PMID- 31081107 OWN - NLM STAT- MEDLINE DCOM- 20200909 LR - 20200909 IS - 2284-0729 (Electronic) IS - 1128-3602 (Linking) VI - 23 IP - 8 DP - 2019 Apr TI - Influence of lncRNA HOTAIR on acute kidney injury in sepsis rats through regulating miR-34a/Bcl-2 pathway. PG - 3512-3519 LID - 17717 [pii] LID - 10.26355/eurrev_201904_17717 [doi] AB - OBJECTIVE: To study the regulatory effect of long non-coding ribonucleic acid (lncRNA) HOX transcript antisense RNA (HOTAIR) on acute kidney injury (AKI) in sepsis rats and its regulatory mechanism. MATERIALS AND METHODS: The sepsis-induced AKI model was established in Sprague-Dawley (SD) male rats through cecal ligation puncture. A total of 30 SD rats were randomly divided into the control group, model group and lncRNA HOTAIR mimic group, with 10 rats in each group. Relative levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) in kidney tissues were detected via enzyme-linked immunosorbent assay (ELISA). Apoptosis of kidney tissues was detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. Moreover, the target gene of miR-34a was searched using the miRNA online database. The messenger RNA (mRNA) expression levels of miR-34a and B-cell lymphoma-2 (Bcl-2) were detected via Reverse Transcription-Polymerase Chain Reaction (RT-PCR). RESULTS: Compared with those in the control group, the rats in the model group showed injured pathological morphology of kidney, elevated contents of TNF-alpha and IL-1beta, and apoptosis in kidney tissues. The target gene of miR-34a was Bcl-2, according to the miRNA online database. MiR-34a level in kidney tissues was upregulated, while the mRNA level of Bcl-2 significantly decreased in the model group. Compared with those in the model group, the pathological morphology of kidney tissues was improved, the content of TNF-alpha and IL-1beta markedly declined, and the apoptotic rate of kidney tissues also reduced in lncRNA HOTAIR mimic group. The miR-34a level in kidney tissues decreased, while the Bcl-2 mRNA level remarkably increased in lncRNA HOTAIR mimic group. CONCLUSIONS: LncRNA HOTAIR overexpression can alleviate AKI in sepsis rats by inhibiting the apoptosis of kidney tissues by downregulating the miR-34a/Bcl-2 signaling pathway. FAU - Jiang, Z-J AU - Jiang ZJ AD - Department of Emergency, Qingpu Branch of Zhongshan Hospital Affiliated to Fudan University, Shanghai, China. 15821363280@163.com. FAU - Zhang, M-Y AU - Zhang MY FAU - Fan, Z-W AU - Fan ZW FAU - Sun, W-L AU - Sun WL FAU - Tang, Y AU - Tang Y LA - eng PT - Journal Article PL - Italy TA - Eur Rev Med Pharmacol Sci JT - European review for medical and pharmacological sciences JID - 9717360 RN - 0 (Bcl2 protein, rat) RN - 0 (HOTAIR long untranslated RNA, rat) RN - 0 (MIRN34 microRNA, rat) RN - 0 (MicroRNAs) RN - 0 (Proto-Oncogene Proteins c-bcl-2) RN - 0 (RNA, Long Noncoding) SB - IM MH - Acute Kidney Injury/*genetics/pathology MH - Animals MH - Apoptosis/genetics MH - Disease Models, Animal MH - Humans MH - Kidney/pathology MH - Male MH - MicroRNAs/*genetics/metabolism MH - Proto-Oncogene Proteins c-bcl-2/*genetics/metabolism MH - RNA, Long Noncoding/*metabolism MH - Rats MH - Sepsis/*complications MH - Signal Transduction/genetics MH - Up-Regulation EDAT- 2019/05/14 06:00 MHDA- 2020/09/10 06:00 CRDT- 2019/05/14 06:00 PHST- 2019/05/14 06:00 [entrez] PHST- 2019/05/14 06:00 [pubmed] PHST- 2020/09/10 06:00 [medline] AID - 17717 [pii] AID - 10.26355/eurrev_201904_17717 [doi] PST - ppublish SO - Eur Rev Med Pharmacol Sci. 2019 Apr;23(8):3512-3519. doi: 10.26355/eurrev_201904_17717.