C3a receptor antagonist ameliorates inflammatory and fibrotic signals in type 2 diabetic nephropathy by suppressing the activation of TGF-β/smad3 and IKBα pathway

PLoS ONE

Volumn 9, Issue 11, 2014, Pages

  Li, Ling ^a   Yin, Qinghua ^a   Tang, Xi ^a   Bai, Lin ^a   Zhang, Jie ^a   Gou, Shenju ^a   Zhu, Hongping ^a   Cheng, Jingqiu ^a   Fu, Ping ^a   Liu, Fang ^a  

^a SICHUAN UNIVERSITY   (China)

Author keywords

[No Author keywords available]

Indexed keywords

ALBUMIN; COLLAGEN TYPE 1; COMPLEMENT COMPONENT C3A; COMPLEMENT COMPONENT C3A RECEPTOR; COMPLEMENT COMPONENT C3A RECEPTOR ANTAGONIST; COMPLEMENT RECEPTOR; CREATININE; I KAPPA B ALPHA; INTERLEUKIN 6; MESSENGER RNA; RECEPTOR BLOCKING AGENT; SMAD3 PROTEIN; TRANSFORMING GROWTH FACTOR BETA; UNCLASSIFIED DRUG; I KAPPA B KINASE; MADH3 PROTEIN, RAT;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BLOOD LEVEL; CONTROLLED STUDY; DIABETIC NEPHROPATHY; DRUG EFFECT; DRUG MECHANISM; ENDOTHELIUM CELL; FUNCTIONAL ASSESSMENT; IMMUNOFLUORESCENCE TEST; KIDNEY FUNCTION; MALE; NON INSULIN DEPENDENT DIABETES MELLITUS; NONHUMAN; PROTEIN DETERMINATION; PROTEIN EXPRESSION; PROTEIN FUNCTION; RAT; REAL TIME POLYMERASE CHAIN REACTION; RENAL GLOMERULAR ENDOTHELIAL CELL; SIGNAL TRANSDUCTION; UREA NITROGEN BLOOD LEVEL; URINARY EXCRETION; WESTERN BLOTTING; ANIMAL; ANTAGONISTS AND INHIBITORS; COMPLICATION; METABOLISM; PATHOPHYSIOLOGY; SPRAGUE DAWLEY RAT;

ANIMALS; BLOTTING, WESTERN; COMPLEMENT C3A; DIABETES MELLITUS, TYPE 2; DIABETIC NEPHROPATHIES; I-KAPPA B KINASE; MALE; RATS; RATS, SPRAGUE-DAWLEY; REAL-TIME POLYMERASE CHAIN REACTION; RECEPTORS, COMPLEMENT; SMAD3 PROTEIN; TRANSFORMING GROWTH FACTOR BETA;

EID: 84912550450     PISSN: None     EISSN: 19326203     Source Type: Journal    
DOI: 10.1371/journal.pone.0113639     Document Type: Article

References (33)

