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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2004.12
- 수록면
- 375 - 383 (9page)
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It has been reported that osteoporosis induced by the deficiency of estrogens in menopause is associated with the unbalance of Ca²? and Pi levels. Proximal tubule is very important organ to regualte Ca²? and Pi level in the body. However, the effect of estrogens on Ca²? and Pi regulation was not elucidated. Thus, we examined the effect of 17-β estradiol (E₂) on Ca²? and Pi uptake in the primary cultured rabbit renal proxiaml tubule cells. In the present study, E₂ (＞10?? M) decreases Ca²? uptake and stimulates Pi uptake over 3 days. E₂-induced decrease of C²? uptake and stimulation of Pi uptake were blocked by actinomycin D (a gene transcription inhibitor), cycloheximide (a protein synthesis inhibitor), tamoxifen, and progesterone (estrogen receptor antagonists). E₂induced decrease of Ca²? uptake and stimulation of Pi uptake were blocked by SQ22536 (an adenylate cyclase inhibitor), Rp-cAMP (a cAMP antagonist), and PKI (a protein kinase A inhibitor). Indeed, E₂ increased cAMP formation. In addition, E₂-induced decrease of Ca²? uptake and stimulation of Pi uptake were blocked by staurosporine, H-7, and bisindolylmaleimide Ⅰ (protein kinase C inhibitors) and E₂ translocated PKC from cytoslic fraction to membrane fraction. In conclusion, E₂ decreased Ca²? uptake and stimulated Pi uptake via cAMP and PKC pathway in the PICs.
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UCI(KEPA) : I410-ECN-0101-2009-510-017342138