The effect of quercetin on expression of SOX9 and subsequent release of type II collagen in spheno-occipital synchondroses of organ-cultured mice

Apichart, Veerawattanatigul; Wong, Ricky W.K.; Rabie, Bakr; Lei, Samuel

doi:10.2319/042111-278.1

Cited by 8 publications

(8 citation statements)

References 21 publications

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“…It can maintain the cartilage homeostasis by regulating the downstream genes involved in the proliferation, apoptosis and synthesis of ECM components in chondrocytes (28–30). This synthesis may, at least partly, be mediated by the transactivation of Sox9, a key transcription factor for cartilage-specific marker genes such as Col II and aggrecan (31,32). Yudoh et al (43) reported that HIF-1α-deficient chondrocytes showed significantly increased levels of apoptosis compared with the control groups.…”

Section: Discussionmentioning

confidence: 99%

“…HIF-1α may inhibit the apoptosis of chondrocytes and regulate the synthesis of ECM (28–30). This synthesis may be mediated by transactivation of sex determining region Y box gene 9 (Sox9), a key transcription factor for chondrocyte-specific genes such as collagen II (Col II) which encode the Col II protein (31,32). Thus, we hypothesized that sodium fluoride (NaF) would induce chondrocytes apoptosis through the downregulation of HIF-1α and cause matrix disruption through the downregulation of HIF-1α via the Sox9 pathway.…”

Section: Introductionmentioning

confidence: 99%

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Sodium fluoride induces apoptosis through the downregulation of hypoxia-inducible factor-1α in primary cultured rat chondrocytes

Meng

Zhang

Liu

et al. 2013

International Journal of Molecular Medicine

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It has been reported that sodium fluoride (NaF) suppresses the proliferation and induces apoptosis of chondrocytes. However, the cellular and molecular mechanisms of the effect have not been elucidated. Therefore, the aim of this study was to evaluate the mechanisms of the effects of NaF on primary cultured rat chondrocytes in vitro. Chondrocytes were treated with NaF at concentrations of 0, 1.5, 2.0, 2.5, 3.0, 3.5 and 4.0 mM. Cell viability decreased and the rate of apoptotic cells increased significantly with the gradient concentration of NaF in a time- and dose-dependent manner. Electron microscopy revealed cytoplasmic, organelle and nuclear alterations in the ultrastructure of chondrocytes exposed to various NaF concentrations. The cell cycle distribution was analyzed by flow cytometry, and the results indicated that NaF induced G2 cell cycle arrest. Western blotting was used to detect the apoptotic pathways. Downregulation of the Bcl-2 protein and upregulation of Bax, cleaved caspase-9, −12 and −3 proteins suggested that NaF was capable of inducing apoptosis through the mitochondrial and endoplasmic reticulum pathways. The results also showed that the levels of hypoxia-inducible factor 1α (HIF-1α), sex determining region Y box gene 9 (Sox9) and the collagen II (Col II) protein of the NaF groups were lower compared to those of the control groups. Thus, NaF may induce apoptosis through the downregulation of HIF-1α and disrupt the synthesis of extracellular matrix (ECM) through the downregulation of HIF-1α via the Sox9 pathway in primary cultured rat chondrocytes.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Sodium fluoride induces apoptosis through the downregulation of hypoxia-inducible factor-1α in primary cultured rat chondrocytes

Meng

Zhang

Liu

et al. 2013

International Journal of Molecular Medicine

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“…In the study of Jiang et al (), a decrease in collagen type I induced by both ultraviolet and hydrogen peroxide was attenuated by quercetin via the inhibition of JNK/c‐Jun activity. Quercetin also increased the expression of collagen type II gene in the spheno‐occipital synchondrosis (Apichart, Wong, Rabie, & Lei, ). The intraperitoneal injection of quercetin to mice significantly increased cadmium‐induced hydroxyproline and total collagen level in the liver (Siddiqi & Zargar, ).…”

Section: Discussionmentioning

confidence: 99%

Dietary quercetin improved the growth, antioxidation, and flesh quality of grass carp (Ctenopharyngodon idella)

Yang

et al. 2019

J World Aquaculture Soc

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To investigate the effects of dietary quercetin on growth, antioxidation, and flesh quality of grass carp, Ctenopharyngodon idella, six diets were prepared with quercetin inclusion rates of 0 (control diet), 0.1, 0.2, 0.4, 0.6, and 0.8 g/kg. Grass carp with a body weight of 13.3 ± 0.1 g were fed with one of the six diets for 60 days. The weight gain (WG) showed a quadratic relationship with dietary quercetin levels; the supplementation of 0.4 g/kg quercetin significantly improved WG (+4.73%) and decreased feed conversion ratio (−0.06) (p < .05) when compared to those of the control group. The intestinal fat ratio was reduced by the addition of 0.2 or 0.4 g/kg of quercetin (p < .05), and serum activities of alkaline phosphatase and superoxide dismutase were increased by the addition of 0.4 and 0.6 g/kg of quercetin (p < .05). The inclusion of 0.2–0.6 g/kg of quercetin increased the contents of delicious amino acids and decreased the cooking loss of flesh (p < .05). Flesh collagen content was increased by the addition of 0.4–0.8 g/kg of quercetin (p < .05). In conclusion, dietary quercetin could improve the growth and enhance the antioxidation and flesh quality of grass carp, with the recommended supplemental level of quercetin was 0.37 g/kg.

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“…Studies specific to the CB have assessed the effects of naturally occurring compounds such as phytoestrogens—quercetin and flavonoids—naringin on the spheno‐occipital synchondrosis (SOS). Using an ex‐vivo culture model, these compounds enhanced growth of the SOS, with increased expression of SOX9 and type II collagen within synchondrosis chondrocytes . Further development of these preliminary studies may provide novel approaches to treat CB growth defects.…”

Section: Mouse Models In the Designing And Testing Of Therapeuticsmentioning

confidence: 96%

Mouse models for the study of cranial base growth and anomalies

Vora

2017

Orthod Craniofacial Res

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The cranial base is a central and integral component of the cranioskeleton, yet little is known about its growth. Despite the dissimilarities between human and murine cranioskeletal form, mouse models are proving instrumental in studying craniofacial growth. The objectives of this review are to summarize recent findings from numerous mouse models that display growth defects in one or more cranial base synchondroses, with accompanying changes in chondrocyte cellular zones. Many of these models also display altered growth of the cranial vault and/or the facial region. FGFR, PTHrP, Ihh, BMP and Wnt/β-catenin, as well as components of primary cilia, are the major genes and signalling pathways identified in cranial base synchondroses. Together, these models are helping to uncover specific genetic influences and signalling pathways operational at the cranial base synchondroses. Many of these genes are in common with those of importance in the cranial vault and the facial skeleton, emphasizing the molecular integration of growth between the cranial base and other cranial regions. Selected models are also being utilized in testing therapeutic agents to correct defective craniofacial and cranial base growth.

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The effect of quercetin on expression of SOX9 and subsequent release of type II collagen in spheno-occipital synchondroses of organ-cultured mice

Cited by 8 publications

References 21 publications

Sodium fluoride induces apoptosis through the downregulation of hypoxia-inducible factor-1α in primary cultured rat chondrocytes

Sodium fluoride induces apoptosis through the downregulation of hypoxia-inducible factor-1α in primary cultured rat chondrocytes

Dietary quercetin improved the growth, antioxidation, and flesh quality of grass carp (Ctenopharyngodon idella)

Mouse models for the study of cranial base growth and anomalies

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