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2007 | 79 | 11 | 720-727
Tytuł artykułu

Cellular and Molecular Basis of Impaired Healing of Diabetic Foot Ulcers

Treść / Zawartość
Warianty tytułu
Języki publikacji
EN
Abstrakty
EN
Słowa kluczowe
Wydawca
Rocznik
Tom
79
Numer
11
Strony
720-727
Opis fizyczny
Daty
wydano
2007-11-01
online
2008-02-11
Twórcy
  • Department of Surgical Research and Transplantology, Medical Research Center, Polish Academy of Sciences, Warsaw
  • Department of Surgical Research and Transplantology, Medical Research Center, Polish Academy of Sciences, Warsaw
Bibliografia
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  • Hinz B: Formation and function of the myofibroblasts during tissue repair. J Invest Dermatol 2007; 127: 526-37.[PubMed][Crossref]
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  • Kauer P, Li A: Adhesive properties of human basal epidermal cells: an analysis of keratinocyte stem cells, transit amplyfying cells and postmitotic differentiating cells. J Invest Dermatol 2000; 114: 413-20.[Crossref]
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  • Santoro MM, Gaudino G: Cellular and molecular facets of keratinocyte reepithelialization during wound healing. Exp Cell Res 2005; 304: 274-86.[Crossref]
  • Usui ML, Underwood RA, Mansbridge JN, et al.: Morphological evidence for the role of suprabasal keratinocytes in wound reepithelialization. Wound Rep Reg 2005; 13: 468-79.[Crossref]
  • Marionnet C, Pierrard C, Vioux-Chagnpleau C, et al.: Interactions between fibroblasts and keratinocytes in morphogenesis of dermal epidermal junction in a model of reconstructed skin. J Dermatol 2006; 126: 971-79.
  • Wang T-W, Sun J-S, Huang Y-C, et al.: Skin basement membrane and extracellular matrix proteins characterization and quantification by real time RT-PCR. Biomaterials 2006; 27: 5059-68.[Crossref][PubMed]
  • Zimny S, Schatz H, Pfohl: Determinants and estimation of healing time in diabetic foot ulcers. J Diab Complic 2002; 16: 327-32.[Crossref]
  • Abbott CA, Vileikyte L, Williamson S, et al.: Multicenter study of the incidence of predictive risk factors for diabetic neuropathic foot ulceration. Diab Care 1998; 21: 1071-75.[Crossref]
  • Shun C-T, Chang Y-C, Wu H-P, et al.: Skin denervation in type 2 diabetes: correlations with diabetic duration and functional impairments. Brain 2004; 127: 1593-1605.
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  • Brack A, Stein C: The role of the peripheral nervous system in immune cells recruitment. Exp Neurol 2003: 184: 44-49.
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  • Galkowska H, Olszewski WL, Wojewodzka U, et al.: Neurogenic factors in the impaired healing of diabetic foot ulcers. J Surg Res 2006; 134: 252-58.[Crossref][PubMed]
  • Candel-Gonzales FJ, Alramadan M, Matesanz M, et al.: Infections in diabetic foot ulcers. Eur J Internal Med 2003; 14: 341-43.[Crossref]
  • Lipsky BA, Berendt AR, Gunner-Deery H, et al.: Diagnosis and treatment of diabetic foot infections. Clin Infect Dis 2004; 39: 885-910.[Crossref]
  • Edwards R, Harding KG: Bacteria and wound healing. Curr Opin Infect Dis 2004; 17: 91-96.[Crossref][PubMed]
  • Jones SG, Edwards R, Thomas DW: Inflammation and wound healing: the role of bacteria in the immuno-regulation of wound healing. Lower Extrem Wounds 2004; 3: 201-08.[Crossref]
  • Loots MAM, Lamme EN, Zeegelaar J, et al.: Differences in cellular infiltrate and extracellular matrix of chronic diabetic and venous ulcers versus acute wounds. J Invest Dermatol 1998; 111: 850-57.[PubMed][Crossref]
  • Nishikawa T, Edelstein D, Brownlee M: The missing link: A single unifying mechanism for diabetic complications. Kidney Internat 2000; 58, (Suppl. 77): S26-30.[Crossref]
  • Tsillibary EC: Microvascular basement membranes in diabetic mellitus. J Pathol 2003; 200: 537-46.[Crossref]
  • Gałkowska H, Olszewski WL, Wojewodzka U: Keratinocyte and dermal vascular endothelial cell capacities remain unimpaired in the margin of chronic venous ulcers. Arch Dermatol Res 2005; 296: 286-95.[PubMed][Crossref]
  • Diegelmann RF: Excessive neutrophils characterize chronic pressure ulcers. Wound Rep Reg 2003; 11: 490-95.[Crossref]
  • Dovi JV, He L-K, DiPietro LA: Accelerated wound closure in neutrophil-depleted mice. J Leukoc Biol 2003; 73: 448-55.[PubMed][Crossref]
  • Galkowska H, Wojewodzka U, Olszewski WL: Low recruitment of immune cells with increased expression of endothelial adhesion molecules in margins of the chronic diabetic foot ulcers. Wound Rep Reg 2005; 13: 248-54.[Crossref]
  • Engelhardt E, Toksoy A, Goebeler M, et al.: Chemokines IL8, GROλ, MCP1, IP10 and Mig are sequentially and differentially expressed during phasespecific infiltration of leukocyte subsets in human wound healing. Am J Pathol 1998; 153: 1849-60.
