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Beta cell dysfunction and dedifferentiation induced by Bone Morphogenetic Protein (BMP)-2 is associated with histone modifications and decreased NeuroD1 chromatin binding {RNA-seq]

ABSTRACT: Beta cell dysfunction and dedifferentiation induced by Bone Morphogenetic Protein (BMP)-2 is associated with histone modifications and decreased NeuroD1 chromatin binding {RNA-seq]

PROVIDER: PRJNA892633 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21987672.fastq.gz	Fastqsanger.gz
	SRR21987673.fastq.gz	Fastqsanger.gz
	SRR21987674.fastq.gz	Fastqsanger.gz
	SRR21987675.fastq.gz	Fastqsanger.gz
	SRR21987676.fastq.gz	Fastqsanger.gz

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Similar Datasets

Beta cell dysfunction and dedifferentiation induced by Bone Morphogenetic Protein (BMP)-2 is associated with histone modifications and decreased NeuroD1 chromatin binding

Project description:Insufficient insulin secretion is a hallmark of type 2 diabetes and has been attributed to beta cell identity loss characterized by a decreased expression of several key beta cell genes. The pro-inflammatory factor BMP-2 is upregulated in islets of Langerhans from diabetic individuals and acts as an inhibitor of beta cell function and proliferation. Exposure to BMP-2 induces expression of Id1-4, Hes-1 and Hey-1, transcriptional regulators associated with loss of differentiation. The aim of this study was to investigate the mechanism of BMP-2 induced beta cell dysfunction and identity loss. Mouse islets exposed to BMP-2 for 10 days showed impaired insulin secretion and beta cell proliferation. BMP-2-induced beta cell dysfunction was associated with decreased expression of beta cell specific identity and proliferation markers such as Ins1, Ucn3 and Ki67 but increased expression of Id1-4, Hes-1 and Hey-1. BMP-2 regulated mRNA expression significantly correlated with corresponding protein expression. BMP-2 induced gene expression changes were associated with a predominant reduction in the H3K27ac mark and a decrease in NeuroD1 chromatin binding activity. These results show that BMP-2-induced beta cell dysfunction is associated with epigenetic changes, predominantly a reduction in H3K27ac and a decrease in NeuroD1 DNA binding resulting in altered beta cell gene expression.

2023-07-20 | PXD036655 | Pride

Beta cell dysfunction and dedifferentiation induced by Bone Morphogenetic Protein (BMP)-2 is associated with histone modifications and decreased NeuroD1 chromatin binding [NeuroD1 ChIP-seq]

Project description:Insufficient insulin secretion is a hallmark of type 2 diabetes and has been attributed to beta cell identity loss characterized by decreased expression of several key beta cell genes. The pro-inflammatory factor BMP-2 is upregulated in islets of Langerhans from diabetic individuals and acts as an inhibitor of beta cell function and proliferation. Exposure to BMP-2 induces expression of Id1-4, Hes-1 and Hey-1, transcriptional regulators associated with loss of differentiation. The aim of this study was to investigate the mechanism of BMP-2 induced beta cell dysfunction and maturity. Mouse islets exposed to BMP-2 for 10 days showed impaired insulin secretion and beta cell proliferation. BMP-2-induced beta cell dysfunction was associated with decreased expression of beta cell specific identity and proliferation markers such as Ins1, Ucn3 and Ki67 but increased expression of Id1-4, Hes-1 and Hey-1. Top 30 most regulated proteins significantly correlated with corresponding mRNA expression. BMP-2 induced gene expression changes were associated with a predominant reduction in acetylation of H3K27 and a decrease in NeuroD1 chromatin binding activity. These results show that BMP-2-induced beta cell dysfunction is associated with epigenetic changes, predominantly a reduction in H3K27ac and a decrease in NeuroD1 DNA binding resulting in altered beta cell gene expression.

