Preview

Нефрология

Расширенный поиск

АПОПТОЗ И ПАТОЛОГИЯ ПОЧЕК

https://doi.org/10.24884/1561-6274-2013-17-4-36-43

Полный текст:

Аннотация

Обзор дает представление о влиянии некоторых молекулярных механизмов апоптоза на развитие нефропатий различного генеза. Описаны пути реализации и значение молекул апоптоза (р53, PUMA, MDM2, р21) в развитии патологии почек, связанных с повреждением клубочков, ишемией, в развитии почечной недостаточности. Охарактеризован тонкий механизм влияния молекулы р53 на онкогенез. Отмечено, что экспрессия р53 определяет нефротоксичность ряда противоопухолевых препаратов. Функции проапоптотического протеина PUMA определены лишь в контексте онкогенеза и нефротоксичности. Рассмотрена роль молекулы MDM2 как предиктора опухолевой пролиферации и эволюции волчаночного нефрита. Описан существенный вклад белка р21 в развитие острой почечной недостаточности, фокально-сегментарного гломерулосклероза, диабетической нефропатии, а также в прогрессирование аутоиммунных процессов в почках. Апоптоз является активным механизмом в развитии хронической болезни почек, и его дальнейшее изучение определяет возможность поиска инновационных подходов в предупреждении, прогнозировании и лечении болезней почек.

Об авторах

Л. Б. Пак
Тихоокеанский государственный медицинский университет
Россия

Кафедра факультетской терапии



А. И. Дубиков
Тихоокеанский государственный медицинский университет
Россия
Кафедра факультетской терапии


Т. А. Кабанцева
клиническая больница № 2, г.Владивосток
Россия
нефрологическое отделение


А. А. Василюк
Тихоокеанский государственный медицинский университет
Россия
кафедра факультетской хирургии и урологии


О. М. Григорян
Тихоокеанский государственный медицинский университет
Россия
V курс лечебного факультета


Список литературы

1. Томилина НА, Бикбов БТ. Эпидемиология хронической почечной недостаточности и новые подходы к классификации и оценке тяжести хронических прогрессирующих заболеваний почек. Тер арх 2005; (6): 87-89

2. Смирнов АВ, Добронравов ВА, Каюков ИГ, Есаян АМ. Хроническая болезнь почек: дальнейшее развитие концепции и классификации. Нефрология 2007; (4): 7-17

3. Цаликова ФД. Апоптоз в патогенезе нефропатий. Нефрология и диализ 1999; (3): 127–130

4. Savill J. Apoptosis and the Kidney. J Am Soc Nephrol 1994; (5): 12-21

5. Ярилин АА. Апоптоз: природа феномена и его роль в норме и при патологии. В: Актуальные проблемы патофизиологии. Мороз Б.Б., ред. Медицина, М., 2001;13-56

6. Chang IY, Kim JN, Jun JY et al. Repression of apurinic/ apyrimidinic endonuclease by p53-dependent apoptosis in hydronephrosis-induced rat kidney. Free Radic Res 2011; 45 (6): 728-34

7. Kerr JF, Wyllie AH,Currie AR. Apoptosis: A basic biological phenomenon with wide-ranging implications in tissue kinetics. Br J Cancer 1972; 26; 239-257

8. Shankland SJ, Hugo C, Coats SR et al. Changes in cell-cycle protein expression during experimental mesangial proliferative glomerulonephritis. Kidney Int 1996; 50 (4): 1230-9

9. Onel KB, Huo D, Hastings D et al. Lack of association of the TP53 Arg72Pro SNP and the MDM2 SNP309 with systemic lupus erythematosus in Caucasian, African American, and Asian children and adults. Lupus 2009; 18 (1): 61-6

10. Salvador JM, Hollander MC, Nguyen AT et al. Mice lacking the p53-effector gene Gadd45a develop a lupus-like syndrome. Immunity 2002; 16 (4): 499-508

11. Liu J, Yang JR, He YN et al. Accelerated senescence of renal tubular epithelial cells is associated with disease progression of patients with immunoglobulin A (IgA) nephropathy. Transl Res 2012; 159 (6): 454-63

