovered form of cell death characterized by iron-dependent accumulation of lipid peroxides, in the pathogenesis of diabetic wound healing. Fibroblasts and vascular endothelial cells exposed to high glucose concentrations in vitro contained elevated levels of reactive oxygen species (ROS), lipid peroxidation products, and ferroptosis-associated proteins, and displayed reduced survival and migration. These effects of high glucose were all significantly reduced by treatment with the ferroptosis inhibitor ferrostatin-1 (Fer-1). Similarly, in a rat model of diabetes, direct application of Fer-1 to the wound site reduced the expression of oxidative stress and inflammation markers and accelerated wound healing via activation of the anti-inflammatory phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway. Our results implicate ferroptosis in wound healing and identify a potential new therapeutic target for difficult-to-treat diabetic wounds.

Caveolin-1/PTRF upregulation constitutes a mechanism for mediating p53-induced cellular senescence: implications for evidence-based therapy of delayed wound healing in diabetes

2013 ◽  
Vol 305 (8) ◽  
pp. E951-E963 ◽  
Author(s):  
Milad S. Bitar ◽  
Samy M. Abdel-Halim ◽  
Fahd Al-Mulla
Keyword(s):  
Oxidative Stress ◽  
Wound Healing ◽  
Cellular Senescence ◽  
Dermal Fibroblasts ◽  
Premature Senescence ◽  
Mrna Levels ◽  
Impaired Wound Healing ◽  
Caveolin 1

A heightened state of oxidative stress and senescence of fibroblasts constitute potential therapeutic targets in nonhealing diabetic wounds. Here, we studied the underlying mechanism mediating diabetes-induced cellular senescence using in vitro cultured dermal fibroblasts and in vivo circular wounds. Our results demonstrated that the total antioxidant capacity and mRNA levels of thioredoxinreductase and glucose-6-phosphate dehydrogenase as well as the ratio of NADPH/NADP were decreased markedly in fibroblasts from patients with type 2 diabetes (DFs). Consistent with this shift in favor of excessive reactive oxygen species, DFs also displayed a significant increase in senescence-associated β-galactosidase activity and phospho-γ-histone H2AX (pH2AX) level. Moreover, the ability of PDGF to promote cell proliferation/migration and regulate the phosphorylation-dependent activation of Akt and ERK1/2 appears to be attenuated as a function of diabetes. Mechanistically, we found that diabetes-induced oxidative stress upregulated caveolin-1 (Cav-1) and PTRF expression, which in turn sequestered Mdm2 away from p53. This process resulted in the activation of a p53/p21-dependent pathway and the induction of premature senescence in DFs. Most of the aforementioned oxidative stress and senescence-based features observed in DFs were recapitulated in a 10-day-old diabetic wound. Intriguingly, we confirmed that the targeted depletion of Cav-1 or PTRF using siRNA- or Vivo-Morpholino antisense-based gene therapy markedly inhibited diabetes/oxidative stress-induced premature senescence and also accelerated tissue repair in this disease state. Overall, our data illuminate Cav-1/PTRF-1 as a key player of a novel signaling pathway that may link a heightened state of oxidative stress to cellular senescence and impaired wound healing in diabetes.

Effects of adiponectin on growth and differentiation of human keratinocytes—Implication of impaired wound healing in diabetes

2008 ◽  
Vol 374 (2) ◽  
pp. 269-273 ◽  
Author(s):  
Kenichiro Kawai ◽  
Akiko Kageyama ◽  
Tomoko Tsumano ◽  
Soh Nishimoto ◽  
Kenji Fukuda ◽  
...  
Keyword(s):  
Wound Healing ◽  
Human Keratinocytes ◽  
Impaired Wound Healing

scholarly journals The Wound Healing Peptide, AES16-2M, Ameliorates Atopic Dermatitis In Vivo

Molecules ◽  
2021 ◽  
Vol 26 (4) ◽  
pp. 1168
Author(s):  
Myun Soo Kim ◽  
Jisun Song ◽  
Sunyoung Park ◽  
Tae Sung Kim ◽  
Hyun Jeong Park ◽  
...  
Keyword(s):  
Wound Healing ◽  
Atopic Dermatitis ◽  
Side Effects ◽  
Low Cost ◽  
Calcineurin Inhibitors ◽  
Human Keratinocytes ◽  
Peripheral Lymph ◽  
Therapeutic Peptides ◽  
Peptide Materials

