Definition of heat shock proteins in the urine, serum and kidney tissue: significance for the assessment of activity and prognosis of chronic glomerulonephritis


如何引用文章

全文:

开放存取 开放存取
受限制的访问 ##reader.subscriptionAccessGranted##
受限制的访问 订阅或者付费存取

详细

Purpose. To evaluate the state of "kidney self-defense" system in patients with chronic glomerulonephritis (CGN) according to the major heat shock protein (HSP) levels in the urine, blood, and kidney; to clarify the significance of the changes of these factors for the assessment of activity and prognosis of CGN. Material and methods. The study included 75 patients with active CGN: 34 - with severe urinary syndrome (Group і), 41 - with nephrotic syndrome (Group II), including 31 - with moderate nephrotic syndrome (Group IIA) and 10 with severe nephrotic syndrome (Group IIB). Transient impairment of renal function as a manifestation of the high CGN activity was revealed in 7 patients from Group I and in 14 from Group II. Control groups consisted of 10 patients with inactive CGN and 10 healthy individuals. Using the ELISA, urine HSP-27 and HSP-70, interleukin (IL)-10 and IL-6 levels; serum levels of antibodies to HSP-70, and HSP-70 expression in the kidney tissue were evaluated. Results. With increasing activity of CGN (primarily an increase of proteinuria, development of nephrotic syndrome, especially in combination with impaired renal function), the imbalance of damaging and protective mechanisms develops. Decrease of serum levels of antibodies to HSP-70 and urine IL-10 levels with an increase of urinary HSP-27, HSP-70 and IL-6 excretion indicate the activity of the inflammatory response in renal tissue and severity of cellular damage in patients with CGN. Progression of these disorders is a poor prognostic sign, indicating the risk of chronization of the disease and poor response to treatment. Thus, in 80% of patients with high (greater than 21 pg/ml) levels of antibodies to HSP-79, response to treatment was obtained within 12 months, in 50% of patients - within 5 months. At the same time, in 57% of patients with antibody titers less than 21 pg ml, nephrotic syndrome persisted despite long-term treatment recommended for these forms of the disease Conclusion. The results of the study demonstrate the significance of HSPs as indicators reflecting the activation of cellular defense mechanisms and extracellular effects of regulation of immune inflammation in the kidney.

全文:

受限制的访问

参考

  1. Kitamura N., Fine L.G. The concept of glomerular self-defense // Kidney Int. - 1999. - Vol. 55. - P. 1639-1671.
  2. Бобкова И.Н., Чеботарева Н.В., Козловская Л.В. и др. Система самозащиты почки: современный взгляд на механизмы, определяющие течение и исход гломерулонефрита // Нефрология и диализ. - 2013. -№ 15(3). - С. 174-183.
  3. Бобкова И.Н., Чеботарева Н.В., Козловская Л.В. и др. Защитное действие белков теплового шока при заболеваниях почек // Клиническая нефрология. - 2011. - № 6. - С. 59- 66.
  4. Welch W.J. Mammalian stress response: Cell physiology, structure/function of stress proteins, and implication for medicine and disease // Physiol Rev. -1992. - Vol. 72. - P. 1063-1081.
  5. Komatsuda A., Wakui H., Imai H. et al. Renal localization of the constitutive 73-kDa heat-shock protein in normal and PAN rats // Kidney Int. - 1992. -Vol. 41. - P. 1204-1212.
  6. Tsagalis G.C., Nikolopoulou N., Sotsiou F. et al. The Expression of heat shock proteins 27 and 70 in lupus nephritis // Hospital Chronicles. - 2006. - Vol. 1(3). - P. 125-129.
  7. Venkataseshan V.S., Marquet E. Heat shock protein 72/73 in normal and diseased kidneys // Nephron. - 1996. - Vol. 73. - P. 442-449.
  8. Ивашкин В.Т., Драпкина О.М. Клиническое значение оксида азота и белков теплового шока. - М: ГЕОТАР-Медиа. - 2011.
  9. Панасенко О.О., Ким М.В., Гусев Н.Б. Структура и свойства малых белков теплового шока // Успехи биологической химии. - 2003. - № 43. -С. 59-98.
  10. Mehlen P., Hickey E., Weber L.A. et al. Large unphosphorylated aggregates as the active form of hsp27 which controls intracellular reactive oxygen species and glutathione levels and generated a protection against TNF-a in NIH-3T3-ras cells // Biochem Biophys Res Commun. - 1997. - Vol. 241. - P. 187-192.
  11. Preville X., Schultz H., Knauf U. et al. Analysis of the role of Hsp27 phosphorylation reveals the importance of the oligomerization state of this small heat shock protein in its protective function against TNF-a and hydrogen peroxide-induced cell death // J Cell Biochem. - 1998. - Vol. 69. -P. 436-452.
  12. Smoyer W.E., Gupta A., Mundel P. et al. Altered expression of glomerular heat shock protein 27 in experimental nephrotic syndrome // J Clin Invest. - 1996. -Vol. 97. - P. 2697-2704.
  13. Чеботарева Н.В., Непринцева Н.В., Еськова О.А. и др. Определение уровня в моче маркеров повреждения и факторов самозащиты подоцитов у больных хроническим гломерулонефритом // Клиническая нефрология. - 2013. - № 4. - С. 33-37.
  14. Morita K., Wakui H., Komatsuda A. et al. Induction of heat-scock proteins HSP73 and HSP90 in rat kidneys after ischemia // Ren Fail. - 1995. - Vol. 17. - P. 405-419.
  15. Komatsuda G., Wakui H., Satoh K. et al. Altered localization of 73-kilodalton heat-shock protein in rat kidneys with gentamicin-induced acute tubular injury // Lab Invest. - 1993. - Vol. 68. - P. 687-695.
  16. Aufricht C., Lu E., Thulin G. et al. ATP releases HSP72 from protein aggregates after renal ischemia // Am J Physiol Renal Physiol. - 1998. -P. 274. - Vol. 268-274.
  17. Mueller T., Bidmon B., Pichler P. et al. Urinary heat shock protein-72 excretion in clinical and experimental renal ischemia // Pediatr Nephrol. - 2003. - Vol. 18. - P. 97-99.
  18. Dodd S.M., Martin J.E., Swash M. et al. Expression of heat shock protein epitopes in renal disease // Clinical Nephrology. - 1993. - Vol. 39(5). -P. 239-244.
  19. Van Eden W., Tholet J.E.R., van der Zee R. et al. Cloning of the mycobacterial epitope recognized by T lymphocyte in adjuvant arthritis // Nature. - 1988. -Vol. 331. - P. 171-173.
  20. Multhoff G., Hightower L.E. Cell surface expression of heat shock proteins and the immune response // Cell Stress Chaperones. - 1996. - Vol. 1. -P. 167-176.
  21. Anderton S.M., van der Zee R., Prakken B. et al. Activation of T cells recognizing self 60-kDa heat shock protein can protect against experimental arthritis // J Exp Med. - 1995. - Vol. 181. - P. 943-952.
  22. Marzec L., Zdrojewski Z., Liberek T. et al. Expression of Hsp 72 protein in chronic kidney disease patients // Scandinavian J Urol and Nephrol. - 2009. -Vol. 43(5). - P. 400-408.
  23. Wu T., Tanguay R.M. Antibodies against heat shock proteins in environmental stresses and diseases: friend or foe? // Cell Stress and Chaperones. - 2006. -Vol. 11(1). - P. 1-12.
  24. Мухин Н.А., Ляшко В.Н., Маргулис Б.А. и др. Амилоидоз и антитела к белкам теплового шока // Терапевтический архив. - 1992. - № 64. -С. 79-82.
  25. Zhang X., Xu Z., Zhou L. et al. Plasma levels of Hsp 70 and anti-Hsp70 antibody predict risk of coronary syndrome // Cell Stress and Chaperones. - 2010. - Vol. 15. - P. 675- 686.
  26. Dulin E., Barreno P.G., Guisasola M.C. Extracellular heat shock protein 70 (HSPA1A) and classical vascular risk factors in a general population // Cell Stress and Chaperones. - 2010. - Vol. 15. - P. 929-937.

补充文件

附件文件
动作
1. JATS XML
下载
##common.cookie##