12. Wang JS, Tseng HH, Shih DF et al. Expression of inducible nitric oxide synthase and apoptosis in human lupus nephritis. Nephron 1997; 77 (4): 404-11

13. Cho DS, Joo HJ, Oh DK, Kang JH, Kim YS, Lee KB, Kim SJ. Cyclooxygenase-2 and p53 expression as prognostic indicators in conventional renal cell carcinoma. Yonsei Med J 2005; 46 (1): 133-40

14. Martínez-Salgado C, Rodríguez-Peña AB, López-Novoa JM. Involvement of small RasGTPases and their effectors in chronic renal disease. Cell Mol Life Sci 2008; 65 (3): 477-92

15. Вильгельм АЭ, Заика АИ, Прасолов ВС. Координированное взаимодействие мультифункциональных членов семейства р53 влияет на важнейшие процессы в многоклеточных организмах. Молекулярная биология 2011;45 (1):180-197

16. Чумаков ПМ. Белок р53 и его универсальные функции в многоклеточном организме. Успехи биологической химии 2007; (47): 3-52

17. Govender D, Harilal P, Hadley GP, Chetty R. p53 protein expression in nephroblastomas: a predictor of poor prognosis. Br J Cancer 1998; 77 (2): 314-8

18. Naesens M. Replicative senescence in kidney aging, renal disease, and renal transplantation. Discov Med 2011; 11 (56): 65-75

19. Vousden KH, Prives C. 2009. Blinded by the light: the growing complexity of p53. Cell 137, 413–431

20. Uzzo RG, Rayman P, Kolenko V, et al. Mechanisms of apoptosis in T cells from patients with renal cell carcinoma. Clin Cancer Res 1999; 5 (5): 1219-29

21. Kucab JE, Phillips DH, Arlt VM. Linking environmental carcinogen exposure to TP53 mutations in human tumours using the human TP53 knock-in (Hupki) mouse model. FEBS J 2010; 277 (12): 2567-83

22. Pedersen AE, Stryhn A, Justesen S et al. Wild type p53- specific antibody and T-cell responses in cancer patients. J Immunother 2011 Nov-Dec; 34 (9): 629-40

23. Van den Berg L, Segun AD, Mersch S et al. Regulation of p53 isoform expression in renal cell carcinoma. Front Biosci (Elite Ed) 2010; 2 : 1042-53

24. Warburton HE, Brady M, Vlatković N et al. p53 regulation and function in renal cell carcinoma. Cancer Res 2005; 65 (15): 6498-503

25. Itoi T, Yamana K, Bilim V et al. Impact of frequent Bcl-2 expression on better prognosis in renal cell carcinoma patients. Br J Cancer 2004; 90 (1): 200-5

26. Kuwahara M, Fujisaki N, Kagawa S et al. Determination of p53 protein and high-risk human papillomavirus DNA in carcinomas of the renal pelvis and ureter. Int J Mol Med 1998; 1 (4): 703-7

27. Vaseva AV, Moll UM. The mitochondrial p53 pathway. Biochim Biophys Acta 2009; 1787 (5): 414-20

28. Qiu LQ, Sinniah R, Hsu SI. Coupled induction of iNOS and p53 upregulation in renal resident cells may be linked with apoptotic activity in the pathogenesis of progressive IgA nephropathy. J Am Soc Nephrol 2004; 15 (8): 2066-78

29. Suzuki T, Matsusaka T, Nakayama M et al. Genetic podocyte lineage reveals progressive podocytopenia with parietal cell hyperplasia in a murine model of cellular/collapsing focal segmental glomerulosclerosis. Am J Pathol 2009; 174 (5): 1675-82

30. Mishra PK, Raghuram GV, Panwar H et al. Mitochondrial oxidative stress elicits chromosomal instability after exposure to isocyanates in human kidney epithelial cells. Free Radic Res 2009; 43 (8): 718-28

31. McLaren BK, Zhang PL, Herrera GA. P53 protein is a reliable marker in identification of renal tubular injury. Appl Immunohistochem Mol Morphol 2004; 12 (3): 225-229

