Corrigendum to "Preoperative sedation in children with congenital heart disease: 50% and 95% effective doses, hemodynamic effects, and safety of intranasal dexmedetomidine". [Journal of Clinical Anesthesia, Volume 81, (2022)/ Article 110908].

Silencing of SNHG6 alleviates hypoxia/reoxygenation-induced cardiomyocyte apoptosis by modulating miR-135a-5p/HIF1AN to activate Shh/Gli1 signalling pathway.

OBJECTIVES:To examine the effects of small nucleolar RNA host gene 6 (SNHG6) on apoptosis during myocardial ischemic/reperfusion (I/R) injury and its potential molecular mechanisms.METHODS:In vitro model of I/R was built through exposing mouse HL-1 cardiomyocytes to hypoxia/reoxygenation (H/R) treatment. Quantitative real-time polymerase chain reaction assays were performed to determine gene expression. Cell Counting Kit-8, flow cytometric and western blot assays were conducted to detect cell viability, apoptosis and protein expression. Lactate dehydrogenase (LDH) activity was examined by a commercial detection kit. Dual-luciferase gene reporter and RNA immunoprecipitation experiments were applied for determining the interaction between the molecules.KEY FINDINGS:SNHG6 expression was increased in H/R-challenged cardiomyocytes. Depletion of SNHG6 protected against H/R-induced cardiomyocytes apoptosis. SNHG6 could sponge miR-135a-5p to inhibit its expression. Down-regulation of miR-135a-5p reversed the anti-apoptotic effect caused by SNHG6 knockdown in H/R-induced cardiomyocytes. Hypoxia inducible factor 1 subunit alpha inhibitor (HIF1AN) was identified as a direct target of miR-135a-5p, and knockdown of HIF1AN relieved H/R-induced cardiomyocytes apoptosis. Silencing of SNHG6 activated Shh/Gli1 signalling pathway by regulating miR-135a-5p/HIF1AN. Furthermore, inactivation of Shh/Gli signalling abolished the anti-apoptotic effects of SNHG6 knockdown in H/R-induced cardiomyocytes.CONCLUSIONS:SNHG6 serves as a sponge for miR-135a-5p to promote HIF1AN expression and inactivate Shh/Gli1 signalling, eventually aggravating H/R-induced apoptosis in cardiomyocytes.

Corrigendum to "Preoperative sedation in children with congenital heart disease: 50% and 95% effective doses, hemodynamic effects, and safety of intranasal dexmedetomidine". [Journal of Clinical Anesthesia, Volume 81, (2022)/ Article 110908].

Silencing of SNHG6 alleviates hypoxia/reoxygenation-induced cardiomyocyte apoptosis by modulating miR-135a-5p/HIF1AN to activate Shh/Gli1 signalling pathway.

OBJECTIVES:To examine the effects of small nucleolar RNA host gene 6 (SNHG6) on apoptosis during myocardial ischemic/reperfusion (I/R) injury and its potential molecular mechanisms.METHODS:In vitro model of I/R was built through exposing mouse HL-1 cardiomyocytes to hypoxia/reoxygenation (H/R) treatment. Quantitative real-time polymerase chain reaction assays were performed to determine gene expression. Cell Counting Kit-8, flow cytometric and western blot assays were conducted to detect cell viability, apoptosis and protein expression. Lactate dehydrogenase (LDH) activity was examined by a commercial detection kit. Dual-luciferase gene reporter and RNA immunoprecipitation experiments were applied for determining the interaction between the molecules.KEY FINDINGS:SNHG6 expression was increased in H/R-challenged cardiomyocytes. Depletion of SNHG6 protected against H/R-induced cardiomyocytes apoptosis. SNHG6 could sponge miR-135a-5p to inhibit its expression. Down-regulation of miR-135a-5p reversed the anti-apoptotic effect caused by SNHG6 knockdown in H/R-induced cardiomyocytes. Hypoxia inducible factor 1 subunit alpha inhibitor (HIF1AN) was identified as a direct target of miR-135a-5p, and knockdown of HIF1AN relieved H/R-induced cardiomyocytes apoptosis. Silencing of SNHG6 activated Shh/Gli1 signalling pathway by regulating miR-135a-5p/HIF1AN. Furthermore, inactivation of Shh/Gli signalling abolished the anti-apoptotic effects of SNHG6 knockdown in H/R-induced cardiomyocytes.CONCLUSIONS:SNHG6 serves as a sponge for miR-135a-5p to promote HIF1AN expression and inactivate Shh/Gli1 signalling, eventually aggravating H/R-induced apoptosis in cardiomyocytes.