Ka Hye In, Han Sora, Jeong Ae Lee, Lee Sunyi, Yong Hyo Jeong, Boldbaatar Ariundavaa, Joo Hyun Jeong, Soh Su Jung, Park Ji Young, Lim Jong-Seok, Lee Myung Sok, Yang Young
Department of Biological Sciences, Sookmyung Women's University, Seoul 04310, Republic of Korea.
J Microbiol Biotechnol. 2017 Jun 28;27(6):1180-1188. doi: 10.4014/jmb.1702.02049.
Neuronatin (NNAT) is known to regulate ion channels during brain development and plays a role in maintaining the structure of the nervous system. A previous in silico analysis showed that was overexpressed in the adipose tissue of an obese rodent model relative to the wild type. Therefore, the aim of the present study was to investigate the function of in the adipose tissue. Because obesity is known to systemically induce low-grade inflammation, the expression level was examined in the adipose tissue obtained from C57BL/6 mice administered lipopolysaccharide (LPS). Unexpectedly, the expression level decreased in the white adipose tissue after LPS administration. To determine the role of NNAT in inflammation, 3T3-L1 cells overexpressing were treated with LPS. The level of the p65 subunit of nuclear factor-kappa B (NF-κB) and the activity of NF-κB luciferase decreased following LPS treatment. These results indicate that NNAT plays an anti-inflammatory role in the adipose tissue.
已知神经调节素（NNAT）在大脑发育过程中调节离子通道，并在维持神经系统结构中发挥作用。先前的计算机分析表明，相对于野生型，肥胖啮齿动物模型的脂肪组织中NNAT表达上调。因此，本研究的目的是探讨NNAT在脂肪组织中的功能。由于已知肥胖会系统性地诱导低度炎症，因此检测了给予脂多糖（LPS）的C57BL/6小鼠脂肪组织中NNAT的表达水平。出乎意料的是，给予LPS后白色脂肪组织中NNAT表达水平降低。为了确定NNAT在炎症中的作用，用LPS处理过表达NNAT的3T3-L1细胞。LPS处理后，核因子κB（NF-κB）的p65亚基水平和NF-κB荧光素酶活性降低。这些结果表明，NNAT在脂肪组织中发挥抗炎作用。
