Sericin suppresses high glucose-induced EMT in mouse podocytes via miR-30a-5p and its target Snai1.
Pak J Pharm Sci
; 36(5): 1457-1466, 2023 Sep.
Article
em En
| MEDLINE
| ID: mdl-37869922
ABSTRACT
The effect of sericin in high glucose (HG)-induced podocyte injury and the mechanisms involving Snai1 and miR-30a-5p were investigated. Bioinformatics and dual-luciferase reporter assay evaluated the relationship of Snai1 with miR-31a-5p. Podocyte injury mouse induced by HG were randomly divided into control (5.5mmol/L D-glucose), HG (30mmol/L D-glucose), HG + Sericin (30mmol/L D-glucose+600µg/ml sericin), miR-30a-5p inhibitor NC (sericin+30mmol/L D-glucose+miR-30a-5p inhibitor negative control) and miR-30a-5p inhibitor groups (sericin+30mmol/L D-glucose+miR-30a-5p inhibitor). The migration ability of podocytes was detected by Transwell assay. The expressions of Snai1, podocin, E-cadherin, FSP-1, ZO-1, α-SMA, Desmin, and miR-30a-5p were assessed with RT-qPCR and Western blot. Snai1 was one direct target of miR-30a-5p. HG group had significantly larger number of migrated podocytes and higher levels of Snai1, FSP-1, α-SMA and Desmin, but significantly lower levels of podocin, ZO-1 and E-cadherin than control and HG + Sericin group. These effects of sericin were reversed by miR-30a-5p inhibitor, as evidenced by increased podocyte migration and increased expressions of Snai1, α-SMA, FSP-1 and Desmin, whereas decreased expressions of podocin, ZO-1 and E-cadherin. Sericin may protect podocytes from damage caused by HG via up-regulating epithelial phenotype markers, down-regulating mesenchymal phenotype markers, and reducing migration of podocytes. The mechanism may be through targeting miR-30a-5p and its target Snai1.
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Base de dados:
MEDLINE
Assunto principal:
MicroRNAs
/
Sericinas
/
Podócitos
/
Transição Epitelial-Mesenquimal
Limite:
Animals
Idioma:
En
Revista:
Pak J Pharm Sci
Assunto da revista:
FARMACIA
/
FARMACOLOGIA
/
QUIMICA
Ano de publicação:
2023
Tipo de documento:
Article
País de afiliação:
China