Anti-antioxidant impacts of circZNF609 silence in HaCaT cells through regulating miR-145

Abstract

Background: CircZNF609 (cZNF609) is previously revealed as an essential mediator in oxidative stress. This paper determined the role of cZNF609 in skin oxidative damage to evaluate its importance in pressure ulcer. Methods: HaCaT cells treated by H 2 O 2 were considered as a cell model of pressure ulcer. The role of cZNF609 in the model was checked by conducting CCK-8 assay, FITC-PI double-staining, ROS detection and Western blot. The downstream gene and signalling of cZNF609 were studied by utilizing qRT-PCR and Western blot. Results: HaCaT cells were remarkably damaged by H 2 O 2 , as evidenced by the viability loss, apoptosis and ROS generation. It was coupled with the elevated expression of p53, p16, Bax and the activated forms of caspase-3 and PARP. Meanwhile, cZNF609 was high-expressed in response to H 2 O 2. The oxidative stress driven by H 2 O 2 was alleviated by transfection with cZNF609 specific siRNA. Further, the antiantioxidant impacts of cZNF609 silence were impeded by miR-145 silence. The inhibition of JNK and p38MAPK pathways induced by cZNF609 silence was impeded by miR-145 silence. Conclusion: The protective function of cZNF609 silence in H 2 O 2-injured HaCaT cells was revealed in vitro. Silence of cZNF609 exhibited its impact possibly through regulating miR-145, and JNK and p38MAPK pathways.

Role of microRNAs in Pressure Ulcer Immune Response, Pathogenesis, and Treatment

“…When hydrogen peroxide-injured keratinocytes were treated with circular RNA ZNF609 silencer, there is an upregulation of miR-145. This increase in miR-145 resulted in lower ROS generation, decreased keratinocyte p53 and caspase 3 expression, and improved cell viability [87]. When miR-145 was silenced, there was a loss of anti-oxidant effects.…”

“…When miR-145 was silenced, there was a loss of anti-oxidant effects. miR-145 inhibits JNK and p38-MAPK signaling pathways, which are activated by ROS [87,121]. JNK has been shown to have a complex role in pressure ulcer pathophysiology, increasing ROS production but inhibiting apoptotic activity [84,87,121].…”

“…miR-145 inhibits JNK and p38-MAPK signaling pathways, which are activated by ROS [87,121]. JNK has been shown to have a complex role in pressure ulcer pathophysiology, increasing ROS production but inhibiting apoptotic activity [84,87,121]. Increased levels of p38-MAPK have been shown to contribute to the ischemia-reperfusion injury seen in pressure ulcer pathogenesis, and miR-145 may downregulate this expression [23,25,87].…”

Emerging Clues of Regulatory Roles of Circular RNAs through Modulating Oxidative Stress: Focus on Neurological and Vascular Diseases

“…Researchers found that in HaCaT cells treated with H 2 O 2 , which were considered a cell model of pressure ulcers, circZNF609 silencing may reduce oxidative stress by regulating miR-145 [106]. CircNFIX is abundant, conservative, and stable in H9c2 cells.…”

Protective effect of dimethyl fumarate for the development of pressure ulcers after cutaneous ischemia‐reperfusion injury

“…Skin oxidative damage is considered to be the main factor in the pathogenesis of PU. 26,27 Therefore, recent studies reported that antioxidant drug have been considered as potential agents for improving the treatment of PU for clinical application. 10,28,29 Moreover, we recently demonstrated the usability of OKD48 mice to quantify the oxidative stress level using cutaneous I/R injury mice model.…”