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Glutathione enhances fibroblast collagen contraction and protects keratinocytes from apoptosis in hyperglycaemic culture
dc.contributor.authorDeveci, Mustafaen_US
dc.contributor.authorGilmont, Robert R.en_US
dc.contributor.authorDunham, W. R.en_US
dc.contributor.authorMudge, B. P.en_US
dc.contributor.authorSmith, D. J.en_US
dc.contributor.authorMarcelo, Cynthia L.en_US
dc.date.accessioned2010-06-01T21:29:44Z
dc.date.available2010-06-01T21:29:44Z
dc.date.issued2005-02en_US
dc.identifier.citationDeveci, M.; Gilmont, R.R.; Dunham, W.R.; Mudge, B.P . ; Smith, D.J.; Marcelo, C.L. (2005). "Glutathione enhances fibroblast collagen contraction and protects keratinocytes from apoptosis in hyperglycaemic culture." British Journal of Dermatology 152(2): 217-224. <http://hdl.handle.net/2027.42/74552>en_US
dc.identifier.issn0007-0963en_US
dc.identifier.issn1365-2133en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/74552
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=15727631&dopt=citationen_US
dc.description.abstractBackground  Cutaneous wound healing is relatively slow in patients with diabetes. Objectives  To test the hypothesis that this defect in healing of wounds in patients with diabetes results from dysfunction of skin fibroblasts and epidermal keratinocytes and that this dysfunction is related to disrupted intracellular glutathione (GSH) homeostasis. Methods  We investigated the effects of esterified GSH on the contraction of fibroblasts in a fibroblast-populated collagen lattice and on keratinocyte apoptosis. Results  High glucose medium (hyperglycaemia) reduced the contraction ability of fibroblasts ( P <  0·05). The normalization of glucose medium concentrations for hyperglycaemic fibroblasts did not restore the contraction capacity. The percentage of apoptotic keratinocytes was statistically higher in hyperglycaemic cells ( P <  0·05). GSH media concentrations ranging from 0·1 to 100 µmol L −1 restored the ability of hyperglycaemic fibroblasts to contract the gels in a concentration-dependent manner. Primary human keratinocytes grown in hyperglycaemic medium were more susceptible to apoptosis, and treatment with esterified GSH rescued the keratinocytes from apoptosis. Conclusions  These data suggest that intracellular GSH can normalize skin cell functions disrupted by in vitro cell growth under hyperglycaemic conditions.en_US
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dc.format.extent3109 bytes
dc.format.mimetypeapplication/pdf
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dc.publisherBlackwell Science Ltden_US
dc.rights2005 British Association of Dermatologistsen_US
dc.subject.otherApoptosisen_US
dc.subject.otherDiabetesen_US
dc.subject.otherFibroblast Contractionen_US
dc.subject.otherGlutathioneen_US
dc.subject.otherWound Healingen_US
dc.titleGlutathione enhances fibroblast collagen contraction and protects keratinocytes from apoptosis in hyperglycaemic cultureen_US
dc.typeArticleen_US
dc.subject.hlbsecondlevelDermatologyen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationum† Biophysics Research Division, University of Michigan, Medical Center, Kresge I R 5659, Ann Arbor, MI 48109, U.S.A.en_US
dc.contributor.affiliationother* Department of Plastic and Reconstructive Surgeryen_US
dc.identifier.pmid15727631en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/74552/1/j.1365-2133.2004.06329.x.pdf
dc.identifier.doi10.1111/j.1365-2133.2004.06329.xen_US
dc.identifier.sourceBritish Journal of Dermatologyen_US
dc.identifier.citedreferenceMellin TN, Cashen DE, Ronan JJ et al. Acidic fibroblast growth factor accelerates dermal wound healing in diabetic mice. J Invest Dermatol 1995; 103: 850 – 5.en_US
dc.identifier.citedreferenceTomasek JJ, Haaksma CJ, Eddy RJ, Vaughan MB. Fibroblast contraction occurs on release of tension in attached collagen lattices: dependency on an organized actin cytoskeleton and serum. Anat Rec 1992; 232: 359 – 68.en_US
dc.identifier.citedreferenceGermain L, Jean A, Auger FA, Garrel DR. Human wound healing fibroblasts have greater contractile properties than dermal fibroblasts. J Surg Res 1994; 57: 268 – 73.en_US
dc.identifier.citedreferenceObara K, Nikcevic G, Pestic L et al. Fibroblast contractility without an increase in basal myosin light chain phosphorylation in wild type cells and cells expressing the catalytic domain of myosin light chain kinase. J Biol Chem 1995; 270: 18734 – 7.en_US
dc.identifier.citedreferenceHehenberger K, Heilborn JD, Brismar K, Hansson A. Inhibited proliferation of fibroblasts derived from chronic diabetic wounds and normal dermal fibroblasts treated with high glucose associated with increased formation of l-lactate. Wound Repair Regen 1998; 6: 135 – 41.en_US
dc.identifier.citedreferenceMorocutti A, Sethi M, Hayward A et al. Glutathione reverses the growth abnormalities of skin fibroblasts from insulin-dependent diabetic patients with nephropathy. J Am Soc Nephrol 1998; 9: 1060 – 6.en_US
