Fig. 8: Early hypertrophic differentiation of tmem165-deficient mouse ATDC5 cells. | Cell Death & Disease

Fig. 8: Early hypertrophic differentiation of tmem165-deficient mouse ATDC5 cells.

From: TMEM165 a new player in proteoglycan synthesis: loss of TMEM165 impairs elongation of chondroitin- and heparan-sulfate glycosaminoglycan chains of proteoglycans and triggers early chondrocyte differentiation and hypertrophy

Fig. 8

A Fold changes of chondrogenic markers expression in wild-type mouse ATDC5 cells and tmem165-knockout cells. RT-qPCR analysis of the mRNA levels of chondrogenic markers SOX9, Col2A, and Aggrecan, and (B) of hypertrophic markers Ihh and OCN. qPCR values were normalized for the housekeeping gene ribosomal protein S29 and are expressed as the relative expression compared with control. Data are expressed as mean ± S.D. Statistical analysis was performed with an unpaired Student’s t test (n = 3; *p < 0.05; **p < 0.01). C Mineralization of wild-type and tmem165-deficient mouse ATDC5 cells analyzed by Alizarin red staining at Days 0, 14, 21, and 28. Representative images from three independent experiments are shown. D Loss of TMEM165 function impairs Golgi Mn2+ homeostasis necessary for glycosyltransferase polymerization activities leading to blockage in the elongation of GAG chains of proteoglycans. Blockage in the elongation of GAG chains by loss of TMEM165 may account for dysregulation of TGF/BMP and Ihh signaling, and therefore in defects in chondrocyte differentiation and maturation. However, other mechanisms can’t be ruled-out.

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