Abstract
Acute kidney injury (AKI) is a common and fatal complication in inflammatory sepsis. Several microRNAs (miRNAs or miRs) have been identified to control sepsis. MiR-103a-3p has been reported to take part in the various inflammatory response. However, its role in AKI remains unclear. The present research aimed to explore the role and mechanisms of miR-103a-3p in AKI. Neurogenic sepsis mouse model and lipopolysaccharide-induced HK-2 and 293 cell models were established. The renal functions in each group of mice were measured. After evaluating the biological functions of C-X-C motif chemokine 12 (CXCL12) and miR-103a-3p on HK-2 and HEK-293 T cells, their interaction was determined. Detection of CXCL12 and apoptosis and inflammation-related factors in renal tissue was done. MiR-103a-3p was significantly repressed in the sepsis model, while CXCL12 was elevated. Furthermore, miR-103a-3p inversely controlled CXCL12. Knockdown of miR-103a-3p or overexpression of CXCL12 could significantly inhibit the progression of HK-2 and HEK293 cells, whereas elevated miR-103a-3p or knockdown of CXCL12 showed the opposite effects. Collectively, miR-103a-3p heightens renal cell damage caused by sepsis by targeting CXCL12.