Investigation of AGE, their receptor and NF-κB activation and apoptosis in patients with ATTR and Gelsolin amyloidosis

Histology and Histopathology

Volumn 25, Issue 6, 2010, Pages 691-699

  Anan, Intissar ^a   Kiuru Enari, Sari ^b   Obayashi, Konen ^a   Ranløv, Poul Jørgen ^c   Ando, Yukio ^d  

^a UMEÅ UNIVERSITY HOSPITAL   (Sweden)

^b HELSINKI UNIVERSITY CENTRAL HOSPITAL   (Finland)

^c Hoersholm Hospital   (Denmark)

^d KUMAMOTO UNIVERSITY   (Japan)

Author keywords

Amyloidosis; Apoptosis; NF B; Rage and immunohistochemistry

Indexed keywords

ADVANCED GLYCATION END PRODUCT; ADVANCED GLYCOSYLATION END PRODUCT RECEPTOR; ADVANCED GLYCOSYLATION END-PRODUCT RECEPTOR; AMYLOID; BIOLOGICAL MARKER; CONGO RED; GELSOLIN; IMMUNOGLOBULIN ENHANCER BINDING PROTEIN; IMMUNOGLOBULIN RECEPTOR; NFKB1 PROTEIN, HUMAN; PREALBUMIN;

ADULT; AGED; AMYLOIDOSIS; APOPTOSIS; APPENDIX; ARTICLE; CHEMISTRY; FEMALE; GASTROINTESTINAL TRACT; HEART MUSCLE; HUMAN; IMMUNOHISTOCHEMISTRY; KIDNEY; MALE; METABOLISM; MIDDLE AGED; PATHOLOGY; RECTUM;

ADULT; AGED; AMYLOID; AMYLOIDOSIS; APOPTOSIS; APPENDIX; BIOLOGICAL MARKERS; CONGO RED; FEMALE; GASTROINTESTINAL TRACT; GELSOLIN; GLYCOSYLATION END PRODUCTS, ADVANCED; HUMANS; IMMUNOHISTOCHEMISTRY; KIDNEY; MALE; MIDDLE AGED; MYOCARDIUM; NF-KAPPA B P50 SUBUNIT; PREALBUMIN; RECEPTORS, IMMUNOLOGIC; RECTUM;

EID: 77953371033     PISSN: 02133911     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

References (40)

