Advanced glycation end products stimulate osteoblast apoptosis via the MAP kinase and cytosolic apoptotic pathways.
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D. Graves | L. Gerstenfeld | M. Alikhani | Z. Alikhani | P. Trackman | Louis Gerstenfeld | Dana T Graves | Mani Alikhani | Zoubin Alikhani | Coy Boyd | Christine M MacLellan | Markos Raptis | Rongkun Liu | Nicole Pischon | Philip C Trackman | N. Pischon | Rongkun Liu | M. Raptis | Coy M Boyd | Christine M Maclellan
[1] D. Graves,et al. Diabetes enhances mRNA levels of proapoptotic genes and caspase activity, which contribute to impaired healing. , 2006, Diabetes.
[2] T. Niwa,et al. Advanced glycation end product modification of bone proteins and bone remodelling: hypothesis and preliminary immunohistochemical findings , 2005, Annals of the rheumatic diseases.
[3] M. Noda,et al. Histological evidence of the altered distribution of osteocytes and bone matrix synthesis in klotho-deficient mice. , 2005, Archives of histology and cytology.
[4] S. Kato,et al. Advanced Glycation End‐Products Attenuate Human Mesenchymal Stem Cells and Prevent Cognate Differentiation Into Adipose Tissue, Cartilage, and Bone , 2005, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.
[5] H. Genant,et al. Osteoblast-derived PTHrP is a potent endogenous bone anabolic agent that modifies the therapeutic efficacy of administered PTH 1-34. , 2005, The Journal of clinical investigation.
[6] D. Graves,et al. Advanced Glycation End Products Enhance Expression of Pro-apoptotic Genes and Stimulate Fibroblast Apoptosis through Cytoplasmic and Mitochondrial Pathways* , 2005, Journal of Biological Chemistry.
[7] D. Graves,et al. FOXO1 Functions as a Master Switch That Regulates Gene Expression Necessary for Tumor Necrosis Factor-induced Fibroblast Apoptosis* , 2005, Journal of Biological Chemistry.
[8] D. Graves,et al. TNF‐α in vivo stimulates apoptosis in fibroblasts through caspase‐8 activation and modulates the expression of pro‐apoptotic genes , 2004, Journal of cellular physiology.
[9] P. Gane,et al. The triggering of human peritoneal mesothelial cell apoptosis and oncosis by glucose and glycoxydation products. , 2004, Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association.
[10] S. Yagihashi,et al. Reduced cell replication and induction of apoptosis by advanced glycation end products in rat Schwann cells. , 2004, Biochemical and biophysical research communications.
[11] D. Graves,et al. Diabetes alters the response to bacteria by enhancing fibroblast apoptosis. , 2004, Endocrinology.
[12] E. Romagnoli,et al. Skeletal involvement in patients with diabetes mellitus , 2004, Diabetes/metabolism research and reviews.
[13] R. Weinstein,et al. Glucocorticoids act directly on osteoblasts and osteocytes to induce their apoptosis and reduce bone formation and strength. , 2004, Endocrinology.
[14] B. Ortwerth,et al. 2-Ammonio-6-(3-oxidopyridinium-1-yl)hexanoate (OP-lysine) Is a Newly Identified Advanced Glycation End Product in Cataractous and Aged Human Lenses* , 2004, Journal of Biological Chemistry.
[15] A. Ashkenazi,et al. Tumor Necrosis Factor An Apoptosis JuNKie? , 2004, Cell.
[16] A. Schwartz,et al. Diabetes Mellitus: Does it Affect Bone? , 2003, Calcified Tissue International.
[17] S. Vatner,et al. Glycation end-product cross-link breaker reduces collagen and improves cardiac function in aging diabetic heart. , 2003, American journal of physiology. Heart and circulatory physiology.
[18] S. Chae,et al. JNK/SAPK is required in nitric oxide-induced apoptosis in osteoblasts , 2003, Archives of pharmacal research.
[19] G. Stein,et al. Advanced glycation end-products pentosidine and N " -carboxymethyllysine are elevated in serum of patients with osteoporosis , 2003 .
[20] J. Boehm,et al. p38 MAP kinases: key signalling molecules as therapeutic targets for inflammatory diseases , 2003, Nature Reviews Drug Discovery.
[21] D. Graves,et al. A role for advanced glycation end products in diminished bone healing in type 1 diabetes. , 2003, Diabetes.
[22] M. Kasuga,et al. Methylglyoxal induces apoptosis through activation of p38 mitogen-activated protein kinase in rat mesangial cells. , 2003, Kidney international.
[23] D. Saudek,et al. Advanced glycation endproducts and osteoarthritis , 2003, Current rheumatology reports.
[24] S. Erkaya,et al. Evaluation of bone turnover in postmenopausal patients with type 2 diabetes mellitus using biochemical markers and bone mineral density measurements , 2003, Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology.
[25] G. Johnson,et al. Mitogen-Activated Protein Kinase Pathways Mediated by ERK, JNK, and p38 Protein Kinases , 2002, Science.
[26] T. Kataoka,et al. H-Ras/Mitogen-activated Protein Kinase Pathway Inhibits Integrin-mediated Adhesion and Induces Apoptosis in Osteoblasts* , 2002, The Journal of Biological Chemistry.
