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Mus musculus

ABSTRACT: LIM-Domain-Binding 1 maintains the terminally-differentiated state of pancreatic β-cells

PROVIDER: PRJNA331049 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3948030.fastq.gz	Fastqsanger.gz
	SRR3948040.fastq.gz	Fastqsanger.gz
	SRR3948050.fastq.gz	Fastqsanger.gz
	SRR3948060.fastq.gz	Fastqsanger.gz
	SRR3948070.fastq.gz	Fastqsanger.gz

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Project description:Pancreatic islet endocrine cell and endothelial cell (EC) interactions mediated by vascular endothelial growth factor-A (VEGF-A) signaling are important for islet endocrine cell differentiation and the formation of highly vascularized islets. To dissect how VEGF-A signaling modulates intra-islet vasculature and innervation, islet microenvironment, and β cell mass, we transiently increased VEGF-A production by β cells. VEGF-A induction dramatically increased the number of intra-islet ECs but led to β cell loss. After withdrawal of the VEGF-A stimulus, β cell mass, function, and islet structure normalized as a result of a robust, but transient, burst in proliferation of pre-existing β cells. Bone marrow-derived macrophages (MΦs) recruited to the site of β cell injury were crucial for the β cell proliferation, which was independent of pancreatic location and circulating factors such as glucose. Identification of the signals responsible for the proliferation of adult, terminally differentiated β cells will improve strategies aimed at β cell regeneration and expansion.

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