长链非编码RNA H19通过JNK信号通路促进海绵体神经损伤后平滑肌细胞凋亡

Abstract

JNK/ Bcl-2/ Bax pathway participates in corpus cavernosal smooth muscle cells apoptosis during early period after cavernosal nerve (CN) crush injury (CNCI). Nevertheless, the regulation mechanisms of long noncoding RNA H19 in apoptosis during early stage after CN injury are still poorly understood. The rats in sham group were not direct injury to the CNs. The rats in CNCI group were performed to bilateral CN crush injury. The ICP/MAP rate and smooth muscle content were significantly lower than that in the sham group. Primary CCSMCs were prepared from the tissues samples after completing erectile function detection. Phosphorylated-JNK level was increased significantly, and the expression of Bax and Bcl-2 was elevated and declined in CNCI group respectively. Except for Bcl-2, the mRNA levels of H19, JNK and Bax were significantly increased in CNCI group. After H19 siRNA transfection, for the mRNA and protein levels, JNK and Bax were declined, while Bcl-2 was enhanced. LncRNA H19 might be involved in regulation of Bcl-2, Bax via JNK signalling pathway in CCSMCs apoptosis after CN injury.