1. Anan I., El-Salhy M., Nyhlin N. and Suhr O.B. (2000). Liver transplantation restores endocrine cells in patients with familial amyloidotic polyneuropathy. Transplantation 70, 794-799.
2. Ando Y., Nyhlin N., Suhr O., Holmgren G., Uchida K., El-Salhy M., Yamashi T., Terasaki H., Nakamura M., Uchino M. and Ando M. (1997). Oxidative stress is found in amyloid deposits in systemic amyloidosis. Biochem. Biophys. Res. Commun. 232, 497-502.
3. Andrade C. (1952). A peculiar form of peripheral polyneuropathy: familial atypical generalized amyloidosis with special involvement of the peripheral nerves. Brain 75, 408-427.
4. Benson M. (2003). The hereditary amyloidosis. Best. Pract. Res. Clin. Rheumatol. 17, 909-927.
5. Brownlee M., Cerami A. and Vlassara H. (1988). Advanced glycosylation end products in tissue and the biochemical basis of diabetic complications. N. Engl. J. Med. 318, 1315-1321.
6. Bucciarelli L.G., Kaneko M., Ananthakrishnan R., Harja E., Lee L.K., Hwang Y.C., Lerner S., Bakr S., Li Q., Lu Y., Song F., Qu W., Gomez T., Zou Y.S., Yan S.F., Schmidt A.M. and Ramasamy R. (2006). Receptor for advanced-glycation end products: key modulator of myocardial ischemic injury. Circulation 113, 1226-1234.
7. Henle T. and Miyata T. (2003). Advanced glycation end products in uremia. Adv. Ren. Replace. Ther. 10, 321-331.
8. Kawaji T., Ando Y., Ando E., Nakamura M., Hirata A. and Tanihara H. (2004). A case of vitreous amyloidosis without systemic symptoms in familial amyloidotic polyneuropathy. Amyloid 11, 257-259.
9. Kiuru S. (1998). Gelsolin-related familial amyloidosis, Finnish type (FAF), and its variants found worldwide. Amyloid 5, 55-66.
10. Koyama Y., Takeishi Y., Arimoto T., Niizeki T., Shishido T., Takahashi H., Nozaki N., Hirono O., Tsunoda Y., Nitobe J., Watanabe T. and Kubota I. (2007). High serum level of pentosidine, an advanced glycation end product (AGE), is a risk factor of patients with heart failure. J. Card. Fail. 13, 199-206.
11. Lander H.M., Tauras J.M., Ogiste J.S., Hori O., Moss R.A., Schmidt A.M. (1997). Activation for the receptor for AGE triggers p21 ras dependent mitogen activated protein kinase pathway regulated by oxidative stress. J. Biol. Chem. 272, 17810-17814.
12. Lobato L., Beirao I., Guimaraes S.M., Droz D., Guimaraes S., Grunfeld J. and Noel L. (1998). Familial amyloid polyneuropathy type I (Portugese): distribution and characterization of renal amyloiddeposits. Am. J. Kidney Dis. 31, 940-946.
13. Lobato L., Beirão I., Silva M., Bravo F., Silvestre F., Guimarães S., Sousa A., Noël L.H. and Sequeiros J. (2003). Familial ATTR amyloidosis: microalbuminuria as a predictor of symptomatic disease and clinical nephropathy. Nephrol. Dial. Transplant. 18, 532-538.
14. Matsunaga N., Anan I., Forsgren S., Nagai R., Rosenberg P., Horiuchi S., Ando Y. and Suhr O.B. (2002). Advanced glycation end products (AGE) and the receptor for AGE are present in gastrointestinal tract of familial amyloidotic polyneuropathy patients but do not induce NF-kappaB activation. Acta Neuropathol. 104, 441-447.
15. Matsunaga N., Anan I., Rosenberg P., Nagai R., Lundström O., Horiuchi S., Ando Y. and Suhr O.B. (2005). Advanced glycation end product is implicated in amyloid-related kidney complications. Scand. J. Clin. Lab. Invest. 65, 263-271.
16. Maury C.P. (1993). Homozygous familial amyloidosis, Finnish type: demonstration of glomerular gelsolin-derived amyloid and nonamyloid tubular gelsolin. Clin. Nephrol. 40, 53-56.
17. Maury C.P., Kere J., Tolvanen R. and de la Chapelle A. (1990). Finnish hereditary amyloidosis is caused by a single nucleotide substitution in the gelsolin gene. FEBS Lett. 276, 75-77.
18. Monnier V.M., Glomb M., Elgawish A. and Sell D.R. (1996). The mechanism of collagen cross-linking in diabetes: a puzzle nearing resolution. Diabetes 45, S67-72.
19. Nyhlin N., El-Salhy M., Sandström O. and Suhr O. (1997). Evaluation of immunohistochemical staining of human duodenal endocrine cells after microwave antigen retrieval. Histochem. J. 29, 177-181.
