Smad4 regulates growth plate chondrocyte proliferation, columnar organization and proteoglycan synthesis

2013 ◽  
Author(s):  
Whitaker Amanda ◽  
Berthet Ellora ◽  
Cantu Andrea ◽  
Laird Diana ◽  
Alliston Tamara
Keyword(s):  
Growth Plate ◽  
Proteoglycan Synthesis ◽  
Chondrocyte Proliferation ◽  
Growth Plate Chondrocyte ◽  
Columnar Organization

Suppression of growth plate chondrocyte proliferation by corticosteroids

2000 ◽  
Vol 14 (7) ◽  
pp. 612-615 ◽  
Author(s):  
G. Klaus ◽  
C. Jux ◽  
P. Fernandez ◽  
J. Rodriguez ◽  
R. Himmele ◽  
...  
Keyword(s):  
Growth Plate ◽  
Chondrocyte Proliferation ◽  
Growth Plate Chondrocyte

scholarly journals The Role of p27Kip1 in the Regulation of Growth Plate Chondrocyte Proliferation in Mice

2006 ◽  
Vol 60 (3) ◽  
pp. 288-293 ◽  
Author(s):  
Joyce A M Emons ◽  
Rose Marino ◽  
Ola Nilsson ◽  
Kevin M Barnes ◽  
Naomi Even-Zohar ◽  
...  
Keyword(s):  
Growth Plate ◽  
Chondrocyte Proliferation ◽  
Growth Plate Chondrocyte ◽  
Regulation Of Growth

scholarly journals DHEA Suppresses Longitudinal Bone Growth by Acting Directly at Growth Plate through Estrogen Receptors

Endocrinology ◽  
2011 ◽  
Vol 152 (4) ◽  
pp. 1423-1433 ◽  
Author(s):  
Hongzhi Sun ◽  
Weijin Zang ◽  
Bo Zhou ◽  
Lin Xu ◽  
Shufang Wu
Keyword(s):  
Estrogen Receptor ◽  
Growth Plate ◽  
Bone Growth ◽  
Nuclear Factor Κb ◽  
Binding Activity ◽  
Skeletal Maturation ◽  
Chondrocyte Apoptosis ◽  
Chondrocyte Proliferation ◽  
Longitudinal Bone Growth ◽  
Growth Plate Chondrocyte

Abstract Dehydroepiandrosterone (DHEA) is produced by the adrenal cortex and is the most abundant steroid in humans. Although in some physiological and pathological conditions the increased secretion of DHEA and its sulfated form is associated with accelerated growth rate and skeletal maturation, it is unclear whether DHEA can affect longitudinal bone growth and skeletal maturation by acting directly at the growth plate. In our study, DHEA suppressed metatarsal growth, growth plate chondrocyte proliferation, and hypertrophy/differentiation. In addition, DHEA increased the number of apoptotic chondrocytes in the growth plate. In cultured chondrocytes, DHEA reduced chondrocyte proliferation and induced apoptosis. The DHEA-induced inhibition of metatarsal growth and growth plate chondrocyte proliferation and hypertrophy/differentiation was nullified by culturing metatarsals with DHEA in the presence of ICI 182,780, an inhibitor of estrogen receptor, but not in the presence of Casodex, an inhibitor of androgen receptor. Lastly, nuclear factor-κB DNA binding activity was inhibited by the addition of DHEA in the medium of cultured chondrocyte. Our findings indicate that DHEA suppressed bone growth by acting directly at growth plate through estrogen receptor. Such growth inhibition is mediated by decreased chondrocyte proliferation and hypertrophy/differentiation and by increased chondrocyte apoptosis.

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