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Upregulation of renal renin-angiotensin system in mouse diabetic nephropathy.
Jpn J Vet Res. 2005 Aug; 53(1-2):13-26.JJ

Abstract

The aim of this study was to clarify the role of the renal renin-angiotensin system (RAS) in diabetic nephropathy (DN), which was induced by injection of streptozotocin (STZ). Male CBA/N and CBA/J mice were compared in this study. The former possesses a single renin gene, Ren1, whereas the latter carries two renin genes, Ren1 and Ren2. To examine the molecular dynamics of renal RAS, including renin, angiotensinogen (Agt), angiotensin-converting enzyme (Ace), angiotensin type 1 (Agtr1) and type 2 (Agtr2) receptors in experimental DN, we performed laser-microdissection (LMD) followed by reverse transcriptase nested polymerase chain reaction using each specific primer pairs and immunohistochemistry for renin and angiotensin II. CBA/N mice had a higher response after injection of STZ than CBA/J mice, showing a significant increase of the kidney/body weight ratio, although there was no significant difference between the two strains for the blood glucose level or pancreatic beta-cell response. The onset of renal pathological changes associated with DN was earlier and more severe in CBA/N mice than in CBA/J mice. Distinct immunoreactivities for renin and angiotensin II were newly distributed on the flattened epithelial cells in the dilated distal tubules in the cortex as well as the collecting ducts in the cortex and medulla, and were demonstrated more intensely in CBA/N mice than in CBA/J mice. Microdissectional analysis in both DN models revealed a higher incidence of RAS-related gene expression in CBA/J, Ren 1 Ren 2 mice than in CBA/N, Ren 1 mice. These findings suggest that intrarenal RAS plays an important role in the onset of renal pathological changes associated with DN. Additionally, Ren 1 mice have more severe histopathological nephropathy than Ren1 Ren2 mice, followed by marked production of angiotensin II.

Authors+Show Affiliations

Laboratory of Anatomy, Department of Biomedical Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo 060-0818, Japan.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16190318

Citation

Tamura, Jun, et al. "Upregulation of Renal Renin-angiotensin System in Mouse Diabetic Nephropathy." The Japanese Journal of Veterinary Research, vol. 53, no. 1-2, 2005, pp. 13-26.
Tamura J, Konno A, Hashimoto Y, et al. Upregulation of renal renin-angiotensin system in mouse diabetic nephropathy. Jpn J Vet Res. 2005;53(1-2):13-26.
Tamura, J., Konno, A., Hashimoto, Y., & Kon, Y. (2005). Upregulation of renal renin-angiotensin system in mouse diabetic nephropathy. The Japanese Journal of Veterinary Research, 53(1-2), 13-26.
Tamura J, et al. Upregulation of Renal Renin-angiotensin System in Mouse Diabetic Nephropathy. Jpn J Vet Res. 2005;53(1-2):13-26. PubMed PMID: 16190318.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Upregulation of renal renin-angiotensin system in mouse diabetic nephropathy. AU - Tamura,Jun, AU - Konno,Akihiro, AU - Hashimoto,Yoshiharu, AU - Kon,Yasuhiro, PY - 2005/9/30/pubmed PY - 2005/10/26/medline PY - 2005/9/30/entrez SP - 13 EP - 26 JF - The Japanese journal of veterinary research JO - Jpn. J. Vet. Res. VL - 53 IS - 1-2 N2 - The aim of this study was to clarify the role of the renal renin-angiotensin system (RAS) in diabetic nephropathy (DN), which was induced by injection of streptozotocin (STZ). Male CBA/N and CBA/J mice were compared in this study. The former possesses a single renin gene, Ren1, whereas the latter carries two renin genes, Ren1 and Ren2. To examine the molecular dynamics of renal RAS, including renin, angiotensinogen (Agt), angiotensin-converting enzyme (Ace), angiotensin type 1 (Agtr1) and type 2 (Agtr2) receptors in experimental DN, we performed laser-microdissection (LMD) followed by reverse transcriptase nested polymerase chain reaction using each specific primer pairs and immunohistochemistry for renin and angiotensin II. CBA/N mice had a higher response after injection of STZ than CBA/J mice, showing a significant increase of the kidney/body weight ratio, although there was no significant difference between the two strains for the blood glucose level or pancreatic beta-cell response. The onset of renal pathological changes associated with DN was earlier and more severe in CBA/N mice than in CBA/J mice. Distinct immunoreactivities for renin and angiotensin II were newly distributed on the flattened epithelial cells in the dilated distal tubules in the cortex as well as the collecting ducts in the cortex and medulla, and were demonstrated more intensely in CBA/N mice than in CBA/J mice. Microdissectional analysis in both DN models revealed a higher incidence of RAS-related gene expression in CBA/J, Ren 1 Ren 2 mice than in CBA/N, Ren 1 mice. These findings suggest that intrarenal RAS plays an important role in the onset of renal pathological changes associated with DN. Additionally, Ren 1 mice have more severe histopathological nephropathy than Ren1 Ren2 mice, followed by marked production of angiotensin II. SN - 0047-1917 UR - https://www.unboundmedicine.com/medline/citation/16190318/Upregulation_of_renal_renin_angiotensin_system_in_mouse_diabetic_nephropathy_ L2 - http://www.medicalonline.jp/meteo_linkout.php?issn=0047-1917&volume=53&issue=1-2&spage=13 DB - PRIME DP - Unbound Medicine ER -