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Deletion of clock gene Bmal1 impaired the chondrocyte function due to disruption of the HIF1α-VEGF signaling pathway
Removing the clock gene Bmal1 harms cartilage cell function by disturbing low-oxygen and blood vessel signals
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Abstract
Bmal1 ablation in mice resulted in shorter growth plates and reduced chondrocyte proliferation.
- Bmal1 knockout mice exhibited growth retardation during puberty.
- Both the length of the whole growth plate and the proliferation zone were shorter in Bmal1 ablated mice compared to controls.
- Deletion of Bmal1 led to decreased chondrocyte proliferation and increased apoptosis in the growth plate.
- Loss of Bmal1 decreased the expression of VEGF and HIF1α, while increasing levels of MMP13 and Runx2.
- In cultured chondrocytes, Bmal1 ablation similarly reduced proliferation and HIF1α and VEGF expression while elevating apoptosis.
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