ArticleMolecular metabolism2020
Overexpression of Gjb4 impairs cell proliferation and insulin secretion in primary islet cells.
Article in Molecular metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 16 citations in OpenAlex.
- Systematic cell-type resolved transcriptomes of 8 tissues in 8 lab and wild-derived mouse strains capture global and local expression variation.Cell genomics · 2026Article
- Determining gene specificity from multivariate single-cell RNA sequencing data.bioRxiv : the preprint server for biology · 2025Article
- Targeting GJB4 to inhibit tumor growth and induce ferroptosis in pancreatic cancer.Frontiers in oncology · 2025Article
- Transcriptomic heterogeneity of non-beta islet cells is associated with type 2 diabetes development in mouse models.Diabetologia · 2025Article
- A unique polygenic mouse model of obesity exhibits a distinct immunological profile that may offer protection against systemic inflammation, diabetes, and behavioral impairments.Frontiers in immunology · 2025Article
- Optimal tagging strategies for illuminating expression profiles of genes with different abundance in zebrafish.Communications biology · 2023Article
- Heterogeneous Development of β-Cell Populations in Diabetes-Resistant and -Susceptible Mice.Diabetes · 2022Article
- Identification of Novel Genes Involved in Hyperglycemia in Mice.International journal of molecular sciences · 2022Article
- Characterization of the microRNA transcriptomes and proteomics of cochlear tissue-derived small extracellular vesicles from mice of different ages after birth.Cellular and molecular life sciences : CMLS · 2022Article
- Positively selected genes in the hoary bat (PeerJ · 2022Article
- Enriched Alternative Splicing in Islets of Diabetes-Susceptible Mice.International journal of molecular sciences · 2021Article
- Alternative exon splicing and differential expression in pancreatic islets reveals candidate genes and pathways implicated in early diabetes development.Mammalian genome : official journal of the International Mammalian Genome Society · 2021Article
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveAltered gene expression contributes to the development of type 2 diabetes (T2D); thus, the analysis of differentially expressed genes between diabetes-susceptible and diabetes-resistant mouse models is an important tool for the determination of candidate genes that participate in the pathology. Based on RNA-seq and array data comparing pancreatic gene expression of diabetes-prone New Zealand Obese (NZO) mice and diabetes-resistant B6.V-ob/ob (B6-ob/ob) mice, the gap junction protein beta 4 (Gjb4) was identified as a putative novel T2D candidate gene.
methodsGjb4 was overexpressed in primary islet cells derived from C57BL/6 (B6) mice and INS-1 cells via adenoviral-mediated infection. The proliferation rate of cells was assessed by BrdU incorporation, and insulin secretion was measured under low (2.8 mM) and high (20 mM) glucose concentration. INS-1 cell apoptosis rate was determined by Western blotting assessing cleaved caspase 3 levels.
resultsOverexpression of Gjb4 in primary islet cells significantly inhibited the proliferation by 47%, reduced insulin secretion of primary islets (46%) and INS-1 cells (51%), and enhanced the rate of apoptosis by 63% in INS-1 cells. Moreover, an altered expression of the miR-341-3p contributes to the Gjb4 expression difference between diabetes-prone and diabetes-resistant mice.
conclusionsThe gap junction protein Gjb4 is highly expressed in islets of diabetes-prone NZO mice and may play a role in the development of T2D by altering islet cell function, inducing apoptosis and inhibiting proliferation.
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