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IRE1a Negative Regulates Chondrocyte Differentiation

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Abstract:

We present evidences demonstrating that overexpression of IRE1a inhibits chondrocyte differentiation, as revealed by reduced expression of Col,,SOX9, ColX, MMP-13, IHH, Runx2. Furthmore, IRE1a-mediated inhibition of chondrogenesis depends on its enzymatic activity, since its point mutant lacking enzymatic activity completely loses this activity. The RNase and Kinase domains of IRE1a C-terminal is necessary for its full enzymatic activity and inhibition of chondrocyte differentiation. Mechanism studies demonstrate that granulin-epithelin precursor (GEP),a growth factor known to stimulate chondrogenesis, induced IRE1a expression in chondrogenesis. In addition, IRE1a inhibits GEP-mediated chondrocyte differentiation as a negative regulator. Altered expression of IRE1a in chondrocyte hypertrophy was accompanied by altered levels of IHH and PTHrP.Collectively,IRE1a may be a novel regulator of chondrocyte differentiation by 1) inhibition GEP-mediated chondrocyte differentiation as a negative regulator; 2) promoting IHH/PTHrP signaling.

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Periodical:

Advanced Materials Research (Volumes 998-999)

Pages:

265-268

DOI:

https://doi.org/10.4028/www.scientific.net/AMR.998-999.265

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Online since:

July 2014

Authors:

Feng Jin Guo*, Fei Xia, Rong Jiang, Mei Ling Li

Keywords:

BMP2, Chondrogenesis, GEP, Inositol-Requiring Enzyme-1a(IRE1a), Unfolded Protein Response

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© 2014 Trans Tech Publications Ltd. All Rights Reserved

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