2009 Fiscal Year Final Research Report
Calcium-sensing receptor expression is regulated by glial cells missing-2 in human parathyroid cells
| Project/Area Number |
20790598
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Kidney internal medicine
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| Research Institution | Showa University |
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Principal Investigator |
MIZOBUCHI Masahide Showa University, 医学部・内科学講座腎臓内科学部門, 助教 (90465203)
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| Project Period (FY) |
2008 – 2009
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| Keywords | 二次性副甲状腺機能亢進症 / Gcm2 / 副甲状腺細胞 / Ca感知受容体 / ビタミンD受容体 |
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| Research Abstract |
Glial cells missing-2 (Gcm2) is the key regulating transcription factor for parathyroid gland development. The role of Gcm2 in parathyroid cell physiology, however, has not been fully studied. In this study, we examined the effects of Gcm2 silencing on cultured human parathyroid cells. Collagenase-dispersed human parathyroid cells from patients with chronic kidney disease were infected with lentivirus expressing shRNA for human Gcm2. Seventy-two hours after infection, mRNA was processed and analyzed for Gcm2, PTH, vitamin D receptor (VDR), calcium-sensing receptor (CaR), 25-hydroxyvitamin D3 1-a-hydroxylase (1-OHase), and proliferating cell nuclear antigen (PCNA) by real-time PCR (qPCR). CaR mRNA and protein were significantly reduced by Gcm2 silencing, however, VDR, PTH, 1-OHase, and PCNA were not significantly affected. Further analysis of CaR mRNA indicated that transcripts containing exon 1B, derived by transcription from CaR promoter 2, were downregulated by Gcm2 silencing. These results indicate that one function of Gcm2 is to maintain high levels of CaR expression in parathyroid cells.
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