2023-07-12 | GSE216232 | GEO

Beta cell dysfunction and dedifferentiation induced by Bone Morphogenetic Protein (BMP)-2 is associated with histone modifications and decreased NeuroD1 chromatin binding [NeuroD1 ChIP-seq]

Project description:Beta cell dysfunction and dedifferentiation induced by Bone Morphogenetic Protein (BMP)-2 is associated with histone modifications and decreased NeuroD1 chromatin binding [NeuroD1 ChIP-seq]

| PRJNA892632 | ENA

Beta cell dysfunction and dedifferentiation induced by Bone Morphogenetic Protein (BMP)-2 is associated with histone modifications and decreased NeuroD1 chromatin binding {RNA-seq]

2023-07-12 | GSE216231 | GEO

Beta cell dysfunction and dedifferentiation induced by Bone Morphogenetic Protein (BMP)-2 is associated with histone modifications and decreased NeuroD1 chromatin binding

Project description:Beta cell dysfunction and dedifferentiation induced by Bone Morphogenetic Protein (BMP)-2 is associated with histone modifications and decreased NeuroD1 chromatin binding

| PRJNA892627 | ENA

Beta cell dysfunction and dedifferentiation induced by Bone Morphogenetic Protein (BMP)-2 is associated with histone modifications and decreased NeuroD1 chromatin binding [Histone ChIP-seq]

2023-07-12 | GSE216230 | GEO

Beta cell dysfunction and dedifferentiation induced by Bone Morphogenetic Protein (BMP)-2 is associated with histone modifications and decreased NeuroD1 chromatin binding [Histone ChIP-seq]

| PRJNA892634 | ENA

Proteomic profiling of murine melanoma treated with bone morphogenetic protein (BMP) signaling inhibitor

Project description:Melanoma is a highly aggressive skin cancer, which has the fastest and second fastest growing incidence of any cancer in men and women, respectively. Although melanoma accounts for 5% of skin cancers, it is responsible for 80% of deaths related to skin cancers. The lifetime risk of melanoma is currently estimated to be 1 in 75 and is rising every year. The present study shows that inhibition of bone morphogenetic protein (BMP) signaling pathway is a potential target for treating metastatic melanoma. To characterize the underlying signaling mechanism, comparative proteomic profile of the mouse melanoma tissue treated with and BMP inhibitor (LDN193189) with untreated controls was performed using liquid chromatography-tandem mass spectrometry. Our mass spectrometry data analysis leads to identification of a total of 3231 nonredundant proteins. Of the 3231 proteins, 117 were up-regulated (fold change≥ 1.5) while 14 were down-regulated (fold change ≤ 0.66). Pathway enrichment analysis showed that altered proteins were primarily grouped into: regulation of actin cytoskeleton, phagosomes, proteoglycans in cancer, Focal adhesion, ECM receptor interaction and fatty acid metabolism pathway. Our studies suggest that inhibition of the BMP signaling cascade with small molecule inhibitors decreased the expression of the MT1 and MT2 (metallothionine 1 and 2) which are well known for the antiapoptotic, antioxidant, proliferative, and angiogenic effects in cancer.

2022-02-15 | PXD016088 | Pride

Beta cell dysfunction and dedifferentiation induced by Bone Morphogenetic Protein (BMP)-2 is associated with histone modifications and decreased NeuroD1 chromatin binding

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-07-12 | GSE216233 | GEO

Beta cell dysfunction induced by bone morphogenetic protein (BMP)-2 is associated with histone modifications and decreased NeuroD1 chromatin binding.

Project description:Insufficient insulin secretion is a hallmark of type 2 diabetes and has been attributed to beta cell identity loss characterized by decreased expression of several key beta cell genes. The pro-inflammatory factor BMP-2 is upregulated in islets of Langerhans from individuals with diabetes and acts as an inhibitor of beta cell function and proliferation. Exposure to BMP-2 induces expression of Id1-4, Hes-1, and Hey-1 which are transcriptional regulators associated with loss of differentiation. The aim of this study was to investigate the mechanism by which BMP-2 induces beta cell dysfunction and loss of cell maturity. Mouse islets exposed to BMP-2 for 10 days showed impaired glucose-stimulated insulin secretion and beta cell proliferation. BMP-2-induced beta cell dysfunction was associated with decreased expression of cell maturity and proliferation markers specific to the beta cell such as Ins1, Ucn3, and Ki67 and increased expression of Id1-4, Hes-1, and Hey-1. The top 30 most regulated proteins significantly correlated with corresponding mRNA expression. BMP-2-induced gene expression changes were associated with a predominant reduction in acetylation of H3K27 and a decrease in NeuroD1 chromatin binding activity. These results show that BMP-2 induces loss of beta cell maturity and suggest that remodeling of H3K27ac and decreased NeuroD1 DNA binding activity participate in the effect of BMP-2 on beta cell dysfunction.

| S-EPMC10322916 | biostudies-literature

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