Peptide materials have recently been considered for use in various industrial fields. Because of their efficacy, safety, and low cost, therapeutic peptides are studied for various diseases, including atopic dermatitis (AD). AD is a common inflammatory skin disease impairing the patient’s quality of life. Various therapies, such as treatments with corticosteroids, calcineurin inhibitors, and antibody drugs, have been applied, but numerous side effects have been reported, including skin atrophy, burning, and infection. In the case of antibody drugs, immunogenicity against the drugs can be a problem. To overcome these side effects, small peptides are considered therapeutic agents. We previously identified the small wound healing peptide AES16-2M with a sequence of REGRT, and examined its effects on AD in this study. Interestingly, the administration of AES16-2M downregulated the AD disease score, ear thickness, serum IgE, and thymic stromal lymphopoietin (TSLP) in AD mice. The thickness of the epidermal layer was also improved by AES16-2M treatment. In addition, quantities of IL-4-, IL-13-, and IL-17-producing CD4 T cells from peripheral lymph nodes and spleens were reduced by injection of AES16-2M. Furthermore, the expression of TSLP was significantly reduced in AES16-2M-treated human keratinocytes. Therefore, these results suggest that AES16-2M can be a novel candidate for AD treatment.

Mycophenolic acid affects basic functions of human keratinocytes in the IMPDH-dependent manner

2013 ◽  
Vol 91 (5) ◽  
pp. 333-340 ◽  
Author(s):  
J. Borowczyk ◽  
E. Laczna ◽  
K. Sporniak-Tutak ◽  
Z. Madeja ◽  
J. Drukala
Keyword(s):  
Wound Healing ◽  
Mycophenolic Acid ◽  
De Novo ◽  
Human Keratinocytes ◽  
Pcr Analysis ◽  
Dependent Manner ◽  
Differentiation Markers ◽  
Impaired Wound Healing ◽  
Basic Functions

Clinical studies suggest that the immunosuppressant MPA is associated with impaired wound healing. It is believed that the main cause of impairment is the inhibition of inflammatory response. However, it is unknown whether MPA may directly affect epidermal cells. The aim of our study was to examine the direct influence of mycophenolic acid, the selective blocker of de novo purine synthesis, on human epidermal keratinocyte morphology, proliferation, motile activity, and differentiation in in vitro culture. The number of keratinocytes cultured in the presence of MPA was counted and cell motility was measured by a time-lapse computer-aided method. Cell morphology was determined by flow and image cytometry methods. Real-time RT-PCR analysis was employed to investigate the expression of markers of differentiation. We showed that MPA induces irreversible inhibition of cell proliferation, causes cell enlargement and impairs cell locomotion in a time-dependent manner. The level of expression of differentiation markers was significantly reduced by MPA treatment. All these effects were reversed by the addition of guanine. Our results indicated that MPA impairs basic functions of human skin keratinocytes via intracellular guanosine nucleotide depletion, which may be directly reflected in wound healing problems in patients treated with this immunosuppressant.

scholarly journals Verbascoside Protects Gingival Cells against High Glucose-Induced Oxidative Stress via PKC/HMGB1/RAGE/NFκB Pathway

Antioxidants ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1445
Author(s):  
Pei-Fang Hsieh ◽  
Cheng-Chia Yu ◽  
Pei-Ming Chu ◽  
Pei-Ling Hsieh
Keyword(s):  
Oxidative Stress ◽  
Wound Healing ◽  
High Glucose ◽  
Inhibitory Effect ◽  
Diabetic Patients ◽  
Impaired Wound Healing ◽  
Stress Indicator ◽  
Patients With Diabetes ◽  
Nfκb Pathway ◽  
Oral Wound Healing

