scholarly journals Abnormal Response of the Proliferation and Differentiation of Growth Plate Chondrocytes to Melatonin in Adolescent Idiopathic Scoliosis

2014 ◽  
Vol 15 (9) ◽  
pp. 17100-17114 ◽  
Author(s):  
William Wang ◽  
Gene Man ◽  
Jack Wong ◽  
Tzi-Bun Ng ◽  
Kwong-Man Lee ◽  
...  
Bone ◽  
2008 ◽  
Vol 43 ◽  
pp. S96
Author(s):  
Man Chi Wai ◽  
Yeung Hiu Yan ◽  
Wang Wei Jun ◽  
Lee Kwong Man ◽  
Ng Kin Wah ◽  
...  

2007 ◽  
Vol 282 (46) ◽  
pp. 33698-33706 ◽  
Author(s):  
Shufang Wu ◽  
Janna K. Flint ◽  
Geoffrey Rezvani ◽  
Francesco De Luca

NF-κB is a group of transcription factors involved in cell proliferation, differentiation, and apoptosis. Mice deficient in the NF-κB subunits p50 and p52 have retarded growth, suggesting that NF-κB is involved in bone growth. Yet, it is not clear whether the reduced bone growth of these mice depends on the lack of NF-κB activity in growth plate chondrocytes. Using cultured rat metatarsal bones and isolated growth plate chondrocytes, we studied the effects of two NF-κB inhibitors (pyrrolidine dithiocarbamate (PDTC) or BAY11-7082 (BAY)), p65 short interference RNA (siRNA), and of the overexpression of p65 on chondrocyte proliferation, differentiation, and apoptosis. To further define the underlying mechanisms, we studied the functional interaction between NF-κB p65 and BMP-2 in chondrocytes. PDTC and BAY suppressed metatarsal linear growth. Such growth inhibition resulted from decreased chondrocyte proliferation and differentiation and from increased chondrocyte apoptosis. In cultured chondrocytes, the inhibition of NF-κB p65 activation (by PDTC and BAY) and expression (by p65 siRNA) led to the same findings observed in cultured metatarsal bones. In contrast, overexpression of p65 in cultured chondrocytes induced chondrocyte proliferation and differentiation and prevented apoptosis. Although PDTC, BAY, and p65 siRNA reduced the expression of BMP-2 in cultured growth plate chondrocytes, the overexpression of p65 increased it. The addition of Noggin, a BMP-2 antagonist, neutralized the stimulatory effects of p65 on chondrocyte proliferation and differentiation, as well as its anti-apoptotic effect. In conclusion, our findings indicate that NF-κB p65 expressed in growth plate chondrocytes facilitates growth plate chondrogenesis and longitudinal bone growth by inducing BMP-2 expression and activity.


2010 ◽  
Vol 51 (3) ◽  
pp. 188-196 ◽  
Author(s):  
Shoufeng Wang ◽  
Yong Qiu ◽  
Zhaolong Ma ◽  
Caiwei Xia ◽  
Feng Zhu ◽  
...  

2010 ◽  
pp. no-no ◽  
Author(s):  
Gene Chi-wai Man ◽  
William Wei-jun Wang ◽  
Benson Hiu-yan Yeung ◽  
Simon Kwong-man Lee ◽  
Bobby Kin- ah Ng ◽  
...  

PPAR Research ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Lai Wang ◽  
Yvonne Y. Shao ◽  
R. Tracy Ballock

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.


2007 ◽  
Vol 193 (1) ◽  
pp. 75-84 ◽  
Author(s):  
Ola Nilsson ◽  
Elizabeth A Parker ◽  
Anita Hegde ◽  
Michael Chau ◽  
Kevin M Barnes ◽  
...  

In the growth plate, stem-like cells in the resting zone differentiate into rapidly dividing chondrocytes of the proliferative zone and then terminally differentiate into the non-dividing chondrocytes of the hypertrophic zone. To explore the molecular switches responsible for this two-step differentiation program, we developed a microdissection method to isolate RNA from the resting (RZ), proliferative (PZ), and hypertrophic zones (HZ) of 7-day-old male rats. Expression of approximately 29 000 genes was analyzed by microarray and selected genes verified by real-time PCR. The analysis identified genes whose expression changed dramatically during the differentiation program, including multiple genes functionally related to bone morphogenetic proteins (BMPs). BMP-2 and BMP-6 were upregulated in HZ compared with RZ and PZ (30-fold each, P < 0.01 and 0.001 respectively). In contrast, BMP signaling inhibitors were expressed early in the differentiation pathway; BMP-3 and gremlin were differentially expressed in RZ (100- and 80-fold, compared with PZ, P < 0.001 and 0.005 respectively) and growth differentiation factor (GDF)-10 in PZ (160-fold compared with HZ, P < 0.001). Our findings suggest a BMP signaling gradient across the growth plate, which is established by differential expression of multiple BMPs and BMP inhibitors in specific zones. Since BMPs can stimulate both proliferation and hypertrophic differentiation of growth plate chondrocytes, these findings suggest that low levels of BMP signaling in the resting zone may help maintain these cells in a quiescent state. In the lower RZ, greater BMP signaling may help induce differentiation to proliferative chondrocytes. Farther down the growth plate, even greater BMP signaling may help induce hypertrophic differentiation. Thus, BMP signaling gradients may be a key mechanism responsible for spatial regulation of chondrocyte proliferation and differentiation in growth plate cartilage.


2018 ◽  
pp. 88-98 ◽  
Author(s):  
Alla Mikhailovna Zaidman ◽  
Elena Leonidovna Strokova ◽  
Vyacheslav Viktorovich Novikov ◽  
Aleksandr Sergeyevich Vasyura ◽  
Mikhail Vitalyevich Mikhailovsky ◽  
...  

2009 ◽  
Vol 610-613 ◽  
pp. 1070-1075
Author(s):  
Li Yu ◽  
Ming Qiao Tang ◽  
Wei Qun Yan

Objective:To observe the effect of human platelet extracts on proliferation and differentiation of rabbit growth-plate chondrocytes in monolayer and fabrication of tissue engineering cartilage in vitro. Method: To determine the effects of platelet extracts at different concentrations on proliferation and differentiation of rabbit growth-plate chondrocytes using 3H-TdR、PNP and HE staining. Results: Platelet extracts had very strong stimulative effects on proliferation and differentiation of chondrocytes, especially the hypertropization (termination) of chondrocytes.


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