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Granulosa cell-derived serum TNF-α mediates inflammation and apoptosis in renal tubular cells through NF-κB signaling and indicates PCOS-related kidney injury.

ABSTRACT: Serum TNF-α plays a key role in mediating inflammation and apoptosis in renal tubular cells and indicates PCOS-related kidney injury.

ORGANISM(S): Mus musculus

PROVIDER: GSE229106 | GEO | 2023/12/06

REPOSITORIES: GEO

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Granulosa cell-derived serum TNF-α mediates inflammation and apoptosis in renal tubular cells through NF-κB signaling and indicates PCOS-related kidney injury.

Project description:Granulosa cell-derived serum TNF-α mediates inflammation and apoptosis in renal tubular cells through NF-κB signaling and indicates PCOS-related kidney injury.

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IGF2BP2-regulated alternative splicing of NFIC causes excessive granulosa cell proliferation in PCOS [IRIP-seq]

Project description:The expression of IGF2BP2 in GCs from PCOS patients was detected using RT-qPCR and western blot. We captured IGF2BP2-interacting transcripts, global transcriptome together with alternative splicing by RNA immunoprecipitation sequencing (RIP-seq) and RNA sequencing (RNA-seq). KGN cells transfected with IGF2BP2 overexpressing plasmids and nuclear factor 1 C-type (NFIC) siRNAs, were applied to CCK-8, EdU and TUNEL assays. IGF2BP2 was highly expressed in GCs from PCOS patients. As a RBP, it preferentially bound to the 3’and 5’UTRs of mRNAs with GGAC motif and a newly found GAAG motif. The overexpression of IGF2BP2 changed the transcriptome profile of KGN cells. IGF2BP2 functioned to regulate alternative splicing events (ASEs) and promote cell proliferation through inhibiting exon skipping events of NFIC. In conclusion, we demonstrated that IGF2BP2 promotes granulosa cell proliferation via regulating alternative splicing of NFIC in PCOS. The findings help to better understand the roles of IGF2BP2 in the pathogenesis of PCOS.

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