Silencing circular ANRIL protects HK-2 cells from lipopolysaccharide-induced inflammatory injury through up-regulating microRNA-9

Abstract

Circular antisense non-coding RNA in the INK4 locus (cANRIL) participated in inflammation of endothelial cells. However, whether cANRIL is associated with inflammatory injury of HK-2 cells, thereby affecting chronic kidney disease has not been investigated. We tested the hypothesis that cANRIL participated in inflammatory response in vitro. HK-2 cells were stimulated by lipopolysaccharides (LPS). RT-qPCR was executed for cANRIL expression assessment. After transfection, cell viability, apoptosis, inflammatory cytokines and ROS generation were appraised to evaluate the impact of silencing cANRIL on LPS-induced inflammatory injury. The regulatory relationship between cANRIL and microRNA-9 (miR-9) was verified. In addition, whether miR-9 affected LPS-induced inflammatory injury was measured after miR-9 inhibitor transfection. Western blot was utilized to detect NF-jB and JNK/p38 pathway-related proteins. The results showed that LPS promoted cANRIL expression and cell injuries in HK-2 cells. Furthermore, silencing cANRIL alleviated inflammatory injuries by promoting viability, suppressing apoptosis, inflammatory cytokines and ROS generation in HK-2 cells. In addition, miR-9 expression was accelerated by silencing cANRIL. Meanwhile, miR-9 down-regulation invalidated the effect of silencing cANRIL on inflammation and NF-jB and JNK/p38 pathways. The study clarified that silencing cANRIL hindered NF-jB and JNK/p38 pathways by positively regulating miR-9, thereby protecting HK-2 cells from LPS-induced injury.

Long non-coding RNA CDKN2B-AS1 regulates high glucose-induced human mesangial cell injury via regulating the miR-15b-5p/WNT2B axis

“…Another research indicated that CDKN2B-AS1 decreased the protective role of Rhein via elevating inflammation response in uric acid nephropathy rats [32]. Deng et al suggested that CDKN2B-AS1 knockdown reduced the inflammation response of lipopolysaccharide-treated HK-2 cells via increasing miR-9 expression [33]. Herein, CDKN2B-AS1 silencing decreased viability, ECM accumulation, inflammation response, and induced cell cycle arrest of HG-induced HMCs.…”

Silencing of circular RNA ANRIL attenuates oxygen–glucose deprivation and reoxygenation-induced injury in human brain microvascular endothelial cells by sponging miR-622

“…Moreover, inhibition of NF-κB activation was shown to reduce cerebral ischemic injury in CI/R rats, which can be attributed, at least in part, to the reduction of inflammation and apoptosis following ischemic injury [32]. It has been reported that silencing of circ_ANRIL protects HK-2 cells from lipopolysaccharide (LPS)-induced inflammatory damage by inhibiting the activation of the NF-κB and c-Jun N-terminal kinase (JNK)/p38 pathways [33]. Here, our results also revealed that silencing of circ_ ANRIL inhibited the activation of the NF-κB pathway in OGD/R-induced HBMECs by sponging miR-622.…”

The correlation of serum long non‐coding RNA ANRIL with risk factors, functional outcome, and prognosis in atrial fibrillation patients with ischemic stroke

“…The oxidative damage induced by thrombosis in patients with AF is a hot topic in recent years. Studies have found that lncRNA ANRIL can induce thrombosis in the following ways: (a) LncRNA ANRIL can induce DNA damage in endothelial cells under oxidative stress and plays an important role in the occurrence and development of endothelial inflammation 24 . (b) A large number of studies have pointed out that under oxidative stress, lncRNA ANRIL can promote the release of myeloperoxidase, and can induce the body to produce a variety of free radicals, promote the formation of cardiovascular plaques, and induce thrombosis 25 .…”