The Mechanism Of HNRNPA2B1 Mediates Pri-miR-873 Nuclear Translocation In Intracerebral Hemorrhage Of Mice

Objective: To investigate the changes in the expression of HNRNPA2B1 after ICH in mice and further investigate whether HNRNPA2B1 affect pri-mi R-873 nuclear translocation after ICH in mice;to investigate the relationship between mi R-873 and RIPK3(a key protein of necroptosis)after ICH in mice;whether modulation of HNRNPA2B1 affect the RIPK1/RIPK3 signaling pathway of necroptosis and neurological deficits after ICH in mice.Methods: A mice model of ICH was established by collagenase,and changes in mice behavior were assessed by behavioral assays.Changes in the expression of HNRNPA2B1 and RIPK3 were measured by western blot analysis,and changes in pri-mi R-873 and mi R-873 were detected by q RT-PCR.,changes in the expression of HNRNPA2B1 and RIPK3 were measured again by western blot analysis after knocking out of HNRNPA2B1,and the changes of pri-mi R-873 and mi R-873 were detected by q RT-PCR.The presence of interaction between mi R-873 and RIPK3 were detected by luciferase assay.Results: The expression of HNRNPA2B1 was elevated after ICH in mice.After knocking out of HNRNPA2B1,behavioral scores were increased and brain edema was reduced after ICH in mice.The expression of pri-mi R-873 was decreased and the expression of mi R-873 was increased after knocking out of HNRNPA2B1.Mi R-873 bound to RIPK3(a key protein for necroptosis)after ICH in mice.The expression of HNRNPA2B1 was positively correlated with RIPK3.Conclusion: High expression of HNRNPA2B1 inhibited pri-mi R873 nuclear translocation after ICH in mice.Mi R-873 bound to RIPK3(a key protein for necroptosis)after ICH in mice.Knocking out of HNRNPA2B1 inhibited the RIPK1/RIPK3 signaling pathway of necroptosis,while reducing neurological deficits,cerebral edema and cognitive deficits after ICH in mice.