scholarly journals Valproic Acid Impacts the Growth of Growth Plate Chondrocytes

2020 ◽  
Vol 17 (10) ◽  
pp. 3675
Author(s):  
Hueng-Chuen Fan ◽  
Shih-Yu Wang ◽  
Yi-Jen Peng ◽  
Herng-Sheng Lee
Keyword(s):  
Valproic Acid ◽  
Short Stature ◽  
Growth Plate ◽  
Caspase 3 ◽  
Skeletal Growth ◽  
Growth Plate Chondrocytes ◽  
Protein Levels ◽  
Rat Growth ◽  
Cox 2 ◽  
Bone Abnormalities

A range of bone abnormalities including short stature have been reported to be associated with the use of antiepileptic drugs (AEDs) in children. Exactly how AEDs impact skeletal growth, however, is not clear. In the present study, rat growth plate chondrocytes were cultured to study the effects of AEDs, including valproic acid (VPA), oxcarbazepine (OXA), levetiracetam (LEV), lamotrigine (LTG), and topiramate (TPM) on the skeletal growth. VPA markedly reduced the number of chondrocytes by apoptosiswhile other AEDs had no effect. The apoptosis associated noncleaved and cleaved caspase 3, and caspases were increased by exposure to VPA, which up-regulated cyclooxygenase 2 (COX-2) mRNA and protein levels likely through histone acetylation. The COX-2 inhibitor NS-398 attenuated the effects of VPA up-regulating COX-2 expression and decreased VPA-induced caspase 3 expression. The use of VPA in children should be closely monitored or replaced, where appropriate, by AEDs which do not apparently affect the growth plate chondrocytes.

Autoradiographic Evidence of Opioid Binding Sites in Rat Growth Plate Chondrocytes

1992 ◽  
Vol 55 (3) ◽  
pp. 357-359 ◽  
Author(s):  
Manuel Freire-Garabal ◽  
Maria Teresa Castaño ◽  
Angel Belmonte ◽  
Javier Jorge ◽  
José Couceiro ◽  
...  
Keyword(s):  
Growth Plate ◽  
Binding Sites ◽  
Growth Plate Chondrocytes ◽  
Opioid Binding ◽  
Rat Growth

scholarly journals Nicotine Acts on Growth Plate Chondrocytes to Delay Skeletal Growth through the α7 Neuronal Nicotinic Acetylcholine Receptor

PLoS ONE ◽  
2008 ◽  
Vol 3 (12) ◽  
pp. e3945 ◽  
Author(s):  
Atsuo Kawakita ◽  
Kazuki Sato ◽  
Hatsune Makino ◽  
Hiroyasu Ikegami ◽  
Shinichiro Takayama ◽  
...  
Keyword(s):  
Acetylcholine Receptor ◽  
Growth Plate ◽  
Nicotinic Acetylcholine Receptor ◽  
Skeletal Growth ◽  
Neuronal Nicotinic Acetylcholine Receptor ◽  
Growth Plate Chondrocytes ◽  
Nicotinic Acetylcholine

Rat growth plate chondrocytes express low levels of 25-hydroxy-1α-hydroxylase

2004 ◽  
Vol 89-90 ◽  
pp. 143-147 ◽  
Author(s):  
Ulrike Hügel ◽  
Lutz Weber ◽  
Jörg Reichrath ◽  
Otto Mehls ◽  
Günter Klaus
Keyword(s):  
Growth Plate ◽  
Growth Plate Chondrocytes ◽  
Rat Growth ◽  
Low Levels

scholarly journals Apoptosis of Growth Plate Chondrocytes Occurs through a Mitochondrial Pathway

2007 ◽  
Vol 77 (1) ◽  
pp. 129-134 ◽  
Author(s):  
Cristina C. Teixeira ◽  
Aida P. Padron Costas ◽  
Yelena Nemelivsky
Keyword(s):  
Cytochrome C ◽  
Growth Plate ◽  
Caspase 3 ◽  
Mitochondrial Pathway ◽  
Chondrocyte Apoptosis ◽  
Cytochrome C Release ◽  
Growth Plate Chondrocytes ◽  
Chondrocyte Viability ◽  
Induced Apoptosis ◽  
Free Media

