A Review on Role of Advanced Glycation End products (AGEs) in Rheumatoid Arthritis
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2015,
Vol. 3 No. 1 > A Review on Role of Advanced Glycation End products (AGEs) in Rheumatoid Arthritis
Authors
- Ravinder Kumar
Chitkara College of Pharmacy, Chitkara University, Rajpura, Punjab-140401
- Sandeep Arora
Chitkara College of Pharmacy, Chitkara University, Rajpura, Punjab-140401
- Pratima Syal
Chitkara College of Pharmacy, Chitkara University, Rajpura, Punjab-140401
- Mayank Sippy
Chitkara College of Pharmacy, Chitkara University, Rajpura, Punjab-140401
Keywords
Advance glycated end products, RAGE, Rheumatoid arthritis
Abstract
Rheumatoid arthritis (RAa) is a systemic inflammatory connective tissue disease with polyarthritis as a prominent feature; however, extra-articular symptoms and signs are always present. Aadvanced glycation end products with ability of cross-linking of proteins characteristic fluorescence and reaction with AaGEe-specific receptor RAaGEe (receptor for AaGEes). AaGEes action as well as AaGEe formation is directly related to both to inflammation and oxidative stress. RAaGEe is a 35-kDa polypeptide whose gene is located at the junction of the class II and III HLAla regions on chromosome. ligation of RAaGEe has been shown to activate p21ras and mitogen-activated protein (MAaP) kinase, and stimulate nuclear translocation of the transcription factor NF-κB, thereby, resulting in the transcription of target genes thus may induce chronic cellular activation and tissue damage.
References
- A Agarwal S K, Narsimulu G, Handa R, Misra A, Aggarwal S, Kumar U, Naidu M, Agnihotri N, Parikh S (2002). The Indian experience: A multicenter assessment of its safety & effectiveness in the treatment of active rheumatoid arthritis. Journal of Indian Rheumatology Association, 10: 32-35.
- A Ames P, Murat A, Isenberg DA and Nourooz-Z (1999). Oxidative stress in systemic lupus erythematosus and allied conditions with vascular involvement. Rheumatology (Oxford), 38(6):529–534.
- A Arshad A and Mohammed S (2005). Mortality in rheumatoid arthritis: Time to take it seriously. Journal of Rheumatology, 8:154–158.
- Basta G, Lazzerini G, Massaro M, Simoncini T, Tanganelli P, Fu C, Kislinger T, Stern DM, Schmidt AM, Caterina R (2002). Advanced glycation end products activate endothelium through signal-transduction receptor RAGE: a mechanism for amplification of inflammatory responses. Circulation, 105: 816–22. http://dx.doi.org/10.1161/hc0702.104183
- Baynes JW, Thorpe SR (2000). Glycoxidation and lipoxidation in atherosclerosis, Free Radical Biology & Medicine, 28: 1708– 1716. http://dx.doi.org/10.1016/S0891-5849(00)00228-8
- Burmester G, Bruno S, Gernot K and Raimund W (1997). Mononuclear phagocytes and rheumatoid synovitis: mastermind or workhorse in arthritis. Arthritis Rheum, 40:5–18. http://dx.doi.org/10.1002/art.1780400104
- David H, Adrian F, Georg N, Frank E, Remy C, Oliver D, Markus B, Lukas E, Michel N, Renate G, Thomas F, Steffen G, Frank R (2002). Anti-tumour necrosis factor-α treatment improves endothelial dysfunction in patients with rheumatoid arthritis. Circulation, 106:2184-2187. http://dx.doi.org/10.1161/01.CIR.0000037521.71373.44
- Feldmann M, Brennan FM, Maini RN (1996). Role of cytokines in rheumatoid arthritis. Annu Rev Immunol, 14:397–440.
- Gerli R, Goodson NJ (2005). Cardiovascular involvement in rheumatoid arthritis. Lupus, 14:1-4. http://dx.doi.org/10.1002/art.20851
- Harry M, James M, Tauras, Jason S, Osamu H, Rebecca A. (1997). Activation of the receptor for advanced glycation end products triggers a p21(ras) – dependent mitogen-activated protein kinase pathway regulated by oxidant stress. Journal of Biological Chemistry, 272(28): 17810–17814. http://dx.doi.org/10.1074/jbc.272.28.17810
- Hofmann MA, Drury S, Fu C, Qu W, Taguchi A, Lu Y, Avila C, Kambham N, Bierhaus A, Nawroth P, Neurath MF, Slattery T, Beach D, McClary J, Nagashima M, Morser J, Stern D, Schmidt AM (1999). RAGE mediates a novel proinflammatory axis: the cell surface receptor for S100/calgranulin polypeptides. Cell, 97:889–901. http://dx.doi.org/10.1016/S0092-8674(00)80801-6
- Hofmann MA, Drury S, Hudson BI, Gleason MR, Qu W, Lu Y, Lalla E, Chitnis S, Monteiro J, Stickland MH, Bucciarelli LG, Moser B, Moxley G, Itescu S, Grant PJ, Gregersen PK,
- Stern DM, Schmidt AM (2002). RAGE and arthritis: the G82S polymorphism amplifies the inflammatory response. Genes Immun, 3:123-135. http://dx.doi.org/10.1002/art.10262
- Hou FF, Jiang JP, Guo JQ, Wang GB, Zhang X, Stern DM, Schmidt AM, Owen WF (2002). Receptor for advanced glycation end products on human synovial fibroblasts: role in the pathogenesis of dialysis-related amyloidosis. Journal of the American Society of Nephrology, 13:1296–306.
