Role of long non-coding RNA Peg13 in apoptosis of developing primary neurons following sevoflurane injury / 上海交通大学学报（医学版）

Objective • To investigate the role of long non-coding RNA (lncRNA) Peg13 (paternally expressed 13) in the apoptosis of developing primary neurons following sevoflurane injury. Methods • Primary neurons were prepared from fetal mice with 14.5 d of gestational age. The expression of lncRNA Peg13 after sevoflurane treatment was detected by quantitative PCR. The localization of lncRNA Peg13 in primary neurons was detected by in situ hybridization. Peg13 overexpression and knockdown plasmids were constructed and transfected into primary neurons. The morphology of primary neurons was observed by fluorescence microscope. Cell vability was assessed by CCK-8 assay. Cell apoptosis was determined by TUNEL assay and Western blotting. Results • The expression of lncRNA Peg13 in primary neurons decreased in a time-dependent manner after sevoflurane treatment. LncRNA Peg13 was widely expressed in the cytoplasm and axon of primary neuron. Overexpression of lncRNA Peg13 resulted in decreased sevoflurane-induced apoptosis. The primary neurons were restored to normal morphology with increased cell vability. The percentage of TUNEL-positive cells was decreased. The expression ratio of Bcl-2/Bax was increased and the expression of casepase-3 was decreased. However, knockdown of lncRNA Peg13 aggravated the sevoflurane-induced apoptosis. The primary neurons had visible morphological deterioration and decreased cell vability, with increased percentage of TUNEL-positive cells, decreased ratio of Bcl-2/Bax, and increased expression of casepase-3. Conclusion • LncRNA Peg13 may alleviate sevoflurane-induced apoptosis in developing primary neurons.

TRPV1 Activation in Primary Cortical Neurons Induces Calcium-Dependent Programmed Cell Death

Transient receptor potential cation channel, subfamily V, member 1 (TRPV1, also known as vanilloid receptor 1) is a receptor that detects capsaicin, a pungent component of chili peppers, and noxious heat. Although its function in the primary nociceptor as a pain receptor is well established, whether TRPV1 is expressed in the brain is still under debate. In this study, the responses of primary cortical neurons were investigated. Here, we report that 1) capsaicin induces caspase-3-dependent programmed cell death, which coincides with increased production of nitric oxide and peroxynitrite ; that 2) the prolonged capsaicin treatment induces a steady increase in the degree of capase-3 activation, which is prevented by the removal of capsaicin; 3) and that blocking calcium entry and calcium-mediated signaling prevents capsaicin-induced cell death. These results indicate that cortical neurons express TRPV1 whose prolonged activation causes cell death.