1. Association AD (2012) Diagnosis and classification of diabetes mellitus. Diabetes Care 35 Suppl 1: S64-71.
2. Shaw JE, Sicree RA, Zimmet PZ (2010) Global estimates of the prevalence of diabetes for 2010 and 2030. Diabetes Res Clin Pract 87: 4-14.
3. Brownlee M (2005) The pathobiology of diabetic complications: a unifying mechanism. Diabetes 54: 1615-1625.
4. Liu J, Wang D, Chen Y, Sun H, He S, et al. (2013) 1H NMR-based metabonomic analysis of serum and urine in a nonhuman primate model of diabetic nephropathy. Mol Biosyst 9: 2645-2652.
5. Ahmed N (2005) Advanced glycation endproducts-role in pathology of diabetic complications. Diabetes Res Clin Pract 67: 3-21.
6. Forbes JM, Cooper ME (2013) Mechanisms of diabetic complications. Physiol Rev 93: 137-188.
7. Hansen TK, Forsblom C, Saraheimo M, Thorn L, Waden J, et al. (2010) Association between mannose-binding lectin, high-sensitivity C-reactive protein and the progression of diabetic nephropathy in type 1 diabetes. Diabetologia 53: 1517-1524.
8. Hansen TK, Gall MA, Tarnow L, Thiel S, Stehouwer CD, et al. (2006) Mannose-binding lectin and mortality in type 2 diabetes. Arch Intern Med 166: 2007-2013.
9. Ostergaard J, Hansen TK, Thiel S, Flyvbjerg A (2005) Complement activation and diabetic vascular complications. Clin Chim Acta 361: 10-19.
10. Ricklin D, Lambris JD (2013) Complement in immune and inflammatory disorders: pathophysiological mechanisms. J Immunol 190: 3831-3838.
11. Bao L, Osawe I, Haas M, Quigg RJ (2005) Signaling through up-regulated C3a receptor is key to the development of experimental lupus nephritis. J Immunol 175: 1947-1955.
12. Bao L, Wang Y, Haas M, Quigg RJ (2011) Distinct roles for C3a and C5a in complement-induced tubulointerstitial injury. Kidney Int 80: 524-534.
13. Tang Z, Lu B, Hatch E, Sacks SH, Sheerin NS (2009) C3a mediates epithelial-to-mesenchymal transition in proteinuric nephropathy. J Am Soc Nephrol 20: 593-603.
14. Peake PW, O'Grady S, Pussell BA, Charlesworth JA (1999) C3a is made by proximal tubular HK-2 cells and activates them via the C3a receptor. Kidney Int 56: 1729-1736.
15. Liu F, Gou R, Huang J, Fu P, Chen F, et al. (2011) Effect of anaphylatoxin C3a, C5a on the tubular epithelial-myofibroblast transdifferentiation in vitro. Chin Med J (Engl) 124: 4039-4045.
16. Satchell SC, Braet F (2009) Glomerular endothelial cell fenestrations: an integral component of the glomerular filtration barrier. Am J Physiol Renal Physiol. 296: F947-F956.
17. Maezawa Y, Takemoto M, Yokote K (2014) Cell biology of diabetic nephropathy: Roles of endothelial cells, tubulointerstitial cells and podocytes. J Diabetes Invest. doi: 10.1111/jdi.12255.
18. Satchell S (2012) The glomerular endothelium emerges as a key player in diabetic nephropathy. Kidney Int. 82(9): 949-51.
19. Navarro-González JF, Mora-Fernández C (2008) The role of inflammatory cytokines in diabetic nephropathy. J Am Soc Nephrol.19(3): 433-42.
20. Sanchez AP, Sharma K (2009) Transcription factors in the pathogenesis of diabetic nephropathy. Expert Rev Mol Med. 11: e13.
21. Bottinger EP, Bitzer M (2002) TGF-beta signaling in renal disease. J Am Soc Nephrol 13: 2600-2610.
22. Danda RS, Habiba NM, Rincon-Choles H, Bhandari BK, Barnes JL, et al. (2005) Kidney involvement in a nongenetic rat model of type 2 diabetes. Kidney Int 68: 2562-2571.
23. Brown KM, Sacks SH, Sheerin NS (2007) Mechanisms of disease: the complement system in renal injury-new ways of looking at an old foe. Nat Clin Pract Nephrol 3: 277-286.
24. Proctor LM, Arumugam TV, Shiels I, Reid RC, Fairlie DP, et al. (2004) Comparative anti-inflammatory activities of antagonists to C3a and C5a receptors in a rat model of intestinal ischaemia/reperfusion injury. Br J Pharmacol. 142(4): 756-64.
25. Oberg BP, McMenamin E, Lucas FL, McMonagle E, Morrow J, et al. (2004) Increased prevalence of oxidant stress and inflammation in patients with moderate to severe chronic kidney disease. Kidney Int 65: 1009-1016.
26. Cachofeiro V, Goicochea M, de Vinuesa SG, Oubina P, Lahera V, et al. (2008) Oxidative stress and inflammation, a link between chronic kidney disease and cardiovascular disease. Kidney Int Suppl:S4-9.
27. Tak PP, Firestein GS (2001) NF-kappaB a key role in inflammatory diseases. J Clin Invest 107: 7-11.
28. Lawrence T (2009) The nuclear factor NF-kappaB pathway in inflammation. Cold Spring Harb Perspect Biol 1: a001651.
29. Kim YS, Kim JS, Kwon JS, Jeong MH, Cho JG, et al. (2010) BAY 11-7082, a nuclear factor-kappaB inhibitor, reduces inflammation and apoptosis in a rat cardiac ischemia-reperfusion injury model. Int Heart J 51: 348-353.
30. Liu Y (2006) Renal fibrosis: new insights into the pathogenesis and therapeutics. Kidney Int 69: 213-217.
31. Lan HY (2011) Diverse roles of TGF-beta/Smads in renal fibrosis and inflammation. Int J Biol Sci 7: 1056-1067.
32. Jinnin M, Ihn H, Tamaki K (2006) Characterization of SIS3, a novel specific inhibitor of Smad3, and its effect on transforming growth factor-beta1-induced extracellular matrix expression. Mol Pharmacol 69: 597-607.
33. Locatelli M, Buelli S, Pezzotta A, Corna D, Perico L, et al. (2014) Shiga toxin promotes podocyte injury in experimental hemolytic uremic syndrome via activation of the alternative pathway of complement. J Am Soc Nephrol. 25: 1786-1798.