20. Olofsson B.O. (1983). Cardiac involvement in familial amyloidosis with polyneuropathy. Int. J. Cardiol. 4, 379-382.
21. Picken M.M. (2006). New insights into systemic amyloidosis: the importance of diagnosis of specific type. Curr. Opin. Nephrol. Hypertens. 16, 196-203.
22. Ranløv I., Alves I.L., Ranløv P.J., Husby G., Costa P.P. and Saraiva M.J. (1992). A Danish kindred with familial amyloid cardiomyopathy revisited: identification of a mutant transthyretin-methionine111 variant in serum from patients and carriers. Am. J. Med. 93, 3-8.
23. Robbins J. (1976). Thyroxine-binding proteins. Prog. Clin. Biol. Res. 5, 331-355.
24. Ruderman N., Wiliamson J. and Brownlee M. (1992). Glucose and diabetic vascular disease. FASEB J. 6, 2905-2914.
25. Saito A., Takeda T., Sato K., Hama H., Tanuma A., Kaseda R., SuzukiY. and Gejyo F. (2005). Significance of proximal tubular metabolism of advanced glycation end products in kidney diseases. Ann. N. Y. Acad. Sci. 1043, 637-643.
26. Sanchorawala V. (2006). Light-Chain (AL) Amyloidosis: Diagnosis and treatment. Clin. J. Am. Soc. Nephrol. 1, 1331-1341.
27. Saraiva M.J., Costa P.P., Birken S. and Goodman D.S. (1983). Presence of an abnormal transthyretin (prealbumin) in Portuguese patients with familial amyloidotic polyneuropathy. Trans. Assoc. Am. Physicians 96, 261-270.
28. Schmidt A.M., Yan S.D. and Stern D.M. (1995). The dark side of glucose. Nature Med. 1, 1002-1004.
29. Singh R., Barden A., Mori T. and Beilin L. (2001). Advanced glycation end-products: a review. Diabetologia 44, 129-146.
30. Sousa M.M., Yan S.D., Stern D. and Saraiva M.J. (2000). Interaction of the receptor for advanced glycation end products (RAGE) with transthyretin triggers nuclear transcription factor κB (NFκB) activation. Lab. Invest. 80, 1101-1110.
31. Suhr O., Danielsson A. and Steen L. (1992). Bile acid malabsorption caused by gastrointestinal motility dysfunction? An investigation of gastrointestinal disturbances in familial amyloidosis with polyneuropathy. Scand. J. Gastroenterol. 27, 201-207.
32. Suhr O.B., Lindqvist P., Olofsson B.O., Waldenström A. and BackmanC. (2006). Myocardial hypertrophy and function are related to age at onset in familial amyloidotic polyneuropathy. Amyloid 13, 154-159.
33. Svendsen I.H., Steensgaard-Hansen F. and Nordvåg B.Y. (1998). A clinical, echocardiographic and genetic characterization of a Danish kindred with familial amyloid transthyretin methionine 111 linked cardiomyopathy. Eur. Heart J. 19, 782-789.
34. Svendsen I.H., Steensgaard-Hansen F. and Nordvåg B.Y. (1999). Hereditary amyloid cardiomyopathy related to a mutation at transthyretin protein number 111. A clinical, genetic and echocardiographic study of an affected Danish family. Ugeskr. Laeger. 161, 4995-4999.
35. Tanji N., Markowitz G.S., Fu C., Kislinger T., Taguchi A., Pischetsrieder M., Stern D., Schmidt A.M. and D'Agati V.D. (2000). Expression of advanced glycation end products and their cellular receptor RAGE in diabetic nephropathy and nondiabetic renal disease. J. Am. Soc. Nephrol. 11, 1656-1666.
36. Thornalley P.J. (1998). Cell activation by glycated proteins, AGE receptors receptor recognition factors and functional classification of AGE. Cell Mol. Biol. 44, 1013-1023.
37. Tsutsui H. (2004). Novel pathophysiological insight and treatment strategies for heart failure--lessons from mice and patients. Circ. J. 68, 1095-2003.
38. Valen G. (2004). Signal transduction through nuclear factor kappa B in ischemia-reperfusion and heart failure. Basic Res. Cardiol. 99, 1-7.
39. Valen G., Yan Z.Q. and Hansson G.K. (2001). Nuclear factor kappa-B and the heart. J. Am. Coll. Cardiol. 38, 307-314.
40. Xiang G., Schinzel R., Simm A., Sebekova K. and Heidland A. (2001). Advanced glycation end products impair protein turnover in LLCPK1: amelioration by trypsin. Kidney Int. Suppl. 78, S53-S57.