Abstract Objective: To determine the role of mitochondria in chondrocyte apoptosis induced by inorganic phosphate (Pi). Materials and Methods: Chondrocytes isolated from the growth plates of chick embryo tibia were treated with Pi in serum-free media; chondrocyte viability, mitochondrial membrane potential, cytochrome c release from mitochondria, caspase 3 activity, endonuclease activity, and DNA fragmentation were investigated. Results: Exposure to Pi for 24 hours induced apoptosis in growth plate chondrocytes through a pathway that involved loss of mitochondrial function, release of cytochrome c into the cytoplasm, increases in caspase 3 and endonuclease activities, and fragmentation of DNA. Conclusions: This study suggests that mitochondria are important players in Pi-induced apoptosis.

scholarly journals 17β-Estradiol Regulates Rat Growth Plate Chondrocyte Apoptosis Through a Mitochondrial Pathway Not Involving Nitric Oxide or MAPKs

Endocrinology ◽  
2011 ◽  
Vol 152 (1) ◽  
pp. 82-92 ◽  
Author(s):  
M. Zhong ◽  
D. H. Carney ◽  
B. D. Boyan ◽  
Z. Schwartz
Keyword(s):  
Nitric Oxide ◽  
Growth Plate ◽  
Caspase 3 ◽  
Growth Zone ◽  
Mapk Signaling ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Dependent Manner ◽  
Growth Plate Chondrocytes ◽  
Bax Protein ◽  
17Β Estradiol

Abstract Estrogens cause growth plate closure in both males and females, by decreasing proliferation and inducing apoptosis of postproliferative growth plate chondrocytes. In vitro studies using 17β-estradiol (E2) conjugated to bovine serum albumin (E2-BSA) show that rat costochondral growth plate resting zone chondrocytes also respond to E2. Moreover, they are regulated by E2-BSA via a protein kinase C and ERK MAPK signaling pathway that is functional only in female cells. To better understand how E2 regulates apoptosis of growth plate chondrocytes, rat resting zone chondrocytes cells were treated with E2 or E2-BSA. E2 caused apoptosis in male and female resting zone and growth zone chondrocytes in a dose-dependent manner, based on elevated DNA fragmentation, terminal deoxynucleotidyl transferase dUTP nick end labeling staining and caspase-3 activation. E2 also up-regulated p53 and Bax protein (Bcl-2-associated X protein) levels and induced release of cytochrome C from the mitochondria, indicating a mitochondrial apoptotic pathway. The apoptotic effect of E2 did not involve elevated nitric oxide production or MAPKs. It was reduced by ICI 182780, which is an estrogen receptor (ER) antagonist and blocked by antibodies to Erα36, a membrane-associated ER. E2-BSA reduced cell viability and increased caspase-3 activity; ICI 182780 had no effect, but anti-ERα36 antibodies blocked the effect. The results indicate that estrogen is able to directly affect the cell population kinetics of growth plate chondrocytes by regulating apoptosis, as well as proliferation and differentiation in both resting zone and growth zone cells. They also have provided further information about the physiological functions of estrogen on longitudinal bone growth.

scholarly journals Interaction of IGF-I and 1α,25(OH)2D3 on receptor expression and growth stimulation in rat growth plate chondrocytes

1998 ◽  
Vol 53 (5) ◽  
pp. 1152-1161 ◽  
Author(s):  
Günter Klaus ◽  
Lutz Weber ◽  
Julian Rodríguez ◽  
Porfirio Fernández ◽  
Thomas Klein ◽  
...  
Keyword(s):  
Growth Plate ◽  
Growth Stimulation ◽  
Receptor Expression ◽  
Growth Plate Chondrocytes ◽  
Igf I ◽  
Rat Growth

Primary culture of rat growth plate chondrocytes: an in vitro model of growth plate histotype, matrix vesicle biogenesis and mineralization

Bone ◽  
2004 ◽  
Vol 34 (6) ◽  
pp. 961-970 ◽  
Author(s):  
Rama Garimella ◽  
Xiahong Bi ◽  
Nancy Camacho ◽  
Joseph B Sipe ◽  
H.Clarke Anderson
Keyword(s):  
Primary Culture ◽  
Growth Plate ◽  
In Vitro Model ◽  
Matrix Vesicle ◽  
Growth Plate Chondrocytes ◽  
Vesicle Biogenesis ◽  
Rat Growth ◽  
Vitro Model

Isolation of a plasma membrane-enriched fraction from collagenase-suspended rachitic rat growth plate chondrocytes

1983 ◽  
Vol 1 (3) ◽  
pp. 319-324 ◽  
Author(s):  
William W. Bohn ◽  
Ross M. Stein ◽  
Howard H. T. Hsu ◽  
David C. Morris ◽  
H. Clarke Anderson
Keyword(s):  
Plasma Membrane ◽  
Growth Plate ◽  
Growth Plate Chondrocytes ◽  
Rat Growth
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