- Inmaculada D, Rincon M, Agustin E (2003). Atherosclerotic cardiovascular disease in rheumatoid arthritis. Current Rheumatology Reports, 5:278–286. http://dx.doi.org/10.1007/s11926-003-0006-8
- J. R. Chen, M. Takahashi, M. Suzuki, K. Kushida, S. Miyamoto and T. Inoue (1999). Comparison of the concentrations of pentosidine in the synovial fluid, serum and urine of patients with rheumatoid arthritis and osteoarthritis. Rheumatology (Oxford), Dec; 38(12): 1275–1278.
- James R, Claire E, Haire R, Erikson N, Walter D, William P, James E, Vernon G, Pierre M, Lynell, Steven W, Harry K, and Gerald F (1996). Treatment of rheumatoid arthritis with methotrexate alone, sulfasalazine and hydroxychloroquine or a combination of all three medications. The New England Journal of Medicine, 334: 1287-1291. http://dx.doi.org/10.1056/NEJM199605163342002
- Javier RG, Jesus R. Requena and Santiago R S (1998). Increased concentrations of serum pentosidine in rheumatoid arthritis. Clin Chem, 44:250–255.
- Jianfeng Li and Schmidt AM (1997). Characterization and functional analysis of the promoter of RAGE, the receptor for advanced glycation endproducts. The Journal of Biological Chemistry, 272:16498–506. http://dx.doi.org/10.1074/jbc.272.26.16498
- Joan M, Richard WM, Roy M, John R, Schiff MH, Edward C, Mark C, Wasko MC, Larry W, Arthur L, Joseph M and Barbara K (2000). A comparison of etanercept and methotrexate in patients with early rheumatoid arthritis. N The New England Journal of Medicine, 343:1586- 1592. http://dx.doi.org/10.1056/NEJM200011303432201
- Keystone EC, Kavanaugh AF, Sharp JT, Tannenbaum H, Hua Y, Teoh LS, Fischkoff SA, Chartash EK (2004) . Radiographic, clinical, and functional outcomes of treatment with adalimumab (a human anti-tumor necrosis factor monoclonal antibody) in patients with active rheumatoid arthritis receiving concomitant methotrexate therapy. Arthritis Rheum, 50:1400-1441. http://dx.doi.org/10.1002/art.20217
- L Lipsky PE, Van H, Clair EW, Furst DE, Breedveld FC, Kalden JR, Smolen JS, Weisman M, Emery P, Feldmann M, Harriman GR, Maini RN (2000). Infliximab and Methotrexate in the treatment of rheumatoid arthritis. The New England Journal of Medicine, 343:1595-1601. http://dx.doi.org/10.1056/NEJM200011303432202
- L Lynden J Roberts, Leslie G Cleland, Susanna M Proudman and Ranjeny Thomas (2005). Early combination disease modifying antirheumatic drugs treatment for rheumatoid arthritis. MJA 184(3): 122-125.
- Makita Z, Vlassara H, Cerami A and Bucala R (1992). Immunochemical detection of advanced glycosylation end products in vivo, Journal of Biological Chemistry, 267: 5133–5138.
- Megan L. Krause, Shreyasee Amin, and Ashima Mako (2014). Ther Adv Musculoskelet Dis. 6(5):169–184. http://dx.doi.org/10.1177/1759720X14551568
- Michaëlsson E, Broddefalk J, Engström A, Kihlberg J, Holmdahl R (1996). Antigen processing and presentation of a naturally glycosylated protein elicits major histocompatibility complex class II-restricted, carbohydrate-specific T cells. European Journal of Immunology, 26(8):1906–1910.
- Miguel A. Gonzalez G, Tomas R. Vazquez-rodriguez, Rheumatology Division; Carlos Gonzalez-Juanatey, Javier L (2005). Division of Preventive Medicine and Public Health, School of Medicine, University of Cantabria, Santander, Spain., Rheumatoid arthritis: A disease associated with accelerated atherogenesis. Semin. Arthritis Rheum, 35:8-17.
- Mitsuhiro I, Masahiro Y, Tetsushi A, Akira O, Akiko U, Norio O, Sachiko A, Kensuke M, Paul J and Hirofumi M (2004). Expression of Toll-like receptor 2 on CD16+ blood monocytes and synovial tissue macrophages in rheumatoid arthritis. Arthritis Rheum, 50:1457–67. http://dx.doi.org/10.1002/art.20219
- Miyata T, Ishiguro N, Yasuda Y, Ito T, Nangaku M, Iwata H, Kurokawa K (1998). Increased pentosidine, an advanced glycation end product, in plasma and synovial fluid from patients with rheumatoid arthritis and its relation with inflammatory markers. Biochemical and Biophysical Research Communications, 244:45–9. http://dx.doi.org/10.1006/bbrc.1998.8203
- Nakayama M, Izumi G, Nemoto Y, Shibata K, Hasegawa T, Numata M, Wang K, Kawaguchi Y, Hosoya T (1999). Suppression of N (epsilon)-(carboxymethyl)lysine generation by the antioxidant N-acetylcysteine. Perit Dial Int, 19(3): 207–210.
