ACS Chem Neurosci. 2021 Apr 7;12(7):1210-1218.doi: 10.1021/acschemneuro.1c00050. Epub 2021 Mar 18.

本文采用的英格恩产品: DNA-Entranster-invivo

LncRNA UC.360+ shRNA Improves Diabetic Cardiac Sympathetic Dysfunction Mediated by the P2X4 Receptor in the Stellate Ganglion



  • 1 Neuropharmacology Laboratory, Physiology Department, Basic Medical School of Nanchang University, Nanchang 330006, P. R. China.
  • 2 Jiangxi Provincial Key Laboratory of Autonomic Nervous Function and Disease, Nanchang, Jiangxi 330006, P. R. China.
  • 3 Clinic Medicine Department, Medical School of Nanchang University, Nanchang 330006, P. R. China.
  • 4 Molecular Pharmacology, RWTH Aachen University, Aachen 52062, Germany.
  • 5 Guangdong Province Key Laboratory of Pharmacodynamic Constituents of TCM and New Drugs Research, College of Pharmacy, Jinan University, Guangzhou 510632, P. R. China.


Diabetic cardiac autonomic neuropathy (DCAN) is a complication that affects more than 60% of diabetic patients. There is evidence for the involvement of P2X4 receptor in DCAN. This study showed that the expression of the long noncoding RNA (lncRNA) UC.360+ was increased in the stellate ganglion (SG) of type 2 diabetes mellitus (DM) rats, and in situ hybridization revealed a clear presence of UC.360+ in SG neurons. The potential roles of UC.360+ in DCAN and its relationship with P2X4 receptor in SG were further explored via application of the short hairpin RNA (shRNA) against lncRNA UC.360+ in DM rats. The abnormal cardiac sympathetic changes in diabetic rats were improved after treatment with lncRNA UC.360+ shRNA. In the SG of these shRNA-treated DM rats, the upregulation of P2X4, tumor necrosis factor-α (TNF-α), interleukin 1β (IL-1β), and phosphorylated ERK1/2 was inhibited. Thus, lncRNA UC.360+ shRNA treatment may improve DCAN mediated by the P2X4 receptor in SG.

Keywords: Diabetes; P2X4 receptor; long noncoding RNA; stellate ganglia.