Peroxisome proliferator activated receptor-γ (PPARγ) represses thyroid hormone signaling in growth plate chondrocytes

Bone ◽  
2005 ◽  
Vol 37 (3) ◽  
pp. 305-312 ◽  
Author(s):  
Lai Wang ◽  
Yvonne Y. Shao ◽  
R. Tracy Ballock
Keyword(s):  
Thyroid Hormone ◽  
Growth Plate ◽  
Peroxisome Proliferator ◽  
Hormone Signaling ◽  
Growth Plate Chondrocytes ◽  
Peroxisome Proliferator Activated Receptor

scholarly journals Leptin Antagonizes Peroxisome Proliferator-Activated Receptor-γSignaling in Growth Plate Chondrocytes

PPAR Research ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Lai Wang ◽  
Yvonne Y. Shao ◽  
R. Tracy Ballock
Keyword(s):  
Growth Plate ◽  
Chondrogenic Differentiation ◽  
Erk Signaling ◽  
Peroxisome Proliferator ◽  
Newborn Rats ◽  
Inhibitory Effects ◽  
Growth Plate Chondrocytes ◽  
Peroxisome Proliferator Activated Receptor ◽  
Proliferation And Differentiation

Leptin is an obesity-associated cytokine-like hormone encoded by theobgene. Recent studies reveal that leptin promotes proliferation and differentiation of chondrocytes, suggesting a peripheral role of leptin in regulating growth plate function. Peroxisome proliferator-activated receptor-γ(PPARγ) is a transcriptional regulator of adipogenesis. Locally, PPARγnegatively regulates chondrogenic differentiation and terminal differentiation in the growth plate. The aim of this study was to test the hypothesis that leptin may suppress the inhibitory effects of PPARγon growth plate chondrocytes. Chondrocytes were collected from distal femoral growth plates of newborn rats and were cultured in monolayer or cell pellets in the presence or absence of leptin and the PPARγagonist ciglitazone. The results show that leptin attenuates the suppressive effects of PPARγon chondrogenic differentiation and T3-mediated chondrocyte hypertrophy. Leptin treatment also leads to a mild downregulation of PPAR mRNA expression and a significant MAPK/ERK-dependent PPARγphosphorylation at serine 112/82. Blocking MAPK/ERK function with PD98059 confirmed that leptin antagonizes PPARγfunction in growth plate chondrocytes through the MAPK/ERK signaling pathway. Furthermore, leptin signaling in growth plate cells is also negatively modulated by activation of PPARγ, implying that these two signaling pathways are mutually regulated in growth plate chondrocytes.

scholarly journals Peroxisome Proliferator-Activated Receptor-γPromotes Adipogenic Changes in Growth Plate Chondrocytes In Vitro

PPAR Research ◽  
2006 ◽  
Vol 2006 ◽  
pp. 1-8 ◽  
Author(s):  
Lai Wang ◽  
Yvonne Y. Shao ◽  
R. Tracy Ballock
Keyword(s):  
Growth Plate ◽  
Adipogenic Differentiation ◽  
Terminal Differentiation ◽  
Cell Types ◽  
Peroxisome Proliferator ◽  
Growth Plate Chondrocytes ◽  
Peroxisome Proliferator Activated Receptor ◽  
Infected Cells ◽  
In Vitro Data

Chondrocytes and adipocytes are two differentiated cell types which are both derived from mesenchymal cells. The purpose of this study was to investigate whether peroxisome proliferator-activated receptor-γ(PPARγ), a transcription factor involved in lineage determination during adipogenesis, is able to induce adipogenic differentiation in growth plate chondrocytes. Isolated epiphyseal chondrocytes were infected with a PPARγadenovirus or treated with the PPARγagonist ciglitazone. Both of these treatments resulted in lipid droplet accumulation and expression of the adipogenic markers aP2, lipoprotein lipase, and adipsin in chondrocytes. Proteoglycan matrix synthesis was decreased in the PPARγ-infected cells, as was the expression of the chondrogenic genes Col2a1 and aggrecan. Growth plate cells transfected with a PPARγexpression plasmid under the control of the collagenα1(II) promoter also demonstrated a similar adipogenic changes. Terminal differentiation of growth plate chondrocytes induced by thyroid hormone was also inhibited by overexpression of PPARγand ciglitazone treatment, with decreased expression of alkaline phosphatase and Runx2/Cbfa1 genes. These in vitro data suggest that PPARγis able to promote adipogenic differentiation in growth plate chondrocytes, while negatively regulating chondrogenic differentiation and terminal differentiation.

Thyroid hormone is required for the phenotype transitions induced by the pharmacological inhibition of calcineurin in adult soleus muscle of rats

2008 ◽  
Vol 294 (1) ◽  
pp. E69-E77 ◽  
Author(s):  
Nathalie Koulmann ◽  
Lahoucine Bahi ◽  
Florence Ribera ◽  
Hervé Sanchez ◽  
Bernard Serrurier ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Soleus Muscle ◽  
Hormone Deficiency ◽  
Peroxisome Proliferator ◽  
Mrna Levels ◽  
Peroxisome Proliferator Activated Receptor ◽  
Thyroid State ◽  
Novel Approach ◽  
A Subunit ◽  
Calcineurin Inhibition

The present experiment was designed to examine the effects of hypothyroidism and calcineurin inhibition induced by cyclosporin A (CsA) administration on both contractile and metabolic soleus muscle phenotypes, with a novel approach to the signaling pathway controlling mitochondrial biogenesis. Twenty-eight rats were randomly assigned to four groups, normothyroid, hypothyroid, and orally treated with either CsA (25 mg/kg, N-CsA and H-CsA) or vehicle (N-Vh and H-Vh), for 3 wk. Muscle phenotype was estimated by the MHC profile and activities of oxidative and glycolytic enzymes. We measured mRNA levels of the peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), the major regulator of mitochondrial content. We also studied the expression of the catalytic A-subunit of calcineurin (CnA) both at protein and transcript levels and mRNA levels of modulatory calcineurin inhibitor proteins (MCIP)-1 and -2, which are differentially regulated by calcineurin activity and thyroid hormone, respectively. CsA-administration induced a slow-to-fast MHC transition limited to the type IIA isoform, which is associated with increased oxidative capacities. Hypothyroidism strongly decreased both the expression of fast MHC isoforms and oxidative capacities. Effects of CsA administration on muscle phenotype were blocked in conditions of thyroid hormone deficiency. Changes in the oxidative profile were strongly related to PGC-1α changes and associated with phosphorylation of p38 MAPK. Calcineurin and MCIPs mRNA levels were decreased by both hypothyroidism and CsA without additive effects. Taken together, these results suggest that adult muscle phenotype is primarily under the control of thyroid state. Physiological levels of thyroid hormone are required for the effects of calcineurin inhibition on slow oxidative muscle phenotype.

Both retinoic acid and 1,25(OH)2 vitamin D3 inhibit thyroid hormone-induced terminal differentiaton of growth plate chondrocytes

2001 ◽  
Vol 19 (1) ◽  
pp. 43-49 ◽  
Author(s):  
R. Tracy Ballock ◽  
Xiaolan Zhou ◽  
Lynn M. Mink ◽  
Daniel H. C. Chen ◽  
Barry C. Mita
Keyword(s):  
Retinoic Acid ◽  
Thyroid Hormone ◽  
Growth Plate ◽  
Vitamin D3 ◽  
Growth Plate Chondrocytes
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