Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0849640 (skin damage)
 1,516 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

MDI 301 is a picolinic acid-substituted ester of 9-cis retinoic acid. It has been shown in the past that MDI 301 increases epidermal thickness, decreases matrix metalloproteinase (MMP) activity, and increases procollagen synthesis in organ-cultured human skin. Unlike all-trans retinoic acid (RA), MDI 301 does not induce expression of proinflammatory cytokines or induce expression of leukocyte adhesion molecules in human skin. In the present study we examined topical MDI 301 treatment for ability to improve the structure and function of skin in three models of skin damage in rodents and for ability to improve abrasion wound healing in these models. MDI 301 was applied daily to the skin of rats treated with the potent corticosteroid, clobetasol propionate, to the skin of diabetic rats (8 weeks posttreatment with streptozotocin) and to the skin of aged (14-16-month-old) rats. In all three models, subsequently induced abrasion wounds healed more rapidly in the retinoid-treated animals than in vehicle-treated controls. Immediately after complete wound closure, tissue from the wound site (as well as from a control site) was put into organ culture and maintained for 3 days. At the end of the incubation period, culture fluids were assessed for soluble type I collagen and for MMPs-2 and -9. In all three models, the level of type I collagen was increased and MMP levels were decreased by MDI 301. In all three models, skin irritation during the retinoid-treatment phase was virtually nonexistent.
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PMID:MDI 301, a nonirritating retinoid, improves abrasion wound healing in damaged/atrophic skin. 1821 83

Diabetic foot ulcerations could result in serious consequences such as amputations. The up-regulation of matrix metalloproteinases and down-regulation of TIMP1 were remarked as distinctive biological characteristics in the diabetic dermal fibroblast. The current study was performed in order to clarify the effect of high glucose on formation of diabetic dermal fibroblast cell. In addition, the effect of MDI 301 on ameliorating diabetic fibroblasts was investigated in this study. The mRNA and protein expression levels of MMPs, TIMP1 and catalase were evaluated against fibroblasts treated with high glucose (30 mM) using qRT-PCR, western blotting and zymography assays. Methods were also employed for investigating the biological effects of MDI 301 on high glucose-induced diabetic fibroblasts. In this study, we found that the unbalance of oxidative stress induced by high glucose concentration play an important role in the formation of diabetic dermal fibroblast from normal cells. In addition, MDI 301, a picolinic acid-substituted ester of 9-cis retinoic acid was employed in this study in order to ameliorate symptoms on diabetic dermal fibroblast induced by high glucose concentration. We found MDI 301 alleviate the effects of high glucose-induced skin damage by balancing the oxidative stress and regulating the MMPs and TIMP1 levels. Our finding indicated that MDI 301 offers the potential for repairing the faulty skin function arising from diabetes.
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PMID:MDI 301, a synthetic retinoid, depressed levels of matrix metalloproteinases and oxidative stress in diabetic dermal fibroblasts. 2842 69