Characterization of Voltage-Sensitive Calcium Channels in Growth Plate Chondrocytes

1997 ◽  
Vol 234 (2) ◽  
pp. 432-438 ◽  
Author(s):  
Michael J. Zuscik ◽  
Thomas E. Gunter ◽  
J.Edward Puzas ◽  
Randy N. Rosier
Keyword(s):  
Calcium Channels ◽  
Growth Plate ◽  
Growth Plate Chondrocytes

L-type calcium channels in growth plate chondrocytes participate in endochondral ossification

2007 ◽  
Vol 101 (2) ◽  
pp. 389-398 ◽  
Author(s):  
Edna E. Mancilla ◽  
Mario Galindo ◽  
Barbara Fertilio ◽  
Mario Herrera ◽  
Karime Salas ◽  
...  
Keyword(s):  
Calcium Channels ◽  
Growth Plate ◽  
Endochondral Ossification ◽  
Growth Plate Chondrocytes

Characterization of the Mineralization Process in Cultures of Rabbit Growth Plate Chondrocytes

1993 ◽  
Vol 156 (2) ◽  
pp. 372-380 ◽  
Author(s):  
Akitoshi Jikko ◽  
Takaaki Aoba ◽  
Hiroshi Murakami ◽  
Yoshiro Takano ◽  
Masahiro Iwamoto ◽  
...  
Keyword(s):  
Growth Plate ◽  
Mineralization Process ◽  
Growth Plate Chondrocytes

scholarly journals Sorting of growth plate chondrocytes allows the isolation and characterization of cells of a defined differentiation status

2010 ◽  
Vol 25 (6) ◽  
pp. 1267-1281 ◽  
Author(s):  
Daniele Belluoccio ◽  
Julia Etich ◽  
Sabrina Rosenbaum ◽  
Christian Frie ◽  
Ivan Grskovic ◽  
...  
Keyword(s):  
Growth Plate ◽  
Growth Plate Chondrocytes ◽  
Isolation And Characterization ◽  
Differentiation Status

Characterization of a Specific Somatomedin-C Receptor on Isolated Bovine Growth Plate Chondrocytes*

Endocrinology ◽  
1983 ◽  
Vol 112 (6) ◽  
pp. 2128-2136 ◽  
Author(s):  
S. B. TRIPPEL ◽  
J. J. VAN WYK ◽  
M. B. FOSTER ◽  
M. E. SVOBODA
Keyword(s):  
Growth Plate ◽  
Growth Plate Chondrocytes ◽  
Somatomedin C

scholarly journals Characterization of voltage-dependent sodium and calcium channels in mouse pancreatic A- and B-cells

2006 ◽  
Vol 572 (3) ◽  
pp. 691-706 ◽  
Author(s):  
Sheila Vignali ◽  
Veronika Leiss ◽  
Rosi Karl ◽  
Franz Hofmann ◽  
Andrea Welling
Keyword(s):  
B Cells ◽  
Calcium Channels ◽  
Voltage Dependent ◽  
A And B Cells

scholarly journals Expression and Functional Assessment of an Alternatively Spliced Extracellular Ca2+-Sensing Receptor in Growth Plate Chondrocytes

Endocrinology ◽  
2005 ◽  
Vol 146 (12) ◽  
pp. 5294-5303 ◽  
Author(s):  
Luis Rodriguez ◽  
Chialing Tu ◽  
Zhiqiang Cheng ◽  
Tsui-Hua Chen ◽  
Daniel Bikle ◽  
...  
Keyword(s):  
Cell Surface ◽  
Growth Plate ◽  
Inositol Phosphate ◽  
Intact Cell ◽  
Chinese Hamster ◽  
Full Length ◽  
Wild Type ◽  
Growth Plate Chondrocytes ◽  
Matrix Gene ◽  
Alternatively Spliced

The extracellular Ca2+-sensing receptor (CaR) plays an essential role in mineral homeostasis. Studies to generate CaR-knockout (CaR−/−) mice indicate that insertion of a neomycin cassette into exon 5 of the mouse CaR gene blocks the expression of full-length CaRs. This strategy, however, allows for the expression of alternatively spliced CaRs missing exon 5 [Exon5(−)CaRs]. These experiments addressed whether growth plate chondrocytes (GPCs) from CaR−/− mice express Exon5(−)CaRs and whether these receptors activate signaling. RT-PCR and immunocytochemistry confirmed the expression of Exon5(−)CaR in growth plates from CaR−/− mice. In Chinese hamster ovary or human embryonic kidney-293 cells, recombinant human Exon5(−)CaRs failed to activate phospholipase C likely due to their inability to reach the cell surface as assessed by intact-cell ELISA and immunocytochemistry. Human Exon5(−)CaRs, however, trafficked normally to the cell surface when overexpressed in wild-type or CaR−/− GPCs. Immunocytochemistry of growth plate sections and cultured GPCs from CaR−/− mice showed easily detectable cell-membrane expression of endogenous CaRs (presumably Exon5(−)CaRs), suggesting that trafficking of this receptor form to the membrane can occur in GPCs. In GPCs from CaR−/− mice, high extracellular [Ca2+] ([Ca2+]e) increased inositol phosphate production with a potency comparable with that of wild-type GPCs. Raising [Ca2+]e also promoted the differentiation of CaR−/− GPCs as indicated by changes in proteoglycan accumulation, mineral deposition, and matrix gene expression. Taken together, our data support the idea that expression of Exon5(−)CaRs may compensate for the loss of full-length CaRs and be responsible for sensing changes in [Ca2+]e in GPCs in CaR−/− mice.

Sign in / Sign up

Export Citation Format

Share Document