32. Dagher PC, Mai EM, Hato T et al. The p53 inhibitor pifithrin-α can stimulate fibrosis in a rat model of ischemic acute kidney injury. Am J Physiol Renal Physiol 2012; 302 (2): F284-91

33. Hochegger K, Koppelstaetter C, Tagwerker A et al. p21 and mTERT are novel markers for determining different ischemic time periods in renal ischemia-reperfusion injury. Am J Physiol Renal Physiol 2007; 292 (2): F762-8

34. Bhatt K, Zhou L, Mi QS et al. MicroRNA-34a is induced via p53 during cisplatin nephrotoxicity and contributes to cell survival. Mol Med 2010; 16 (9-10): 409-16

35. Wang J, Biju MP, Wang MH et al. Cytoprotective effects of hypoxia against cisplatin-induced tubular cell apoptosis: involvement of mitochondrial inhibition and p53 suppression. J Am Soc Nephrol 2006; 17 (7): 1875-85

36. Wei Q, Dong G, Yang T et al. Activation and involvement of p53 in cisplatin-induced nephrotoxicity. Am J Physiol Renal Physiol 2007; 293 (4): F1282-91

37. Jiang M, Wei Q, Wang J et al. Regulation of PUMA-alpha by p53 in cisplatin-induced renal cell apoptosis. Oncogene 2006; 25 (29): 4056-66

38. Kindt N, Menzebach A, Van de Wouwer M et al. Protective role of the inhibitor of apoptosis protein, survivin, in toxin-induced acute renal failure. FASEB J 2008; 22 (2): 510-21

39. Rincon J, Romero M, Viera N et al. Increased oxidative stress and apoptosis in acute puromycinaminonucleoside nephrosis. Int J ExpPathol 2004; 85 (1): 25-33

40. Fujieda M, Morita T, Naruse K et al. Effect of pravastatin on cisplatin-induced nephrotoxicity in rats. Hum Exp Toxicol 2011; 30 (7): 603-15

41. Kim DH, Jung YJ, Lee JE et al. SIRT1 activation by resveratrol ameliorates cisplatin-induced renal injury through deacetylation of p53. Am J Physiol Renal Physiol 2011; 301 (2): F427-35

42. Kume S, Haneda M, Kanasaki K et al. Silent information regulator 2 (SIRT1) attenuates oxidative stress-induced mesangial cell apoptosis via p53 deacetylation. Free Radic Biol Med 2006; 40 (12): 2175-82

43. Shankar S, Singh G, Srivastava RK. Chemoprevention by resveratrol: molecular mechanisms and therapeutic potential. Front Biosci 2007; 12: 4839-54

44. Nelson DA, Tan TT, Rabson AB et al. Hypoxia and defective apoptosis drive genomic instability and tumorigenesis. Genes Dev 2004; 18 (17): 2095-107

45. Noon AP, Vlatković N, Polański R et al. p53 and MDM2 in renal cell carcinoma: biomarkers for disease progression and future therapeutic targets? Cancer 2010; 116 (4): 780-90

46. Haitel A, Wiener HG, Baethge U et al. MDM2 expression as a prognostic indicator in clear cell renal cell carcinoma: comparison with p53 overexpression and clinicopathological parameters. Clin Cancer Res 2000; 6 (5): 1840-4

47. Moch H, Sauter G, Gasser TC et al. p53 protein expression but not mdm-2 protein expression is associated with rapid tumor cell proliferation and prognosis in renal cell carcinoma. Urol Res 1997; 25 Suppl 1 : S25-30

48. Polanski R, Maguire M, Nield PC et al. MDM2 interacts with NME2 (non-metastatic cells 2, protein) and suppresses the ability of NME2 to negatively regulate cell motility. Carcinogenesis 2011; 32 (8): 1133-42

49. Hashimoto H, Sue Y, Saga Y et al. Roles of p53 and MDM2 in tumor proliferation and determination of the prognosis of transitional cell carcinoma of the renal pelvis and ureter. Int J Urol 2000; 7 (12): 457-63

