Aggravated renal tubular damage and interstitial fibrosis in mice lacking guanylyl cyclase-A (GC-A), a receptor for atrial and B-type natriuretic peptides

Clinical and Experimental Nephrology

Volumn 19, Issue 2, 2015, Pages 197-207

  Yoshihara, Fumiki ^a,b   Tokudome, Takeshi ^a,b   Kishimoto, Ichiro ^a,b   Otani, Kentaro ^a,b   Kuwabara, Atsunori ^a,b   Horio, Takeshi ^a,b   Kawano, Yuhei ^a,b   Kangawa, Kenji ^a,b  

^a NATIONAL CEREBRAL AND CARDIOVASCULAR CENTER   (Japan)

^b KAWASAKI MEDICAL SCHOOL   (Japan)

Author keywords

Angiotensin II; Guanylyl cyclase A; Interstitial fibrosis; Renal tubular atrophy

Indexed keywords

ACTIN; ALPHA-SMOOTH MUSCLE ACTIN, MOUSE; ANGIOTENSIN II; ANTIHYPERTENSIVE AGENT; ATRIAL NATRIURETIC FACTOR RECEPTOR; CADHERIN; DIFFERENTIATION ANTIGEN; HYDRALAZINE; MEMBRANE PROTEIN; MESSENGER RNA; MONOCYTE CHEMOTACTIC PROTEIN 1; MONOCYTE-MACROPHAGE DIFFERENTIATION ANTIGEN; NATRIURETIC PEPTIDE RECEPTOR A; OSTEOPONTIN; PODOCIN; SIGNAL PEPTIDE; SODIUM CHLORIDE; VASOCONSTRICTOR AGENT;

ANIMAL; ATROPHY; BLOOD PRESSURE; CHEMISTRY; DEFICIENCY; DRUG EFFECTS; FIBROSIS; GENE EXPRESSION; GENETICS; KIDNEY TUBULE; KNOCKOUT MOUSE; MALE; METABOLISM; MOUSE; PATHOLOGY;

ACTINS; ANGIOTENSIN II; ANIMALS; ANTIGENS, DIFFERENTIATION; ANTIHYPERTENSIVE AGENTS; ATROPHY; BLOOD PRESSURE; CADHERINS; CHEMOKINE CCL2; FIBROSIS; GENE EXPRESSION; HYDRALAZINE; INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS; KIDNEY TUBULES; MALE; MEMBRANE PROTEINS; MICE; MICE, KNOCKOUT; OSTEOPONTIN; RECEPTORS, ATRIAL NATRIURETIC FACTOR; RNA, MESSENGER; SODIUM CHLORIDE; VASOCONSTRICTOR AGENTS;

EID: 84939895799     PISSN: 13421751     EISSN: 14377799     Source Type: Journal    
DOI: 10.1007/s10157-014-0982-1     Document Type: Article

References (39)