dc.identifier.citedreferenceCheng H, Feldman EL. Bidirectional regulation of p38 kinase and c-jun N-terminal protein kinase by insulin-like growth factor-I. J Biol Chem 1998; 273: 14560 – 5.en_US
dc.identifier.citedreferenceBaumgartner-Parzer SM, Wagner L, Petterman M et al. High-glucose-triggered apoptosis in cultured endothelial cells. Diabetes 1995; 44: 1323 – 7.en_US
dc.identifier.citedreferenceMehlen P, Schulze-Osthoff K, Arrigo A. Small stress proteins as novel regulators of apoptosis. J Biol Chem 1996; 271: 16510 – 14.en_US
dc.identifier.citedreferenceGavrieli Y, Sherman Y, Ben-Sasson SA. Identification of programmed cell death in situ via specific labeling of nuclear DNA fragmentation. J Cell Biol 1992; 119: 493 – 501.en_US
dc.identifier.citedreferenceKashiwagi A, Asahina T, Nishiho Y et al. Glycation, oxidative stress, and scavenging activity. Diabetes 1996; 45 ( Suppl. 3 ): S84 – 6.en_US
dc.identifier.citedreferenceShan XQ, Aw TY, Jones DP. Glutathione-dependent protection against oxidative injury. Pharmacol Ther 1990; 47: 61 – 71.en_US
dc.identifier.citedreferenceMudge B, Harris C, Rees R. Altered glutathione status in two examples of chronic human wounds. Surg Forum 1998; 49: 629.en_US
dc.identifier.citedreferenceBell E, Ivarsson B, Merrill C. Production of a tissue like structure by contraction of collagen lattices by human fibroblasts of different differential potential in vitro. Proc Natl Acad Sci USA 1979; 76: 1274 – 8.en_US
dc.identifier.citedreferenceMarcelo CL, Duel EA, Rhodes LM, Dunham WR. An in vitro model of essential fatty acid deficiency. J Invest Dermatol 1992; 99: 771 – 7.en_US
dc.identifier.citedreferenceKuzuya M, Satake S, Ai S et al. Inhibition of angiogenesis on glycated collagen lattices. Diabetologia 1998; 41: 491 – 9.en_US
dc.identifier.citedreferencePuolakkainen PA, Twardzik DR, Ranchalis JE et al. The enhancement in wound healing by transforming growth factor-β1 (TGF-β1) depends on the topical delivery system. Ann Surg Res 1995; 58: 321 – 9.en_US
dc.identifier.citedreferenceHeggers JP, Elzaim H, Garfield R et al. Effect of the combination of Aloe vera, nitroglycerin, and L-NAME on wound healing in the rat excisional model. J Altern Complement Med 1997; 3: 149 – 53.en_US
dc.identifier.citedreferenceShukla A, Rasik AM, Patnaik GK. Depletion of reduced glutathione, ascorbic acid, vitamin E and antioxidant defence enzymes in a healing cutaneous wound. Free Radic Res 1997; 26: 93 – 101.en_US
dc.identifier.citedreferencePierce GF, Vande Berg J, Rudolph R et al. Platelet-derived growth factor-bb and transforming growth factor beta 1 selectively modulate glycosaminoglycans, collagen, and myofibroblasts in excisional wounds. Am J Pathol 1991; 138: 629 – 46.en_US
dc.identifier.citedreferenceRobson MC, Phillips LG, Thomason LE et al. Platelet-derived growth factor-BB for the treatment of chronic pressure ulcers. Lancet 1992; 339: 23 – 5.en_US
dc.identifier.citedreferenceLiechty KW, Nespit M, Herlyn M et al. Adenoviral-mediated overexpression of platelet-derived growth factor-b corrects ischemic impaired wound healing. J Invest Dermatol 1999; 113: 375 – 83.en_US
dc.identifier.citedreferenceErlich HP, Cremona O, Gabbiani G. The expression of α2β1 integrin and α-smooth muscle actin in fibroblasts grown on collagen. Cell Biochem Func 1998; 16: 129 – 37.en_US
dc.identifier.citedreferenceAsaga H, Kukichi S, Yoshizato K. Collagen gel contraction by fibroblasts requires cellular fibronectin but not plasma fibronectin. Exp Cell Res 1991; 193: 167 – 74.en_US
dc.identifier.citedreferenceMalinda KM, Sidhu GS, Mani H et al. Thymosin β4 accelerates wound healing. J Invest Dermatol 1999; 113: 364 – 8.en_US
dc.identifier.citedreferenceAsensi M, Sastre J, Pallardo FV et al. Ratio of reduced to oxidized glutathione as indicator of oxidative stress status and DNA damage. Methods Enzymol 1997; 299: 267 – 76.en_US
dc.identifier.citedreferenceUrata Y, Yamamoto H, Goto S et al. Long exposure to high glucose concentration impairs the responsive expression of γ-glutamylcystein synthetase by interleukin-1β and tumor necrosis factor-α in mouse endothelial cells. J Biol Chem 1999; 271: 15146 – 52.en_US
dc.identifier.citedreferenceFinco TS, Beg AA, Baldwin AS. Inducible phosphorylation of I kappa B alpha is not sufficient for its dissociation from NF-κB and is inhibited by protease inhibitors. Proc Natl Acad Sci USA 1994; 91: 11884 – 8.en_US
dc.identifier.citedreferenceNakayama K, Shimizu H, Mitomo K et al. A lymphoid cell-specific nuclear factor containing c-rel-like proteins preferentially interacts with interleukin-6 kappa b-related motifs whose activities are repressed in lymphoid cells. Mol Cell Biol 1999; 12: 1736 – 46.en_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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