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
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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