Background:
Podocyte injury and inflammatory response are the core contributors to
the pathogenesis of diabetic nephropathy. This study aims to identify novel regulatory miRNAs
and elucidate their underlying mechanisms, which will help us understand the pathogenesis of
diabetic nephropathy more comprehensively.
background:
Podocyte injury and inflammatory response are the core contributors to the pathogenesis of diabetic nephropathy.
Materials and Methods:
Different glucose concentrations were used to treat podocytes to mimic
the pathology of diabetic nephropathy in vitro. Flow cytometry was used to determine cell
apoptosis. Inflammatory cytokines released by podocytes were measured by using an enzymelinked
immunosorbent assay (ELISA). Western Blot was used to detect the expression of
PRKAB2 protein in podocytes.
objective:
The aim of this study is to identify novel regulatory mirnas and elucidate their underlying mechanisms, which will help us to understand the pathogenesis of diabetic nephropathy more comprehensively.
Results:
Genecard and g: profiler results revealed that miR-29b might be involved in regulating
HG-induced cell injury. QRT-PCR indicated that HG-induced downregulation of miR-29b in
podocytes. MiR-29b knockdown promoted cell apoptosis and inflammatory response in podocytes.
MiR-29b overexpression repressed cell apoptosis and inflammatory response induced by
high glucose treatment in podocytes. Luciferase reporter assay and Western Blot showed that
miR-29b targeted PRKAB2 to negatively regulate PRKAB2 expression directly. Knockdown of
PRKAB2 reversed the increased cell apoptosis and inflammation induced by miR-29b inhibitors.
Conclusion:
MiR-29b plays a role in inhibiting inflammation and apoptosis in high glucose
(HG) treated podocytes by negatively regulating PRKAB2 expression. This study provides new
potential targets and ideas for the treatment of diabetic nephropathy.
result:
Genecard and g: profiler results revealed that miR-29b might be involved in regulating HG-induced cell injury. qRT-PCR indicated that HG induced downregulation of miR-29b in podocytes. miR-29b knockdown promoted cell apoptosis and inflammatory response in podocytes. miR-29b overexpression repressed cell apoptosis and inflammatory response induced by high glucose treatment in podocytes. Luciferase reporter assay and western blot showed that miR-29b targeted PRKAB2 to negative regulate PRKAB2 expression directly. Knockdown of PRKAB2 abolished the increased cell apoptosis and inflammation induced by miR-29b inhibitors.