Novel Insights into the Emerging Role of Neat1 and Its Effects Downstream in the Regulation of Inflammation

Yongli Pan,1,2,* Ting Wang,3,* Zhiqiang Zhao,4,* Wei Wei,2,5,* Xinyu Yang,6 Xianbin Wang,7 Wenqiang Xin2,6 1Department of Neurology, Weifang Medical University, Weifang, Shandong, People’s Republic of China; 2Georg-August-University of Göttingen, Göttingen, Lower Saxony, Germany; 3Department of Radiology, The Second Affiliated Hospital of Baotou Medical College, Baotou, 014030, People’s Republic of China; 4Department of Neurosurgery, Heji Hospital affiliated Changzhi Medical College, Shanxi, People’s Republic of China; 5Department of Neurology, Mianyang Central Hospital, Mianyang, Sichuan, People’s Republic of China; 6Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, People’s Republic of China; 7Department of Emergency Medicine, The Second Affiliated Hospital of Baotou Medical College, Baotou, 014030, People’s Republic of China*These authors contributed equally to this workCorrespondence: Wenqiang XinDepartment of Neurosurgery, Tianjin Medical University General Hospital, Anshan Road No. 154, Tianjin, 300052, People’s Republic of ChinaTel +86– 18526201182, Fax +86– 2260362062, Email xinwenqiangdr@126.com Xianbin WangDepartment of Emergency Medicine, The Second Affiliated Hospital of Baotou Medical College, Baotou, 014030, People’s Republic of ChinaEmail wangxianbin198006@163.comAbstract: Nuclear paraspeckle assembly transcript 1 (Neat1) located at chromosome 11 is a long non-coding RNA that is widely expressed in mammalian cell types, and which is overexpressed in several inflammation-related disorders. Inflammation implies a plethora of mutual interactions between both soluble factors and cells due to various stimuli including tissue injury. Although there is no doubt that inflammation is critically involved in multiple biological and pathological processes alike, the precise mechanisms being involved are still open for debate. In this context, the role of Neat1 as a regulator of inflammation, microglial activation, and lipid accumulation under various inflammatory conditions remains elusive. Herein, we review the regulation of Neat1 and how it modulates the expression of its target genes. Thereafter, we will review the impact of Neat1 on inflammation by activating or inhibiting various signaling pathways, such as microRNAs, AKT, TLR4, TRAF6, and NF-κB.Keywords: Neat1, inflammation, microglia, lipids, microRNA, NF-κB