ISSN:
1432-0827
Keywords:
Cultured cells
;
Vitamin D-resistant rickets
;
Mouse
;
cAMP
;
Alkaline phosphatase
Source:
Springer Online Journal Archives 1860-2000
Topics:
Biology
,
Medicine
,
Physics
Notes:
Abstract Human hypophosphatemic vitamin D-resistant rickets (X-linked hypophosphatemia-XLH) is characterized by hypophosphatemia, a decreased tubular reabsorption of phosphate (Pi) and defective skeleton mineralization. Utilizing a mouse model (Hyp) of XLH, which demonstrates biological abnormalities and skeletal defects of XLH, we analyzed sodium-dependent phosphate transport in isolated osteoblasts derived from the calvaria of normophosphatemic and hypophosphatemic mice. Initial rates of phosphate uptake by normal and Hyp osteoblasts showed similar slopes. Osteoblasts from both normal and Hyp mice exhibited saturable, sodium-dependent phosphate transport with apparent Vmax and Km values not significantly different (normal mice, Vmax=24.30±3.45 nmol/mg prot. 10 min, Km=349.49±95.20 μmol/liter; Hyp mice, Vmax=23.03±3.41 nmol/mg prot. 10 min, Km=453.64±106.93 μmol/liter, n=24). No differences were found in the ability of normal and Hyp osteoblasts to respond to Pi transport after 5 hours of Pi deprivation. Both cell types exhibited a similar increase in cAMP in response to PTH. The accumulated results demonstrate that Pi uptake and transport in normal and Hyp mouse osteoblasts is a sodium-dependent saturable process. As osteoblast Pi uptake and transport is apparently normal in the Hyp mouse model of XLH, the “osteoblastic failure” described for the Hyp mouse should be attributed to other mechanism(s).
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00334333
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