Roles of MK2 gene in angiotensin Ⅱ-induced mouse renal damage
	    		
		   		
		   			
		   		
	    	
    	 
    	10.13431/j.cnki.immunol.j.20240058
   		
        
        	
        		- VernacularTitle:MK2基因在血管紧张素Ⅱ诱导小鼠肾损害中的作用
 
        	
        	
        	
        		- Author:
	        		
		        		
		        		
			        		Lishuang SUN
			        		
			        		
			        		
			        			1
			        			
			        		
			        		
			        		
			        		
			        		;
		        		
		        		
		        		
			        		Yang YU
			        		
			        		;
		        		
		        		
		        		
			        		Yanhong FENG
			        		
			        		
		        		
		        		
		        		
		        		
		        			
			        		
			        		Author Information
			        		
		        		
		        		
			        		
			        		
			        			1. 121000,锦州医科大学附属第三医院超声科
			        		
		        		
	        		
        		 
        	
        	
        	
        	
        		- Keywords:
        			
	        			
	        				
	        				
			        		
				        		Hypertensive nephropathy;
			        		
			        		
			        		
				        		AngiotensinⅡ;
			        		
			        		
			        		
				        		Mitogen-activated protein kinase actitaved protein kinase 2;
			        		
			        		
			        		
				        		Gene knockout
			        		
			        		
	        			
        			
        		
 
        	
            
            
            	- From:
	            		
	            			Immunological Journal
	            		
	            		 2024;40(5):446-451
	            	
            	
 
            
            
            	- CountryChina
 
            
            
            	- Language:Chinese
 
            
            
            	- 
		        	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.