Effect of Nitric Oxide on NGF-Receptor of seminiferous Epithelial Cells
| Project/Area Number |
15591722
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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 |
Urology
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| Research Institution | National Institute of Radiological Sciences |
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Principal Investigator |
ONODA Makoto National Institute of Radiological Sciences, Redox Regulation Research Group, Senior Researcher, レドックス制御研究グループ, 主任研究員 (20260234)
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| Co-Investigator(Kenkyū-buntansha) |
KATSUBE Takanori National Institute of Radiological Sciences, Low Dose Radiation Research Project Group, Researcher, 低線量生体影響研究プロジェクト, 研究員 (10311375)
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| Project Period (FY) |
2003 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2004: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2003: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | Seminiferous Epithelial Cell / Sertoli Cell / NGF / NGF-Receptor / p75 / TRK / Nitric Oxide / Nitric Oxide Synthase / 精巣上皮細 |
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| Research Abstract |
We investigated the effect of nitric oxide (NO) on neurotrophic factor receptors (NGF-R and TRKs) of rat seminiferous epithelial (Sertoli) cells to elucidate some aspects of the role of NO in intratesticular communication between germ cells and epithelial cells.
Immunoreactivity with a specific antibody against NGF gene product localized to germ cells (pachytene spermatocytes and round spermatids) within testis, while gene products of neurotrophic factor receptors such as NGF-R (p75) and Trks (A and B) localized to Sertoli cells. Localization of the NGF-R, TrkA and TrkB in cultured Sertoli cells revealed that the receptors were distributed randomly throughout the cell surface. The diffused immunofluorescence staining represented characteristic immunostaining of plasma membrane receptors that were not pre-clustered in coated pits. In addition, a certain Sertoli cells exhibited that the immunofluorescence staining of these receptors also localized to be in clustered areas of the cells.
Exp
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ression of mRNA of these neurotrophic factor receptors was detected by RT-PCR in total RNA samples obtained from the cultured Sertoli cells, and immunoreactive bands of NGF-R (76kDa), TrkA (140kDa) and TrkB (145kDa) were identified in the extracts of cultured Sertoli cells by the Western blot analyses. Expressions of both proteins and mRNAs of the NGF-R, TrkA and TrkB were apparently decreased in the Sertoli cells treated with NOC18 (an NO donor, 0.4mM) for 24h. Treatment with NO donor also resulted in the decline of the NGF-R, TrkA and TrkB at the supranuclear areas of the cells. This indicates that endocytosis of coated pits including the receptors was eliminated by exogenous NO added to the Sertoli cells in the culture. On the other hand, the culture of Sertoli cells with neurotrophic factors such as BDNF (100ng/ml) and NGF (100ng/ml) revealed the up-regulation of Trk (146kDa) detected the Trk-pan antibody, and the combination-treatment of neurotrophic factor and NO donor eliminated the decrease of Trk (146kDa) induced by the NO donor treatment. These results suggest that Sertoli cells express the neurotrophic factor receptors such as NGF-R, TrkA and TrkB and may regulate the proliferation and differentiation of germ cells through the paracrine regulation mechanism within testis. Furthermore, NO produced excessively within testis during acute or chronic pathophysiological conditions perturbs the expression and localization of neurotrophic factor receptors and in turn the signal transduction for spermatogenesis, whereas the ligands of these receptors such as BDNF and NGF might rescue the receptors from the repression induced by the excessive NO and maintain the regulation of normal spermatogenesis. Less
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Report
(4 results)
Research Products
(13 results)
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[Journal Article] Involvement of illegitimate V(D)J recombination or microhomology-mediated nonhomologous end-joining in the formation of intragenic deletions of the NotchI gene in mouse thymic lymphomas.2004
Author(s)
Tsuji, H., Ishii-Ohba, H, Katsube, T., Ukai, H., Aizawa, S., Doi, M., Hioki, K., Ogiu, T.
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Journal Title
Cancer Research 64
Pages: 8882-8890
Description
「研究成果報告書概要(和文)」より
Related Report
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[Journal Article] Involvement of illegitimate V(D)J recombination or microhomology-mediated nonhomologous end-joining in the formation of intragenic deletions of the NotchI gene in mouse thymic lymphomas.2004
Author(s)
Tsuji, H., Ishii-Ohba, H., Katsube, T., Ukai, H., Aizawa, S., Doi, M., Hioki, K., Ogiu, T.
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Journal Title
Cancer Research 64
Pages: 8882-8890
Description
「研究成果報告書概要(欧文)」より
Related Report
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