Impaired wound healing often occurs in patients with diabetes and causes great inconvenience to them. Aside from the presence of prolonged inflammation, the accumulation of oxidative stress is also implicated in the delayed wound healing. In the present study, we tested the effect of verbascoside, a caffeoyl phenylethanoid glycoside, on the improvement of cell viability and wound healing capacity of gingival epithelial cells under high glucose condition. We showed that verbascoside attenuated the high glucose-induced cytotoxicity and impaired healing, which may be associated with the downregulation of oxidative stress. Our results demonstrated that verbascoside increased the activity of the antioxidant enzyme SOD and reduced the oxidative stress indicator, 8-OHdG, as well as apoptosis. Moreover, verbascoside upregulated the PGC1-α and NRF1 expression and promoted mitochondrial biogenesis, which was mediated by suppression of PKC/HMGB1/RAGE/NFκB signaling. Likewise, we showed the inhibitory effect of verbascoside on oxidative stress was via repression of PKC/HMGB1/RAGE/NFκB activation. Also, our data suggested that the PKC-mediated oxidative stress may lead to the elevated production of inflammatory cytokines, IL-6 and IL-1β. Collectively, we demonstrated that verbascoside may be beneficial to ameliorate impaired oral wound healing for diabetic patients.

scholarly journals Redox Imbalance in T Cell-Mediated Skin Diseases

2010 ◽  
Vol 2010 ◽  
pp. 1-9 ◽  
Author(s):  
Saveria Pastore ◽  
Liudmila Korkina
Keyword(s):  
Oxidative Stress ◽  
Atopic Dermatitis ◽  
Contact Dermatitis ◽  
Skin Diseases ◽  
Redox Balance ◽  
Inflammatory Disorder ◽  
Chronic Inflammatory Disorder ◽  
Physical Chemical ◽  
Chemical Oxidants ◽  
Beneficial Outcome

The skin is permanently exposed to physical, chemical, and biological aggression by the environment. In addition, acute and chronic inflammatory events taking place in the skin are accompanied by abnormal release of pro-oxidative mediators. In this paper, we will briefly overview the homeostatic systems active in the skin to maintain the redox balance and also to counteract abnormal oxidative stress. We will concentrate on the evidence that a local and/or systemic redox dysregulation accompanies the chronic inflammatory disorder events associated to psoriasis, contact dermatitis, and atopic dermatitis. We will also discuss the fact that several well-established treatments for the therapy of chronic inflammatory skin disorders are based on the application of strong physical or chemical oxidants onto the skin, indicating that, in selected conditions, a further increase of the oxidative imbalance may lead to a beneficial outcome.

scholarly journals Type 2 immunity induced by bladder extracellular matrix enhances corneal wound healing

2021 ◽  
Vol 7 (16) ◽  
pp. eabe2635
Author(s):  
Xiaokun Wang ◽  
Liam Chung ◽  
Joshua Hooks ◽  
David R. Maestas ◽  
Andriana Lebid ◽  
...  
Keyword(s):  
Wound Healing ◽  
Immune Responses ◽  
Smooth Muscle Actin ◽  
Treated Group ◽  
Interleukin 4 ◽  
Impaired Wound Healing ◽  
Urinary Bladder Matrix ◽  
Incomplete Healing ◽  
Haze Formation

The avascular nature of cornea tissue limits its regenerative potential, which may lead to incomplete healing and formation of scars when damaged. Here, we applied micro- and ultrafine porcine urinary bladder matrix (UBM) particulate to promote type 2 immune responses in cornea wounds. Results demonstrated that UBM particulate substantially reduced corneal haze formation as compared to the saline-treated group. Flow cytometry and gene expression analysis showed that UBM particulate suppressed the differentiation of corneal stromal cells into α-smooth muscle actin–positive (αSMA+) myofibroblasts. UBM treatments up-regulated interleukin-4 (IL-4) produced primarily by eosinophils in the wounded corneas and CD4+ T cells in draining lymph nodes, suggesting a cross-talk between local and peripheral immunity. Gata1−/− mice lacking eosinophils did not respond to UBM treatment and had impaired wound healing. In summary, stimulating type 2 immune responses in the wounded cornea can promote proregenerative environments that lead to improved wound healing for vision restoration.

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