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来自X连锁低磷血症(Hyp)小鼠的培养肾小管细胞对低磷环境的适应性缺陷。

Defective adaptation to a low phosphate environment by cultured renal tubular cells from X-linked hypophosphatemic (Hyp) mice.

作者信息

Kinoshita Y, Fukase M, Nakada M, Fujita T

出版信息

Biochem Biophys Res Commun. 1987 Apr 29;144(2):763-9. doi: 10.1016/s0006-291x(87)80030-x.

DOI:10.1016/s0006-291x(87)80030-x
PMID:3034262
Abstract

Effects of parathyroid hormone (PTH), low phosphate environment, and 12-O-tetradecanoyl phorbol-13-acetate (TPA) on the phosphate reabsorption by the renal tubular cells from mutant hemizygous hypophosphatemic (Hyp/Y) mice and their littermates (+/Y) were studied using a phosphate accumulation system which had been developed recently. This system mimics phosphate transport at the renal tubules. When cultured in a normal phosphate medium, the characteristics of the phosphate accumulation by Hyp cells was almost identical with that by normal cells; a PTH-induced inhibition and a TPA-induced stimulation of phosphate accumulation. However, when preincubated in a low phosphate medium, the accumulation of phosphate by normal cells increased significantly, while that by Hyp cells did not. These results indicate that the adaptation to the low phosphate environment is defective in Hyp cells and it may be one of the cause of renal phosphate leakage in the Hyp mouse.

摘要

利用最近开发的磷酸盐积累系统,研究了甲状旁腺激素(PTH)、低磷环境和12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯(TPA)对突变半合子低磷血症(Hyp/Y)小鼠及其同窝正常小鼠(+/Y)肾小管细胞磷酸盐重吸收的影响。该系统模拟肾小管的磷酸盐转运。当在正常磷酸盐培养基中培养时,Hyp细胞积累磷酸盐的特性与正常细胞几乎相同;PTH诱导的磷酸盐积累抑制和TPA诱导的磷酸盐积累刺激。然而,当在低磷培养基中预孵育时,正常细胞的磷酸盐积累显著增加,而Hyp细胞则没有。这些结果表明,Hyp细胞对低磷环境的适应性存在缺陷,这可能是Hyp小鼠肾磷酸盐泄漏的原因之一。

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1
Defective adaptation to a low phosphate environment by cultured renal tubular cells from X-linked hypophosphatemic (Hyp) mice.来自X连锁低磷血症(Hyp)小鼠的培养肾小管细胞对低磷环境的适应性缺陷。
Biochem Biophys Res Commun. 1987 Apr 29;144(2):763-9. doi: 10.1016/s0006-291x(87)80030-x.
2
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X-linked hypophosphatemic mice are not hypersensitive to parathyroid hormone.
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Investigation of the mechanism for abnormal renal 25-hydroxyvitamin D3-1-hydroxylase activity in the X-linked Hyp mouse.对X连锁低磷血症小鼠肾脏25-羟维生素D3-1-羟化酶活性异常机制的研究。
Endocrinology. 1984 Aug;115(2):634-9. doi: 10.1210/endo-115-2-634.

引用本文的文献

1
Phosphate transport in osteoblasts from normal and X-linked hypophosphatemic mice.正常小鼠和X连锁低磷血症小鼠成骨细胞中的磷酸盐转运
Calcif Tissue Int. 1994 Jun;54(6):505-10. doi: 10.1007/BF00334333.
2
Molecular biology of hypophosphataemic rickets and oncogenic osteomalacia.低磷性佝偻病和肿瘤性骨软化症的分子生物学
Hum Genet. 1994 Nov;94(5):457-67. doi: 10.1007/BF00211008.
3
Primary cultures of renal epithelial cells from X-linked hypophosphatemic (Hyp) mice express defects in phosphate transport and vitamin D metabolism.来自X连锁低磷血症(Hyp)小鼠的肾上皮细胞原代培养物表现出磷酸盐转运和维生素D代谢缺陷。
Am J Hum Genet. 1988 Sep;43(3):293-303.
4
Crosstransplantation of kidneys in normal and Hyp mice. Evidence that the Hyp mouse phenotype is unrelated to an intrinsic renal defect.正常小鼠和Hyp小鼠之间的肾脏交叉移植。证据表明Hyp小鼠的表型与内在肾脏缺陷无关。
J Clin Invest. 1992 May;89(5):1453-9. doi: 10.1172/JCI115735.