50. Tsao CC, Corn PG. MDM-2 antagonists induce p53- dependent cell cycle arrest but not cell death in renal cancer cell lines. Cancer Biol Ther 2011; 10 (12): 1315-25

51. Allam R, Sayyed S G, Kulkarni OP et al. Mdm2 promotes systemic lupus erythematosus and lupus nephritis. J Am Soc Nephrol 2011; 22 (11): 2016-27

52. Niwa T, Shimizu H. Indoxyl sulfate induces nephrovascular senescence. J Ren Nutr 2012; 22 (1): 102-6

53. Samarakoon R, Overstreet JM, Higgins SP, Higgins PJ. TGF-β1 → SMAD/p53/USF2 → PAI-1 transcriptional axis in ureteral obstruction-induced renal fibrosis. Cell Tissue Res 2012; 347 (1): 117-28

54. Willenbring H, Sharma AD, Vogel A et al. Loss of p21 permits carcinogenesis from chronically damaged liver and kidney epithelial cells despite unchecked apoptosis. Cancer Cell 2008; 14 (1): 59-67

55. Shalitin C, Epelbaum R, Moskovitz B et al. Increased levels of a 21-kDa protein in the circulation of tumor-bearing patients. Cancer Detect Prev 1994; 18 (5): 357-65

56. O’Sullivan GC, Tangney M, Casey G et al. Modulation of p21-activated kinase 1 alters the behavior of renal cell carcinoma. Int J Cancer 2007; 121 (9): 1930-40

57. Whitson JM, Noonan EJ, Pookot D et al. Double strandedRNA-mediated activation of P21 gene induced apoptosis and cell cycle arrest in renal cell carcinoma. Int J Cancer 2009; 125 (2): 446-52

58. Megyesi J, Price PM, Tamayo E et al. The lack of a functional p21(WAF1/CIP1) gene ameliorates progression to chronic renal failure. Proc Natl AcadSci USA 1999; 96 (19): 10830-5

59. Hochegger K, Koppelstaetter-Megyesi J, Udvarhelyi N et al. The p53-independent activation of transcription of p21 WAF1/ CIP1/SDI1 after acute renal failure. Am J Physiol 1996; 271 (6 Pt 2): F1211-6

60. Megyesi J, Andrade L, Vieira JM et al. Positive effect of the induction of p21WAF1/CIP1 on the course of ischemic acute renal failure. Kidney Int 2001; 60 (6): 2164-72

61. Megyesi J, Andrade L, Vieira JM et al. Coordination of the cell cycle is an important determinant of the syndrome of acute renal failure. Am J Physiol Renal Physiol 2002; 283 (4): F810-6

62. Srivastava T, Garola RE, Singh HK. Cell-cycle regulatory proteins in the podocyte in collapsing glomerulopathy in children. Kidney Int 2006; 70 (3): 529-35

63. Balomenos D, Martín-Caballero J, García MI et al. The cell cycle inhibitor p21 controls T-cell proliferation and sex-linked lupus development. Nat Med 2000; 6 (2): 171-6

64. Wolf G. Cell cycle regulation in diabetic nephropathy. Kidney Int Suppl 2000; 77: S59-66

65. Wolf G, Fan YP, Weiss RH. Exogenous attenuation of p21(Waf1/Cip1) decreases mesangial cell hypertrophy as a result of hyperglycemia and IGF-1. J Am Soc Nephrol 2004; 15 (3): 575-84


Для цитирования:


Пак Л.Б., Дубиков А.И., Кабанцева Т.А., Василюк А.А., Григорян О.М. АПОПТОЗ И ПАТОЛОГИЯ ПОЧЕК. Нефрология. 2013;17(4):36-43. https://doi.org/10.24884/1561-6274-2013-17-4-36-43

For citation:


Pak L.B., Dubikov A.I., Kabanceva T.A., Vasilyuk A.A., Grigoryan O.M. APOPTOSIS AND NEPHROPATHIES. Nephrology (Saint-Petersburg). 2013;17(4):36-43. (In Russ.) https://doi.org/10.24884/1561-6274-2013-17-4-36-43

Просмотров: 46


ISSN 1561-6274 (Print)
ISSN 2541-9439 (Online)