Background: Although the pathogenetic mechanism of Diabetic Kidney Disease (DKD) has
not been elucidated, an inflammatory mechanism may be a potential contributor. Monocyte chemotactic
protein-1 (MCP-1) is suggested to be implicated in the development of DKD by playing a role in
the infiltration of monocyte/macrophage. The aim of this study was to investigate the expression of
MCP-1 under high glucose conditions, as well as the effects of microRNA-192 (miR-192) under these
conditions, and to study the regulatory mechanism of MCP-1 in DKD.
Methods: Rat glomerular mesangial cells were cultured in high glucose or isotonic mannitol. The
messenger RNA(mRNA) expression of miR-192, miR-200b, miR-200c, E-box-binding homeobox 1
(Zeb1), and MCP-1 was then detected by real-time PCR, and the protein expression of Zeb1 and MCP-
1 was assessed by western blotting. The rat mesangial cells were transfected with an miR-192 inhibitor,
NC inhibitor , and transfected with siRNA Zeb1, siNC. The cells were then cultured in high glucose
to detect the mRNA expression of miR-192, miR-200b, miR-200c, Zeb1, and MCP-1 using realtime
PCR, and Zeb1 and MCP-1 protein expression were determined by western blotting.
Results: MiR-192, miR-200b, miR-200c, and MCP-1 were overexpressed, whereas Zeb1 was downregulated
when cultured in high glucose (P < 0.05). After transfection with an miR-192 inhibitor, the
expression of miR-192, miR-200b, miR-200c, and MCP-1 was downregulated, whereas Zeb1 was
increased, and these differences were statistically significant (P < 0.05). The observed changes in the
expression in the NC inhibitor transfection group were similar to that of non-transfected cell lines.
Silencing the expression of Zeb1 resulted in a significant increase in the expression of miR-192, miR-
200b, miR-200c, and MCP-1 (P < 0.05). The observed changes in the SiNC transfection group were
similar to those of non-transfected cell lines.
Conclusions: MiR-192 expression was upregulated to increase the expression of inflammatory factor
MCP-1 by inhibiting the expression of Zeb1, which was mediated by breaking the regulatory loop of
Zeb1 and miR-200b/c in rat mesangial cells cultured in high glucose.