Roles of MK2 gene in angiotensin Ⅱ-induced mouse renal damage

SUN Lishuang; YU Yang; FENG Yanhong

doi:10.13431/j.cnki.immunol.j.20240058

Abstract：This study was designed to evaluate the effect and mechanism of mitogen-activated protein kinase(MAPK)activated protein kinase 2(MK2)in Angiotensin Ⅱ(AngⅡ)-induced mouse renal damage.Total of 16 wild type C57BL/6J mice were randomly divided into MK2+/+control group and MK2+/++AngⅡ group,while 16 MK2 knockout C57BL/6J mice were randomly divided into MK2-/-control group and MK2-/-+AngⅡ group.Kidney damage was induced by subcutaneous injection of AngⅡ for 4 weeks.Then corresponding methods were carried out to detect systolic pressure,serum creatinine,24h urinary albumin,glomerulosclerosis index,renal tubulointerstitial injury score,the expression level of phosphorylated MK2(p-MK2),p-p65 nuclear factor-κB(NF-κB),the contents of tumor necrosis factor-α(TNF-α),interleukin-6(IL-6),reactive oxygen species(ROS),superoxide dismutase(SOD)and malondialdehyde(MDA).Compared with the MK2+/+control group,MK2+/++AngⅡ group demonstrated significant increase in systolic blood pressure,serum creatinine,24h urinary albumin,glomerulosclerosis index,renal tubulointerstitial injury score,the expression levels of p-MK2,p-p65 NF-κB expression,and the contents of TNF-α,IL-6,ROS,MDA,while significant decrease in the level of SOD in kidney(P<0.05).Compared with the MK2+/++AngⅡ group,MK2-/-+AngⅡ group showed no significant difference in systolic blood pressure(P>0.05),significant decrease in the serum creatinine,24 h urinary albumin,glomerulosclerosis index,renal tubulointerstitial injury score,the expression levels of p-MK2,p-p65 NF-κB and the contents of TNF-α,IL-6,ROS,MDA,while significant increase in the content of SOD in kidney(P<0.05).In conclusion,MK2 knockout significantly alleviates AngⅡ-induced renal damage and inhibits inflammatory and oxidative stress responses.MK2 is involved in AngⅡ induced renal damage.