2006 Fiscal Year Final Research Report Summary
The role of intercellular communication in repair process of glomerular injury
| Project/Area Number |
17590821
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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 | Niigata University |
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Principal Investigator |
MORIOKA Tetsuo Niigata University, Institute of Medicine and Dentistry, Associate Professor, 医歯学系, 助教授 (00210146)
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| Co-Investigator(Kenkyū-buntansha) |
KUMAGAI Naoki Niigata University, Medical and Dental Hospital, Medical Staff, 医歯学総合病院, 医員 (30377189)
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| Project Period (FY) |
2005 – 2006
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| Keywords | Gap junction / Glomerular mesangial cell / Glomerular endothelial cell / Connexin 37 / Connexin 40 / Connexin 43 / Glomerular sclerosis / Cell adhesion |
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| Research Abstract |
The purpose of this study was to clarify the role of gap junctional intercellular communication (GJIC) in repair process of glomerular injury. Using cell culture system, we investigated the effect of LPS, TNF-α,IFN-γ to the GJIC and connexin expression of cultured human glomerular endothelial cells. Using lucifer yellow as an indicator, dye transfer assay revealed that LPS and TNF-α increased and IFN-γ decreased the GIJC in glomerular endothelial cells. Using real time RT-PCR, mRNA expression of connexin37,40,43 in cultured human endothelial cells was assessed. Cx43 mRNA expression was increased 24 hours after addition of LPS and TNF-α, but decreased after addition of IFN-γ. Cx37,40 mRNA expression was decreased after addition of LPS and TNF-α, but not changed after addition of IFN-γ. We also examined the change of connexin40,43 expression during the course of experimental mesangial proliferative GN model. Immunofluorescence and immunoelectron micropsopic study showed that in normal control rats, Cx40 expressed on the intra and extra-glomerular mesangial cells. Cx40 was presented on the endothelial cells and smooth muscle cells of extra glomerular vessels of kidney. The distribution of Cx43 was similar to that of Cx40. Three to seven days after induction of glomerulonephritis, expression of Cx40 and 43 was decreased. Fourteen days after induction of glomerulonephritis, the expression was recovered similar to normal state. From these data, we concluded that GJIC may contribute to the repair process of glimerular injury.
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