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Merck

Loss of autophagy in chondrocytes causes severe growth retardation.

Autophagy (2019-06-18)
Yoji Horigome, Hiroko Ida-Yonemochi, Satoshi Waguri, Shunichi Shibata, Naoto Endo, Masaaki Komatsu
摘要

Chondrogenesis is accompanied by not only cellular renovation, but also metabolic stress. Therefore, macroautophagy/autophagy is postulated to be involved in this process. Previous reports have shown that suppression of autophagy during chondrogenesis causes mild growth retardation. However, the role of autophagy in chondrocyte differentiation still largely remains unclear. Here, we show the important role of autophagy on chondrogenesis. The transition of mesenchymal cells to chondrocytes was severely impaired by ablation of Atg7, a gene essential for autophagy. Mice lacking Atg7 after the transition exhibited phenotypes severer than mutant mice in which Atg7 was removed before the transition. Atg7-deficient chondrocytes accumulated large numbers of glycogen granules, hardly proliferate and died specifically in the proliferative zone without any ER-stress signal. Our results suggest that the suppression of autophagy in prechondrogenic cells drives compensatory mechanism(s) that mitigate defective chondrogenesis, and that autophagy participates in glycogenolysis to supply glucose in avascular growth plates.Abbreviations: DDIT3/CHOP: DNA damage inducible transcript 3; ER: endoplasmic reticulum; NFE2L2/NRF2: nuclear factor, erythroid derived 2, like 2; SQSTM1/p62: sequestosome 1; STBD1: starch-binding domain-containing protein 1.

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DL-二硫苏糖醇, for molecular biology, ≥98% (HPLC), ≥99% (titration)
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Immobilon®-P PVDF膜, 1 roll, 27 cm x 3.75 m, 0.45 µm pore size, Hydrophobic PVDF Transfer Membrane for western blotting.
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衣霉素 来源于链霉菌
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胰蛋白酶 来源于猪胰腺, lyophilized powder, Type II-S, 1,000-2,000 units/mg dry solid
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阿尔新蓝 8GX, for microscopy (Bact., Bot., Hist.)
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抗肌动蛋白抗体,克隆C4, clone C4, Chemicon®, from mouse
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