LncRNA UC.360+ shRNA Improves Diabetic Cardiac Sympathetic Dysfunction Mediated by the P2X4 Receptor in the Stellate Ganglion.
Liran ShiMinghao SunXinlu RenZijing LiRunan YangXiumei XuLin LiGuilin LiShuangmei LiuGünther SchmalzingHong NieGuodong LiShangdong LiangPublished in: ACS chemical neuroscience (2021)
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.
Keyphrases
- long noncoding rna
- long non coding rna
- poor prognosis
- left ventricular
- rheumatoid arthritis
- diabetic rats
- type diabetes
- oxidative stress
- signaling pathway
- cell proliferation
- binding protein
- neuropathic pain
- spinal cord
- spinal cord injury
- metabolic syndrome
- wound healing
- skeletal muscle
- optic nerve
- weight loss
- atrial fibrillation
- blood pressure
- human health
- insulin resistance
- optical coherence tomography
- smoking cessation