- Nerlich AG, Schleicher ED (1999). N(epsilon)-(carboxymethyl)lysine in atherosclerotic vascular lesions as a marker for local oxidative stress. Atherosclerosis, 144(1): 41–47. http://dx.doi.org/10.1016/S0021-9150(99)00038-6
- Nils Gunnar (2003). Arvidson, Studies on Interleukin-6, Tumour Necrosis Factor alpha, Monocyte Activity, Acute Phase Markers, Glucocorticoids, and Disability. Acta Universitatis Upsaliensis. Disease activity in rheumatoid arthritis. Doctoral thesis at Department of Medical Sciences, Clinical Chemistry, University Hospital, Sweden, 1-86.
- R. Kokkola, E. Sundberg, A.-K. Ulfgren, K. Palmblad, J. Li, H. Wang, L. Ulloa, H. Yang, X.-J. Yan, R. Furie, N. Chiorazzi, K. J. Tracey, U. Andersson, and H. Erlandsson Harris (2002). High mobility group box chromosomal protein 1: a novel proinflammatory mediator in synovitis. Arthritis Rheum, 46: 2598–603. http://dx.doi.org/10.1002/art.10540
- Reddy VP, Beyaz A (2006). Inhibitors of the Maillard reaction and AGE breakers as therapeutics for multiple diseases Drug Discovery Today, volume 11, numbers 13/14, July: 646-654.
- Russell R (1993). The pathogenesis of atherosclerosis: A prospective for the 1990s. Nature, 362:861-869.
- S Drinda, S Franke, C Canet, P Petrow, R Brauer, C Huttich, G Stein, and G Hein (2005). Identification of the receptor for advanced glycation end products in synovial tissue of patients with rheumatoid arthritis. Rheumatol Int, 25: 411– 413. http://dx.doi.org/10.1007/s00296-004-0456-y
- Saravanan V, Hamilton J (2002). Advances in the treatment of rheumatoid arthritis: old verses new therapies. Expert Opin. Pharmacother, 3(7): 1-12.
- Schmid AM, Yan SD, Yan SF, and David MS (2001). The multiligand receptor RAGE as a progression factor amplifying immune and inflammatory responses. J Clin Invest, 108: 949–55. http://dx.doi.org/10.1172/JCI200114002
- Schmidt AM, Yan SD, Wautier JL, Stern D (1999). Activation of receptor for advanced glycation end products: a mechanism for chronic vascular dysfunction in diabetic vasculopathy and atherosclerosis. Circ Res, 84(5): 489–497. http://dx.doi.org/10.1161/01.RES.84.5.489
- Seikoh H (2002). Department of Biochemistry, Kumamoto University School of Medicine, Japan. The liver is the main site for metabolism of circulating advanced glycation end products, Journal of Hepatology, 36: 123–125. http://dx.doi.org/10.1016/S0168-8278(01)00293-8
- Tak PP, Zvaifler NJ, Green DR, Firestein GS (2000). Rheumatoid arthritis and p53: how oxidative stress might alter the course of inflammatory diseases. Immunol Today, 21(2): 78–82. http://dx.doi.org/10.1002/1529-0131(200012)43:12<2619::AID-ANR1>3.0.CO;2-V
- Takahashi M, Kushida K, Ohishi T, Kawana K, Hoshino H, Uchiyama A, Inoue T (1994). Quantitative analysis of cross links pyridinoline and pentosidine in articular cartilage of patients with bone and joint disorders. Arthritis Rheum, 37:724–8. http://dx.doi.org/10.4172/2161-1149.S4-002
- Wolfe F, Mitchell DM, Sibley JT, Fries JF, Bloch DA, Williams CA, Spitz PW, Haga M, Kleinheksel SM, Cathey MA (1994). The mortality of rheumatoid arthritis. Arthritis Rheum, 37:481-494. http://dx.doi.org/10.1002/art.1790070311
- YYang S, Litchfield JE, Baynes JW (2003). AGE-breakers cleave model compounds, but do not break Maillard cross links in skin and tail collagen from diabetic rats. Arch. Biochem. Biophys, 412, 42–46. http://dx.doi.org/10.1016/S0003-9861(03)00015-8
- YYaw K, Rusliza B, Talib H, Hing T, and Nordin N (2013). Receptor for Advanced Glycation End Products and its Involvement in Inflammatory Diseases. International Journal of Inflammation, http://dx.doi.org/10.1155/2013/403460
How to Cite
Ravinder Kumar, Sandeep Arora, Pratima Syal, Mayank Sippy. A Review on Role of Advanced Glycation End products (AGEs) in Rheumatoid Arthritis.
J. Pharm. Technol. Res. Manag.. 2015, 03, 1-10
