Effects Of Mir-128-3P On Kidney Inflammation In Periodontitis

This study aimed to investigate the effects of miR-128-3p in extracellular vesicles (EVs) on kidney inflammation using a rat periodontitis model. Ten-week-old male Wistar rats were divided into two groups; the control (n=8) and the lipopolysaccharides (LPS) group (n=8). LPS group received LPS (Porphyromonas gingivalis, 1 mg/mL, 10 µL) injection in gingiva for 7 days. At the end of the experiment, plasma, periodontal tissue and kidney were collected. Kidney was stained by Hematoxylin and Eosin (H&E) to evaluate glomerular tissue injury score. Real time-PCR were performed to evaluate miR-128-3p, proinflammatory cytokine (IL-1β & TNF-α), and chemokine (CX3CL1 & CXCL7) expression. Bioinformatic analysis was conducted to identify potential target genes of miR-128-3p. The control and LPS groups were compared using Welch t-test. P value of < 0.05 was considered statistically significant. Kidney glomerular tissue injury score in the LPS group was significantly higher than that in the control group. miR-128-3p expression in the gingival tissue and plasma of LPS group were significantly higher, and IL-1β, TNF-α, CX3CL1, and CXCL7 in the kidney of LPS group were also significantly higher. The potential target genes of Activin A receptor type I (Acvr1), Ribosomal Protein S6 Kinase B1 (Rps6kb1), and transforming growth factor beta receptor type 1 (Tgfbr1) were significantly lower in the kidneys of LPS group. EVs-derived miR-128-3p in LPS-induced periodontitis caused kidney inflammation which may be mediated by Acvr1, Rps6kb1, and Tgfbr1.