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URL: http://anatomyjournal.ir/article-1-111-en.html
, Aliasghar Peyvandi2 , Mohsen Noorozian3 , Navid Ahmadi Roozbahani2 , Reza Mastery Farahani3 , Maryam Sadat Khoramgah4 , Hadi Azimi5 , Ayad Bahadori Monfared6 , Hojjat-Allah Abbaszadeh 6
2- Hearing Disorders Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
3- Department of Biology and Anatomical Sciences, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
4- Department of Medical Biotechnology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
5- Department of English Language Teaching, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
6- Department of Health & Community Medicine, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Introduction: SOX9 is a transcriptional activator which is necessary for chondrogenesis. SOX6 are closely related to DNA-binding proteins that critically enhance its function. Therefore, to carry out the growth plate chondrocyte differentiation program, SOX9 and SOX6 collaborate genomewide. Chondrocyte differentiation is also known to be promoted by glucocorticoids through unknown molecular mechanisms.
Methods: We investigated the effects of asynthetic glucocorticoid, dexamethasone (DEX), on SOX9 gene expression in chondrocytes.
Results: SOX9 mRNA was expressed at high levels in these chondrocytes. Treatment with DEX resulted in enhancement of SOX9 mRNA expression. The DEX effect was dose dependent (0·5 nM and 1 nM).
Conclusion: RT-PCR analysis revealed that DEX also enhanced the levels of SOX9 expression. It was observed that DEX had enhancing effect only on SOX9 the expression level was low for SOX6. It can thus be concluded that chondrocyte differentiation can be promoted by DEX via SOX9 enhancement.
Received: 2014/12/22 | Accepted: 2015/03/6 | Published: 2015/05/1
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