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| Regulatory effect of adipokines on miR-506 expression in human adipocytes |
| QIN Zhenying1 ZHONG Fengyu2 CHEN Yao2 LI Jing1 YANG Zi1 WEN Juan3 WANG Yumei4 HU Youfang1 |
1.Department of Children’s Health Care, the First Affiliated Hospital of Nanjing Medical University, Jiangsu Maternal and Child Health Care Hospital, Jiangsu Province, Nanjing 210036, China;
2.the First Clinical Medical College of Nanjing Medical University, Jiangsu Province, Nanjing 210029, China;
3.Medical Research Center, Women’s Hospital of Najing Medical University, Jiangsu Province, Nanjing 210004, China;
4.Department of Screening for Neonatal Diseases, Huai’an Maternity and Child Health Care Hospital Affiliated to Yangzhou University Medical College, Jiangsu Province, Huai’an 223302, China |
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Abstract Objective To investigate the regulatory effect of adipokines tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) on the expression of miR-506 in mature human adipocytes. Methods Real-time fluorescence quantitative polynucleotide chain reaction was used to detect the expression level of miR-506 in human precursor adipocytes and mature adipocytes. TNF-α and IL-6 were treated with 10, 30 ng/mL for 0, 4, 8 and 24 h, and the expression level of miR-506 was detected at each time point. Results The expression level of miR-506 in mature adipocytes was higher than that in precursor adipocytes, and the difference was highly statistically significant (P < 0.01). The expression of miR-506 in mature human adipocytes at 4, 8 and 24 h after treatment with 10 ng/mL TNF-α and IL-6 were not significantly differents from those at 0 h after treatment (P > 0.05). The expression level of miR-506 in mature human adipocytes after treatment with 30 ng/mL TNF-α and IL-6 at 24 h were higher than those after treatment at 0 h, and the differences were statistically significant (all P < 0.05). Conclusion miR-506 expression is regulated by adipokines, which provides theoretical basis for the study of the correlation between miR-506 and inflammatory responses and obesity-related insulin resistance.
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