2011 Fiscal Year Final Research Report
Investigation for anti-renal fibrotic effects of lipid-binding proteins and lipid-activated nuclear receptors and search for new therapeutic reagents
| Project/Area Number |
21591024
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | University of Fukui |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIDA Haruyoshi 福井大学, 医学部, 教授 (80135574)
KASUNO Kenji 福井大学, 医学部, 助教 (60455243)
SUGAYA Takeshi 聖マリアンナ医科大学, 医学部, 客員教授 (40381561)
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| Project Period (FY) |
2009 – 2011
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| Keywords | 腎臓学 / ペルオキシゾーム増殖剤応答性受容体 / 脂肪酸結合蛋白 / 尿細管上皮細胞 / メサンギウム細胞 / 炎症 / アンジテンシンII受容体拮抗薬 |
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| Research Abstract |
Presence and activities of peroxisome proliferator-activated receptor(PPAR)-δandγwere confirmed in human proximal renal tubular epithelial cells and mesangial cells which inflammatory insults targeted mainly during progression of renal injury. An angiotensin II receptor blocker, telmisartan was shown to have PPAR-δandγ-induced transcriptional activities and increase expression of their target genes such as fatty acid-binding protein(FABP) and liver X receptor. Telmisartan also decreased gene expression of monocyte chemoattractant protein-1(MCP-1). In the mouse immortalized proximal renal tubular cell line with over-expression of human liver-type FABP, a putative transporter of PPAR ligands, mouse PPAR-δwas up-regulated and MCP-1 down-regulated. These results suggest that some bioactive molecules with a potential to affect function and dynamism of PPAR and FABP are candidates of new therapeutic reagents for chronic kidney disease.
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