  • Wetzler C, Kaempfer H, Stallmeyer B, et al.: Large and sustained induction of chemokines during impaired wound healing in the genetically diabetic mouse: prolonged persistence of neutrophils and macrophages during the late phase of repair. J Invest Dermatol 2000; 115: 245-53.[Crossref][PubMed]
  • Barker JN, Jones ML, Mitra R, et al.: Modulation of keratinocyte-derived interleukin-8 which is chemotactic for neutrophils and T lymphocytes. Am J Pathol 1991; 139: 869-76.
  • Gibran NS, Ferguson M, Heimbach DM, et al.: Monocyte chemoattractant protein-1 mRNA expression in the human burn wound. J Surg Res 1997; 70: 1-6.[PubMed][Crossref]
  • Nomura S, Shouzu A, Omoto S, et al.: Significance of chemokines and activated platelets in patients with diabetes. Clin Exp Immunol 2000; 121: 437-43.[PubMed]
  • Gałkowska H, Wojewodzka U, Olszewski WL: Chemokines, cytokines and growth factors in keratinocytes and dermal endothelial cells in the margin of chronic diabetic foot ulcers. Wound Rep Reg 2006; 14: 558-65.[Crossref]
  • Elhadd TA, Kennedy G, McLaren M, et al.: Elevated levels of soluble E-selectin in diabetic patients with severe symptomatic peripheral arteries occlusive disease requiring angioplasty. Int Angiol 2000; 19: 171-75.
  • Michel G, Kemeny L, Peter RU, et al.: Interleukin-8 receptor-mediated chemotaxis of normal human epidermal cells. FEBS Lett 1992; 305: 241-43.
  • Rennekampff HO, Hansbrough JF, Kiessig V, et al.: Bioactive interleukin-8 is expressed in wounds and enhances wound healing. J Surg Res 2000; 93: 41-54.[PubMed][Crossref]
  • Boring L, Gosling J, Cleary M, et al.: Decreased lesion formation in CCR2 -/-mice reveals a role for chemokines in the initiation of atherosclerosis. Nature 1998; 394: 894-97.
  • Low QEH, Drugea IA, Duffner LA, et al.: Wound healing in MIP-1λ -/- and MCP-1 -/- mice. Am J Pathol 2001; 159: 457-63.
  • Quatresooz P, Henry F, Paquet P, et al.: Deciphering the impaired cytokine cascades in chronic leg ulcers (review). Internat J Molecul Med 2003; 11: 411-18.
  • Bennett SP, Griffiths GD, Schor AM, et al.: Growth factors in the treatment of diabetic foot ulcers. Br J Surg 2003; 90: 133-46.[Crossref]
  • Edmonds M, Bates M, Doxford M, et al.: New treatments in ulcer healing and wound infection. Diabetes Metab Res Rev 2000; 16 (Suppl 1): S51-54.[Crossref]
  • Jeffcoate W, Price P, Harding KG: Wound healing and treatments for people with diabetic foot ulcers. Diabetes Metab Res Rev 2004; 20(Suppl 1): S78-89.[Crossref]
  • Mulder GD: Diabetic foot ulcers: old problemnew technologies. Nephrol Dial Transplant 2001; 16: 695-98.[PubMed][Crossref]
  • Shure D, Senior RM, Griffin GL, et al.: PDGF AA homodimmers are potent chemoattractants for fibroblasts and neutrophils, and for monocytes activated by lymphocytes or cytokines. Biochem Biophys Res Commun 1992; 186: 1519-24.
  • Arnold F, West DC: Angiogenesis in wound healing. Pharmacol Ther 1991; 52: 407-22.[PubMed][Crossref]
  • Katz MH, Alvarez AF, Kirsner RS, et al.: Human wound fluid from acute wounds stimulates fibroblast and endothelial cell growth. J Am Acad Dermatol 1991; 25: 1054-58.[Crossref]
  • Falanga V, Shen J: Growth factors, signal transduction and cellular responses. In: Falanga V (ed.) Cutaneous wound healing. London: Martin Dunitz, 2001, pp. 81-93.
  • Angiolillo AL, Kanegane H, Sgadari C, et al.: Interleukin 15 promotes angiogenesis in vivo. Biochem Biophys Res Commun 1997; 233: 231-37.[Crossref]
  • Blakytny R, Jude EB, Gibson JM, et al.: Lack of insulin-like growth factor I (IGF I) in the basal keratinocyte layer of diabetic skin and diabetic foot ulcers. J Pathol 2000; 190: 589-94.
