PDL1 triggered from binding eIF3I contributes to ameliorate diabetes associated wound healing defects by regulating IRS4
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE171372 | GEO | 2024/04/02
REPOSITORIES: GEO
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Project description:PDL1 triggered from binding eIF3I contributes to ameliorate diabetes associated wound healing defects by regulating IRS4
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Project description:Transcriptional profiling of SE-14000 stimulated wound healing associated cells (HaCat, NHDF, HMEC-1) comparing control untreated cells. Goal was to determine the effects of SE-14000 to the wound healing associated cells (HaCat, NHDF, HMEC-1).
2020-07-07 | GSE100902 | GEO
Project description:Impaired wound healing is a major complication of diabetes, and despite the associated risks, treatment strategies for diabetic wounds remain limited. This is due, in part, to an incomplete understanding of the underlying pathological mechanisms, including the effects of hyperglycemia on components of the extracellular matrix (ECM). In the current study, we explored whether the expression of thrombospondin 2 (TSP2), a matricellular protein with a demonstrated role in response to injury, was associated with delayed healing in diabetes. First, we found that TSP2 expression was elevated in diabetic mice and skin from patients with diabetes. Then, to determine the contribution of TSP2 to impaired healing in diabetes, we developed a novel diabetic TSP2-deficient model. Though the TSP2-deficient mice developed obesity and hyperglycemia comparable with diabetic control mice, they exhibited significantly improved healing, characterized by accelerated reepithelialization and increased granulation tissue formation, fibroblast migration, and blood vessel maturation. We further found that hyperglycemia increased TSP2 expression in fibroblasts, the major cellular source of TSP2 in wounds. Mechanistically, high glucose increased activation of the hexosamine pathway and nuclear factor-?B signaling to elevate TSP2 expression. Our studies demonstrate that hyperglycemia-induced TSP2 expression contributes to impaired healing in diabetes.
| S-EPMC6754242 | biostudies-literature
Project description:Circulating miRNAs constitute a novel class of disease biomarkers, which are altered in diabetes but the effect of diabetes associated inflammation as seen in chronic wounds is unknown. We here compared the miRNA pattern in diabetic patients in presence or absence of chronic wound with PAD. The clinical plasma samples were obtained from Heart and Diabetes centre, NRW and compared for plasma miRNA levels in 2 pools of 17 T2DM+PAD+Wound patients vs 2 pools from 20 T2DM controls
2015-06-09 | E-GEOD-49885 | biostudies-arrayexpress
Project description:Transcription profiling by array of wounded Nematostella juvenile polyps compared against uninjured animals and animals exposed to the MAPK inhibitor U0126
2014-03-10 | E-MTAB-2341 | biostudies-arrayexpress
Project description:ObjectiveThe redox enzyme p66Shc produces hydrogen peroxide and triggers proapoptotic signals. Genetic deletion of p66Shc prolongs life span and protects against oxidative stress. In the present study, we evaluated the role of p66Shc in an animal model of diabetic wound healing.Research design and methodsSkin wounds were created in wild-type (WT) and p66Shc(-/-) control and streptozotocin-induced diabetic mice with or without hind limb ischemia. Wounds were assessed for collagen content, thickness and vascularity of granulation tissue, apoptosis, reepithelialization, and expression of c-myc and beta-catenin. Response to hind limb ischemia was also evaluated.ResultsDiabetes delayed wound healing in WT mice with reduced granulation tissue thickness and vascularity, increased apoptosis, epithelial expression of c-myc, and nuclear localization of beta-catenin. These nonhealing features were worsened by hind limb ischemia. Diabetes induced p66Shc expression and activation; wound healing was significantly faster in p66Shc(-/-) than in WT diabetic mice, with or without hind limb ischemia, at 1 and 3 months of diabetes duration and in both SV129 and C57BL/6 genetic backgrounds. Deletion of p66Shc reversed nonhealing features, with increased collagen content and granulation tissue thickness, and reduced apoptosis and expression of c-myc and beta-catenin. p66Shc deletion improved response to hind limb ischemia in diabetic mice in terms of tissue damage, capillary density, and perfusion. Migration of p66Shc(-/-) dermal fibroblasts in vitro was significantly faster than WT fibroblasts under both high glucose and hypoxia.Conclusionsp66Shc is involved in the delayed wound-healing process in the setting of diabetes and ischemia. Thus, p66Shc may represent a potential therapeutic target against this disabling diabetes complication.
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Project description:MicroRNA microarray profiling analysis was performed on skin biopsies from unwounded mice, and from mice 1 day or 5 days post-wounding (3 mice per groups)
2013-02-28 | E-MTAB-1518 | biostudies-arrayexpress
Project description:Circulating miRNAs constitute a novel class of disease biomarkers, which are altered in diabetes but the effect of diabetes associated inflammation as seen in chronic wounds is unknown. We here compared the miRNA pattern in diabetic patients in presence or absence of chronic wound with PAD.
2015-06-09 | GSE49885 | GEO
Project description:Polymersomes have been extensively used in the delivery of both small and macromolecular payloads. However, the controlled delivery of gaseous therapeutics (e.g., nitric oxide, NO) remains a grand challenge due to its difficulty in loading of gaseous payloads into polymersomes without premature leakage. Herein, NO-releasing vesicles could be fabricated via the self-assembly of NO-releasing amphiphiles, which were synthesized by the direct polymerization of photoresponsive NO monomers (abbreviated as oNBN, pNBN, and BN). These monomers were rationally designed through the integration of the photoresponsive behavior of N-nitrosoamine moieties and the self-immolative chemistry of 4-aminobenzyl alcohol derivatives, which outperformed conventional NO donors such as diazeniumdiolates (NONOates) and S-nitrosothiols (SNOs) in terms of ease of preparation, stability of storage, and controllability of NO release. The unique design made it possible to selectively release NO by a light stimulus and to regulate the NO release rates. Importantly, the photo-mediated NO release could be manipulated in living cells and showed promising applications in the treatment of corneal wounds. In addition to delivering NO, the current design enabled the synergistic delivery of NO and other therapeutic payloads by taking advantage of NO release-mediated traceless crosslinking of the vesicles.
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Project description:Natural hosts of simian immunodeficiency virus (SIV) avoid AIDS despite lifelong infection. Here, we examined how this outcome is achieved by comparing a natural SIV host, African green monkey (AGM) to an AIDS susceptible species, rhesus macaque (RM). To asses gene expression profiles from acutely SIV infected AGMs and RMs, we developed a systems biology approach termed Conserved Gene Signature Analysis (CGSA), which compared RNA sequencing data from rectal AGM and RM tissues to various other species. We found that AGMs rapidly activate, and then maintain, evolutionarily conserved regenerative wound healing mechanisms in mucosal tissue. The wound healing protein fibronectin shows distinct tissue distribution and abundance kinetics in AGMs. Furthermore, AGM monocytes exhibit an embryonic development and repair/regeneration signature featuring TGF-β and concomitant reduced expression of inflammatory genes compared to RMs. This regenerative wound healing process likely preserves mucosal integrity and prevents inflammatory insults that underlie immune exhaustion in RMs.
| S-EPMC6841668 | biostudies-literature