Abstract：Objective: To investigate the regulatory effects and mechanisms of microRNA-223-3p (miR-223-3p) on the expression of calcium-sensing receptor (CaSR) and the adhesion capacity of calcium oxalate crystals in the formation of calcium oxalate kidney stones. Methods: An in vitro model of calcium oxalate kidney stones was established using rat kidney cells,NRK-52E.The expression levels of CaSR mRNA and protein were assessed using qRT-PCR and Western blot,respectively,while miR-223-3p expression was also evaluated.The target-binding relationship between miR-223-3p and CaSR was validated using a dual-luciferase reporter assay.The effects of overexpressing and silencing miR-223-3p on CaSR expression and calcium oxalate crystal adhesion capacity were analyzed. Results: In the calcium oxalate kidney stone cell model,compared to the control group,the expression of CaSR mRNA and protein was significantly downregulated (P<0.05),while miR-223-3p expression was significantly upregulated (P<0.05).The dual-luciferase reporter assay showed that,compared to the CaSR-WT+miR-NC group,the luciferase activity in the CaSR-WT+miR-223-3p group was significantly decreased (P<0.05),while there was no significant difference in luciferase activity between the CaSR-MT+miR-223-3p and CaSR-MT+miR-NC groups (P>0.05).Under optimal transfection conditions,miR-223-3p overexpression significantly downregulated the levels of CaSR mRNA and protein (both P<0.05),whereas silencing miR-223-3p significantly upregulated their levels (both P<0.05).Compared to the model+miRNA-mimic-NC group,the calcium oxalate crystal adhesion capacity was significantly increased in the model+miR-223-3p-mimic group,while it was significantly decreased in the model+miR-223-3p-inhibitor group (both P<0.05). Conclusion: miR-223-3p targets and inhibits the expression of CaSR,thereby increasing the adhesion capacity of calcium oxalate crystals.Regulating the expression of miR-223-3p may provide new insights for the prevention and treatment of calcium oxalate kidney stones.
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2025, Vol. 31 
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