[27] Ego Seeman,et al. Pathogenesis of bone fragility in women and men , 2002, The Lancet.
[28] M. Bogoyevitch,et al. Identification of the Critical Features of a Small Peptide Inhibitor of JNK Activity* , 2002, The Journal of Biological Chemistry.
[29] H. Vlassara,et al. Diabetes and advanced glycation endproducts , 2002, Journal of internal medicine.
[30] K. Ozono,et al. Role of advanced glycation end products in adynamic bone disease in patients with diabetic nephropathy. , 2001, American journal of kidney diseases : the official journal of the National Kidney Foundation.
[31] D. Barrio,et al. Non-enzymatic glycosylation of a type I collagen matrix: effects on osteoblastic development and oxidative stress , 2001, BMC Cell Biology.
[32] J. Lemonnier,et al. Increased osteoblast apoptosis in apert craniosynostosis: role of protein kinase C and interleukin-1. , 2001, The American journal of pathology.
[33] L. Beilin,et al. Advanced glycation end-products: a review , 2001, Diabetologia.
[34] A. Schmidt,et al. The biology of the receptor for advanced glycation end products and its ligands. , 2000, Biochimica et biophysica acta.
[35] T. Kislinger,et al. Blockade of RAGE suppresses periodontitis-associated bone loss in diabetic mice. , 2000, The Journal of clinical investigation.
[36] J. E. Hale,et al. Alterations of Cartilage and Collagen Expression during Fracture Healing in Experimental Diabetes , 2000, Connective tissue research.
[37] T. Kislinger,et al. N ε-(Carboxymethyl)Lysine Adducts of Proteins Are Ligands for Receptor for Advanced Glycation End Products That Activate Cell Signaling Pathways and Modulate Gene Expression* , 1999, The Journal of Biological Chemistry.
[38] M. Kohno,et al. Specific Activation of the p38 Mitogen-activated Protein Kinase Signaling Pathway and Induction of Neurite Outgrowth in PC12 Cells by Bone Morphogenetic Protein-2* , 1999, The Journal of Biological Chemistry.
[39] C. Y. Wang,et al. NF-kappaB antiapoptosis: induction of TRAF1 and TRAF2 and c-IAP1 and c-IAP2 to suppress caspase-8 activation. , 1998, Science.
[40] A. Parfitt,et al. Inhibition of osteoblastogenesis and promotion of apoptosis of osteoblasts and osteocytes by glucocorticoids. Potential mechanisms of their deleterious effects on bone. , 1998, The Journal of clinical investigation.
[41] T. Kishimoto,et al. Advanced Glycation Endproducts Stimulate Interleukin‐6 Production by Human Bone‐Derived Cells , 1997, Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research.
[42] R. G. Paul,et al. Glycation of collagen: the basis of its central role in the late complications of ageing and diabetes. , 1996, The international journal of biochemistry & cell biology.
[43] J. Baynes,et al. N epsilon-(carboxymethyl)lysine is a dominant advanced glycation end product (AGE) antigen in tissue proteins. , 1995, Biochemistry.
[44] E. Wang,et al. Inhibition of matrix-induced bone differentiation by advanced glycation end-products in rats , 1993, Diabetologia.
[45] T. Lyons,et al. Accumulation of Maillard Reaction Products in Skin Collagen in Diabetes and Aging a , 1992, Annals of the New York Academy of Sciences.
[46] J. Dequeker,et al. Bone mineral homeostasis in spontaneously diabetic BB rats. II. Impaired bone turnover and decreased osteocalcin synthesis. , 1989, Endocrinology.
[47] J. Aubin,et al. Mineralized bone nodules formedin vitro from enzymatically released rat calvaria cell populations , 1986, Calcified Tissue International.
[48] A. Habeeb,et al. Determination of free amino groups in proteins by trinitrobenzenesulfonic acid. , 1966, Analytical biochemistry.
[49] A. Lin,et al. Role of JNK activation in apoptosis: A double-edged sword , 2005, Cell Research.
[50] S. Yamagishi,et al. Possible participation of advanced glycation end products in the pathogenesis of osteoporosis in diabetic patients. , 2005, Medical hypotheses.
[51] Louis C Gerstenfeld,et al. Diabetes causes decreased osteoclastogenesis, reduced bone formation, and enhanced apoptosis of osteoblastic cells in bacteria stimulated bone loss. , 2004, Endocrinology.
[52] G. Stein,et al. Advanced glycation end-products pentosidine and N epsilon-carboxymethyllysine are elevated in serum of patients with osteoporosis. , 2003, Rheumatology.
[53] L. Xing,et al. Apoptosis in Bone Cells , 1998 .
[54] I. Darby,et al. Apoptosis is increased in a model of diabetes-impaired wound healing in genetically diabetic mice. , 1997, International Journal of Biochemistry and Cell Biology.
[55] Rongkun Liu,et al. Tumor Necrosis Factor- (cid:1) Mediates Diabetes-Enhanced Apoptosis of Matrix-Producing Cells and Impairs Diabetic Healing , 2006 .