scholarly journals Immunolocalization of calbindin D28k and vitamin D receptor during root formation of murine molar teeth

2003 ◽  
Vol 273A (2) ◽  
pp. 700-704 ◽  
Author(s):  
Tomoyuki Onishi ◽  
Rena Okawa ◽  
Hiroaki Murakami ◽  
Tomohiro Ogawa ◽  
Takashi Ooshima ◽  
...  
1996 ◽  
Vol 270 (4) ◽  
pp. F677-F681 ◽  
Author(s):  
L. Liu ◽  
A. Khastgir ◽  
J. M. McCauley ◽  
S. T. Dunn ◽  
J. H. Morrissey ◽  
...  

The spatial relationship between vitamin D receptor (VDR) and calbindin D28k [calcium binding protein D28k (CaBP-D28k)] gene expression within the murine kidney was studied by localizing their mRNAs in discrete nephron structures using reverse transcription-polymerase chain reaction (RT-PCR). Primers for beta-actin mRNA were used as a control for the presence of tissue during RT-PCR for CaBP-D28k mRNA. mRNA for CaBP-D28k was found only in distal convoluted tubules (DCTs), connecting tubules (CNTs), and cortical collecting ducts (CCDs). In contrast, VDR mRNA was detected in glomeruli, S2 proximal convoluted tubules, cortical thick ascending limbs of Henle's loop, DCTs, CNTs, and initial CCDs. The presence of both VDR and CaBP-D28k mRNA in DCTs, CNTs, and CCDs is consistent with the hypothesis that cacitriol acts via the VDR to stimulate CaBP-D28k synthesis. Conversely, the presence of VDR mRNA in other parts of the nephron suggests that calcitriol has genomically mediated actions within the kidney in addition to stimulation of CaBP-D28k synthesis.


1999 ◽  
Vol 297 (3) ◽  
pp. 503-512 ◽  
Author(s):  
T. Onishi ◽  
T. Ooshima ◽  
S. Sobue ◽  
M. J. Tabata ◽  
T. Maeda ◽  
...  

1996 ◽  
Vol 39 (4) ◽  
pp. 636-642 ◽  
Author(s):  
I Bailleul-Forestier ◽  
J L Davideau ◽  
P Papagerakis ◽  
I Noble ◽  
C Nessmann ◽  
...  

2004 ◽  
Vol 279 (50) ◽  
pp. 52406-52413 ◽  
Author(s):  
Wei Zheng ◽  
Yixia Xie ◽  
Gang Li ◽  
Juan Kong ◽  
Jian Q. Feng ◽  
...  

Calbindin (CaBP)-D28k and CaBP-D9k are cytosolic vitamin D-dependent calcium-binding proteins long thought to play an important role in transepithelial calcium transport. However, recent genetic studies suggest that CaBP-D28k is not essential for calcium metabolism. Genetic ablation of this gene in mice leads to no calcemic abnormalities. Genetic inactivation of the vitamin D receptor (VDR) gene leads to hypocalcemia, secondary hyperparathyroidism, rickets, and osteomalacia, accompanied by 90% reduction in renal CaBP-D9k expression but little change in CaBP-D28k. To address whether the role of CaBP-D28k in calcium homeostasis is compensated by CaBP-D9k, we generated VDR/CaBP-D28k double knockout (KO) mice, which expressed no CaBP-D28k and only 10% of CaBP-D9k in the kidney. On a regular diet, the double KO mice were more growth-retarded and 42% smaller in body weight than VDRKO mice and died prematurely at 2.5–3 months of age. Compared with VDRKO mice, the double KO mice had higher urinary calcium excretion and developed more severe secondary hyperparathyroidism and rachitic skeletal phenotype, which were manifested by larger parathyroid glands, higher serum parathyroid hormone levels, much lower bone mineral density, and more distorted growth plate with more osteoid formation in the trabecular region. On high calcium, high lactose diet, blood-ionized calcium levels were normalized in both VDRKO and the double KO mice; however, in contrast to VDRKO mice, the skeletal abnormalities were not completely corrected in the double KO mice. These results directly demonstrate that CaBP-D28k plays a critical role in maintaining calcium homeostasis and skeletal mineralization and suggest that its calcemic role can be mostly compensated by CaBP-D9k.


2001 ◽  
Vol 28 (1) ◽  
pp. 89-93 ◽  
Author(s):  
J. R. Garcia-Lozano ◽  
M. F. Gonzalez-Escribano ◽  
A. Valenzuela ◽  
A. Garcia ◽  
A. Nunez-Roldan

2006 ◽  
Vol 175 (4S) ◽  
pp. 260-260
Author(s):  
Nicholas J. Rukin ◽  
Samuel J. Moon ◽  
Dhaval Bodiwala ◽  
Christopher J. Luscombe ◽  
Mark F. Saxby ◽  
...  

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