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FHL2-driven molecular network mediated Septin2 knockdown inducing apoptosis in mesangial cell
- Source :
- PROTEOMICS. 14:2485-2597
- Publication Year :
- 2014
- Publisher :
- Wiley, 2014.
-
Abstract
- The apoptosis of mesangial cells (MCs) plays a critical role in the pathological progress of MesPGN. Septin2, a filamentous GTPase, is implicated in the apoptotic progress of MCs in the rat MesPGN model. However, the molecular mechanism of SEPT2 in MCs apoptosis is not clear. Here, we present the FHL2-driven molecular network as the main mechanism of SEPT2-mediated rat primary MCs apoptosis. First, we proved that the expression of FHL2 and Septin2 were closely related with MCs apoptosis in anti-Thy1 nephritis model. Then, it was found that FHL2 was a new interaction protein of Septin2 and Septin2 knockdown could induce MC apoptosis by FHL2-mediatied signal pathways including p-ERK1 and p-AKT. We applied label-Free quantitative proteomics to identify the mechanism of Septin2/FHL2-regulated apoptosis. Bioinformatics analysis revealed that FHL2-driven molecular network composed of biological functions including glycolysis, oxidative stress, ribonucleotide metabolism, actin cytoskeleton regulation, and signaling pathway, was the main mechanism of SETP2-mediated apoptosis. Furthermore, we showed that the effect of Septin2 knockdown on MC apoptosis could be alleviated by the overexpression of FHL2. Overall, this study illustrated the FHL2-driven molecular network controlling SEPT2-mediated apoptosis in MCs and their potential roles in mesangial proliferative nephritis.
- Subjects :
- SEPT2
LIM-Homeodomain Proteins
Muscle Proteins
Apoptosis
Biology
medicine.disease_cause
Biochemistry
Protein Interaction Mapping
medicine
Animals
Nerve Growth Factors
Molecular Biology
Cells, Cultured
Gene knockdown
Mesangial cell
Actin cytoskeleton
Rats
FHL2
Cell biology
Gene Expression Regulation
Gene Knockdown Techniques
Mesangial Cells
Signal transduction
Septins
Oxidative stress
Signal Transduction
Transcription Factors
Subjects
Details
- ISSN :
- 16159853
- Volume :
- 14
- Database :
- OpenAIRE
- Journal :
- PROTEOMICS
- Accession number :
- edsair.doi.dedup.....a3719e027a11ab0b25ab15c7f3241ed6