  • Yano S, Komine M, Fujimoto M, et al.: Interleukin 15 induces the signals of epidermal proliferation through ERK and PI 3-kinase in a human epidermal keratinocyte cell line, HaCaT. Biochem Biophys Res Commun 2003; 301: 841-47.
  • Krane JF, Murphy DP, Carter DM, et al.: Synergistic effects of epidermal growth factor (EGF) and insulin-like growth factor I/somatomedin c (IGF-1) on keratinocyte proliferation may be mediated by IGF-1 transmodulation of the EGF receptor. J Invest Dermatol 1991; 96: 419-24.
  • Kratz G, Lake M, Ljungstrom K, et al.: Effect of recombinant IGF binding protein-1 on primary cultures of human keratinocytes and fibroblasts: selective enhancement of IGF-1 but not IGF-2 induced cell proliferation. Exp Cell Res 1992; 202: 381-85.[Crossref]
  • Kane CJM, Hebda PA, Mansbridge JN, et al.: Direct evidence for spatial and temporal regulation of transforming growth factor β1 expression during cutaneous wound healing. J Cell Physiol 1991; 148: 157-73.
  • Gałkowska H, Olszewski WL, Wojewodzka U, et al.: Expression of apoptosis-and cell cycle-related proteins in epidermis of venous leg and diabetic foot ulcers. Surgery 2003; 134: 213-20.[Crossref][PubMed]
  • Lobmann R, Ambrosch A, Schultz G, et al.: Expression of matrix proteinases and their inhibitors in the wounds of diabetic and non-diabetic patients. Diabetologia 2002; 45: 1011-16.[PubMed]
  • Lobmann R, Schultz G, Lehnert H: Proteases and the diabetic foot syndrome: mechanisms and therapeutic implications. Diabet Care 2005; 28: 461-71.[Crossref]
  • Cullen B, Smith R, McCulloch E, et al.: Mechanism of action of Promogran, a protease modulating matrix, for the treatment of diabetic foot ulcers. Wound Rep Reg 2002; 10: 16-25.[Crossref]
  • Veves A, Shechan P, Pham HT: A randomized, controlled trial of Promogran (a collagen/ oxidized regenerated cellulose dressing) vs standard treatment in the management of diabetic foot ulcers. Arch Surg 2002; 137: 822-27.
  • Ghatnekar O, Willis M, Persson U: Costeffectiveness of treating deep diabetic foot ulcers with Promogran in four European countries. J Wound Care 2002; 11: 70-74.
  • Chin GA, Thigpin TG, Perrin KJ, et al.: Treatment of chronic ulcers in diabetic patients with a topic metalloproteinase inhibitor, doxycycline. Wounds 2003; 15: 315-23.
  • Saap LJ, Falanga V: Debridement performence index and its correlation with complete closure of diabetic foot ulcers. Wound Rep Reg 2002; 10: 354-59.[Crossref]
  • Lipsky BA: Empirical therapy for diabetic foot infections: are there clinical clues to guide antibiotic selection? Clin Microbiol Infect 2007; 13: 351-53.[Crossref][PubMed]
  • Fu X, Li X, Chehg B, et al.: Engineered growth factors and cutaneous wound healing: success and possible questions in the past 10 years. Wound Rep Reg 2005; 13: 122-30.[Crossref]
  • Koveker GB: Growth factors in clinical practice. Int J Clin Pract 2000; 54: 590-93.[PubMed]
  • Limova M: New therapeutic options for chronic wounds. Dermatol Clin 2002; 20: 357-63.[Crossref][PubMed]
  • Margolis DJ, Bartus C, Hoffstad O, et al.: Effectiveness of recombinant human platelets-derived growth factor for the treatment of diabetic neuropathic foot ulcers. Wound Rep Reg 2005: 13: 531-36.[Crossref]
  • Generini S, Tuveri MA, Matucci-Cerinic M, et al.: Topical application of nerve growth factor in human diabetic foot ulcers. A study of three cases. Exp Clin Endocrinol Diabetes 2004; 112: 542-44.[Crossref]
  • Cavallini M: Autologous fibroblasts to treat deep and complicated leg ulcers in diabetic patients. Wound Rep Reg 2007; 15: 35-38.[Crossref]
  • Caravaggi C, De Giglio R, Pritelli C, et al.: HYAFF 11-based autologous dermal and epidermal grafts in the treatment of nonifected diabetic plantar and dorsal foot ulcers. Diabetic Care 2003; 26: 2853-59.[Crossref]
Typ dokumentu
Bibliografia
Identyfikatory
Identyfikator YADDA
bwmeta1.element.-psjd-doi-10_2478_v10035-007-0112-9
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