ArticleOrganogenesis2026
MLPH/RAB3A accelerates the differentiation of pancreatic stem cells to islet β-cells to control blood glucose in diabetic rats.
Article in Organogenesis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundThis study aimed to determine the potential mechanism by which pancreatic stem cell-derived beta cells (PSCs-β) assist in the body's glucose-lowering capacity in type 1 diabetes (T1D) rats.
methodsWe screened the transcriptomic changes in the pancreatic islets of T1D mice to extract key genes from the GSE169275 dataset. Cell proliferation, cell cycle distribution, apoptosis, PSC-β differentiation ability, and insulin production levels were analyzed after MLPH overexpression/knockdown in PSCs. PSC-β-overexpressing MLPH were transplanted into T1D rats, and the changes in fasting blood glucose level, glucose tolerance and insulin, glucagon and C-peptide contents were examined. After the target genes of MLPH were analysed using the database, immunoprecipitation was introduced for validation. Whether RAB3A is involved in the regulatory effects of MLPH on the proliferation and differentiation of PSCs was further verified.
resultsMLPH overexpression further enhanced the proliferation of PSCs, inhibited apoptosis and accelerated the differentiation of PSCs to PSC-β cells and insulin secretion. After the transplantation of MLPH-overexpressing PSC-β cells, the pancreatic islet tissue damage was restored, the insulin expression was substantially elevated and the glucagon content decreased. RAB3A knockdown counteracted the effects of MLPH on the proliferation, differentiation and insulin secretion of PSCs.
conclusionMLPH overexpression is favourable for the differentiation of PSCs to insulin β-cells. Transplantation of MLPH-overexpressing PSC-β cells restored the ability of T1D rats to manage a glycemic load by promoting RAB3A expression.
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