1. Kasahara M, Mukoyama M, Sugawara A, et al. Ameliorated glomerular injury in mice overexpressing brain natriuretic peptide with renal ablation. J Am Soc Nephrol. 2000;11:1691–701.
2. Suganami T, Mukoyama M, Sugawara A, et al. Overexpression of brain natriuretic peptide in mice ameliorates immune-mediated renal injury. J Am Soc Nephrol. 2001;12:2652–63.
3. Makino H, Mukoyama M, Mori K, et al. Transgenic overexpression of brain natriuretic peptide prevents the progression of diabetic nephropathy in mice. Diabetologia. 2006;49:2514–24.
4. Saito Y. Roles of atrial natriuretic peptide and its therapeutic use. J Cardiol. 2010;56:262–70.
5. Lopez MJ, Wong SK, Kishimoto I, et al. Salt-resistant hypertension in mice lacking the guanylyl cyclase-A receptor for atrial natriuretic peptide. Nature. 1995;378:65–8.
6. Sabrane K, Kruse MN, Fabritz L, et al. Vascular endothelium is critically involved in the hypotensive and hypovolemic actions of atrial natriuretic peptide. J Clin Invest. 2005;115:1666–74.
7. Chen W, Gassner B, Börner S, et al. Atrial natriuretic peptide enhances microvascular albumin permeability by the caveolae-mediated transcellular pathway. Cardiovasc Res. 2012;93:141–51.
8. Ogawa Y, Mukoyama M, Yokoi H, et al. Natriuretic peptide receptor guanylyl cyclase-a protects podocytes from aldosterone-induced glomerular injury. J Am Soc Nephrol. 2012;23:1198–209.
9. Blasi ER, Rocha R, Rudolph AE, Blomme EA, Polly ML, McMahon EG. Aldosterone/salt induces renal inflammation and fibrosis in hypertensive rats. Kidney Int. 2003;63:1791–800.
10. Faulkner JL, Szcykalski LM, Springer F, Barnes JL. Origin of interstitial fibroblasts in an accelerated model of angiotensin II-induced renal fibrosis. Am J Pathol. 2005;167:1193–205.
11. Mitani H, Ishizaka N, Aizawa T, et al. In vivo klotho gene transfer ameliorates angiotensin II-induced renal damage. Hypertension. 2002;39:838–43.
12. Johnson RJ, Alpers CE, Yoshimura A, et al. Renal injury from angiotensin II-mediated hypertension. Hypertension. 1992;19:464–74.
13. Lombardi DM, Viswanathan M, Vio CP, Saavedra JM, Schwartz SM, Johnson RJ. Renal and vascular injury induced by exogenous angiotensin II is AT1 receptor-dependent. Nephron. 2001;87:66–74.
14. Kitayama H, Maeshima Y, Takazawa Y, et al. Regulation of angiogenic factors in angiotensin II infusion model in association with tubulointerstitial injuries. Am J Hypertens. 2006;19:718–27.
15. Ozawa Y, Kobori H, Suzaki Y, Navar LG. Sustained renal interstitial macrophage infiltration following chronic angiotensin II infusions. Am J Physiol Renal Physiol. 2007;292:F330–9.
16. Giachelli CM, Pichler R, Lombardi D, et al. Osteopontin expression in angiotensin II-induced tubulointerstitial nephritis. Kidney Int. 1994;45:515–24.
17. Nath KA. Tubulointerstitial changes as a major determinant in the progression of renal damage. Am J Kidney Dis. 1995;20:1–17.
18. Desmoulière A, Darby IA, Gabbiani G. Normal and pathologic soft tissue remodeling: role of the myofibroblast, with special emphasis on liver and kidney fibrosis. Lab Invest. 2003;83:1689–707.
19. Tokudome T, Horio T, Kishimoto I, et al. Calcineurin-nuclear factor of activated T cells pathway-dependent cardiac remodeling in mice deficient in guanylyl cyclase A, a receptor for atrial and brain natriuretic peptides. Circulation. 2005;111:3095–104.
20. Quesada A, Vargas F, Montoro-Molina S, et al. Urinary aminopeptidase activities as early and predictive biomarkers of renal dysfunction in cisplatin-treated rats. PLoS ONE. 2012;7:e40402.
21. Li P, Oparil S, Novak L, et al. ANP signaling inhibits TGF-beta-induced Smad2 and Smad3 nuclear translocation and extracellular matrix expression in rat pulmonary arterial smooth muscle cells. J Appl Physiol. 2007;102:390–8.
22. Weber NC, Blumenthal SB, Hartung T, Vollmar AM, Kiemer AK. ANP inhibits TNF-alpha-induced endothelial MCP-1 expression–involvement of p38 MAPK and MKP-1. J Leukoc Biol. 2003;74:932–41.
23. Suzuki K, Han GD, Miyauchi N, et al. Angiotensin II type 1 and type 2 receptors play opposite roles in regulating the barrier function of kidney glomerular capillary wall. Am J Pathol. 2007;170:1841–53.
24. Baltatu O, Silva JA Jr, Ganten D, Bader M. The brain renin-angiotensin system modulates angiotensin II-induced hypertension and cardiac hypertrophy. Hypertension. 2000;35(part 2):409–12.
25. Cargill RI, Coutie WJ, Lipworth BJ. The effects of angiotensin II on circulating levels of natriuretic peptides. Br J Clin Pharmacol. 1994;38:139–42.
26. Marin-Grez M, Fleming JT, Steinhausen M. Atrial natriuretic peptide causes pre-glomerular vasodilatation and post-glomerular vasoconstriction in rat kidney. Nature. 1986;324:473–6.
27. Abbate M, Zoja C, Remuzzi G. How does proteinuria cause progressive renal damage? J Am Soc Nephrol. 2006;17:2974–84.
28. Manotham K, Tanaka T, Matsumoto M, et al. Transdifferentiation of cultured tubular cells induced by hypoxia. Kidney Int. 2004;65:871–80.
29. Sun S, Ning X, Zhang Y, et al. Hypoxia-inducible factor-1alpha induces Twist expression in tubular epithelial cells subjected to hypoxia, leading to epithelial-to-mesenchymal transition. Kidney Int. 2009;75:1278–87.
30. Long DA, Mu W, Price KL, et al. Vascular endothelial growth factor administration does not improve microvascular disease in the salt-dependent phase of post-angiotensin II hypertension. Am J Physiol Renal Physiol. 2006;291:F1248–54.
31. Parekh N, Zou AP. Role of prostaglandins in renal medullary circulation: response to different vasoconstrictors. Am J Physiol. 1996;271:F653–8.
32. Zhu Q, Wang Z, Xia M, et al. Silencing of hypoxia-inducible factor-1α gene attenuated angiotensin II-induced renal injury in Sprague-Dawley rats. Hypertension. 2011;58:657–64.
33. Tokudome T, Kishimoto I, Yamahara K, et al. Impaired recovery of blood flow after hind-limb ischemia in mice lacking guanylyl cyclase-A, a receptor for atrial and brain natriuretic peptides. Arterioscler Thromb Vasc Biol. 2009;29:1516–21.
34. Sexton PM, Zhuo J, Mendelsohn FA. Localization and regulation of renal receptors for angiotensin II and atrial natriuretic peptide. Tohoku J Exp Med. 1992;166:41–56.
35. Garg R, Pandey KN. Angiotensin II-mediated negative regulation of Npr1 promoter activity and gene transcription. Hypertension. 2003;41(part 2):730–6.
36. Arise KK, Pandey KN. Inhibition and down-regulation of gene transcription and guanylyl cyclase activity of NPRA by angiotensin II involving protein kinase C. Biochem Biophys Res Commun. 2006;349:131–5.
37. Hu P, Wang J, Zhao XQ, Hu B, Lu L, Qin YH. Overexpressed C-type natriuretic peptide serves as an early compensatory response to counteract extracellular matrix remodeling in unilateral ureteral obstruction rats. Mol Biol Rep. 2013;40:1429–41.
38. Segawa K, Minami K, Jimi N, Nakashima Y, Shigematsu A. C-type natriuretic peptide inhibits rat mesangial cell proliferation by a phosphorylation-dependent mechanism. Naunyn Schmiedebergs Arch Pharmacol. 1998;357:70–6.
39. Canaan-Kühl S, Ostendorf T, Zander K, Koch KM, Floege J. C-type natriuretic peptide inhibits mesangial cell proliferation and matrix accumulation in vivo. Kidney Int. 1998;53:1143–51.