Apoptosis is increased in a model of diabetes-impaired wound healing in genetically diabetic mice.

[1]  Jia Guo,et al.  Neutralization of TGF-β by Anti-TGF-β Antibody Attenuates Kidney Hypertrophy and the Enhanced Extracellular Matrix Gene Expression in STZ-Induced Diabetic Mice , 1996, Diabetes.

[2]  A. Boulton.  The Pathogenesis of Diabetic Foot Problems: an Overview , 1996, Diabetic medicine : a journal of the British Diabetic Association.

[3]  J. Shaw,et al.  The Histology of Diabetic Foot Ulcers , 1996, Diabetic medicine : a journal of the British Diabetic Association.

[4]  W. Waldhäusl,et al.  High-Glucose–Triggered Apoptosis in Cultured Endothelial Cells , 1995, Diabetes.

[5]  John Calvin Reed,et al.  The alpha 5 beta 1 integrin supports survival of cells on fibronectin and up-regulates Bcl-2 expression. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[6]  Z. Werb,et al.  Suppression of ICE and apoptosis in mammary epithelial cells by extracellular matrix , 1995, Science.

[7]  M. Longaker,et al.  Tissue inhibitor of metalloproteinases-1 is decreased and activated gelatinases are increased in chronic wounds. , 1995, The Journal of investigative dermatology.

[8]  L. Aiello,et al.  Vascular endothelial growth factor in ocular fluid of patients with diabetic retinopathy and other retinal disorders. , 1994, The New England journal of medicine.

[9]  R. Clark,et al.  Wound repair in the context of extracellular matrix. , 1994, Current opinion in cell biology.

[10]  G. Morahan,et al.  Genetic and physiological association of diabetes susceptibility with raised Na+/H+ exchange activity. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[11]  R. Bucala,et al.  Pathogenic effects of advanced glycosylation: biochemical, biologic, and clinical implications for diabetes and aging. , 1994, Laboratory investigation; a journal of technical methods and pathology.

[12]  H. Stähelin,et al.  TGF‐βS and TGF‐β type II receptor in human epidermis: Differential expression in acute and chronic skin wounds , 1993 .

[13]  F. Grinnell,et al.  Wound fluid from chronic leg ulcers contains elevated levels of metalloproteinases MMP-2 and MMP-9. , 1993, The Journal of investigative dermatology.

[14]  T. Lyons,et al.  Accumulation of Maillard reaction products in skin collagen in diabetes and aging. , 1993, The Journal of clinical investigation.

[15]  E Ruoslahti,et al.  Expression of transforming growth factor beta is elevated in human and experimental diabetic nephropathy. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[16]  A. Vaheri,et al.  Proteolytic activity in leg ulcer exudate , 1993, Experimental dermatology.

[17]  S. Ben‐Sasson,et al.  Identification of programmed cell death in situ via specific labeling of nuclear DNA fragmentation , 1992, The Journal of cell biology.

[18]  F. Grinnell,et al.  Degradation of Fibronectin and Vitronectin and Vitronectin in Chronic Wound Fluid: Analysis by Cell Blotting, Immunoblotting, and Cell Adhesion Assays , 1992 .

[19]  D. Yue,et al.  Interaction of Ascorbic Acid and Glucose on Production of Collagen and Proteoglycan by Fibroblasts , 1991, Diabetes.

[20]  G. Gabbiani,et al.  Alpha-smooth muscle actin is transiently expressed by myofibroblasts during experimental wound healing. , 1990, Laboratory investigation; a journal of technical methods and pathology.

[21]  R. Rolandi,et al.  Prevention of Diabetes-Increased Aging Effect on Rat Collagen-Linked Fluorescence by Aminoguanidine and Rutin , 1990, Diabetes.

[22]  D. Greenhalgh,et al.  PDGF and FGF stimulate wound healing in the genetically diabetic mouse. , 1990, The American journal of pathology.

[23]  H. Oxlund,et al.  The influence of experimental diabetes and insulin treatments on the biochemical properties of rat skin incisional wounds. , 1987, Acta chirurgica Scandinavica.

[24]  R. Timpl,et al.  Solubilization of protein BM‐40 from a basement membrane tumor with cheating agents and evidence for its identity with osteonectin and SPARC , 1987, FEBS letters.

[25]  G. Gabbiani,et al.  A monoclonal antibody against alpha-smooth muscle actin: a new probe for smooth muscle differentiation , 1986, The Journal of cell biology.

[26]  S. Toledo,et al.  Glucose Toxicity for Human Endothelial Cells in Culture: Delayed Replication, Disturbed Cell Cycle, and Accelerated Death , 1985, Diabetes.

[27]  F. Logerfo,et al.  Current concepts. Vascular and microvascular disease of the foot in diabetes. Implications for foot care. , 1984, The New England journal of medicine.

[28]  D. Rowe,et al.  Construction of DNA sequences complementary to rat alpha 1 and alpha 2 collagen mRNA and their use in studying the regulation of type I collagen synthesis by 1,25-dihydroxyvitamin D. , 1984, Biochemistry.

[29]  M. Khatami,et al.  Stimulation of Retinal Capillary Pericyte Protein and Collagen Synthesis in Culture by High-Glucose Concentration , 1984, Diabetes.

[30]  S. Hsu,et al.  Use of avidin-biotin-peroxidase complex (ABC) in immunoperoxidase techniques: a comparison between ABC and unlabeled antibody (PAP) procedures. , 1981, The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society.

[31]  M. L. Powers,et al.  Effect of glucose and insulin on collagen secretion by human skin fibroblasts in vitro , 1977, Nature.

[32]  C. McCollum,et al.  Venous ulcer fibroblasts compared with normal fibroblasts show differences in collagen but not fibronectin production under both normal and hypoxic conditions. , 1996, The Journal of investigative dermatology.

[33]  A. Desmoulière,et al.  Apoptosis mediates the decrease in cellularity during the transition between granulation tissue and scar. , 1995, The American journal of pathology.

[34]  T. K. Hunt,et al.  Wound healing and wound infection : theory and surgical practice , 1980 .