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Bmp2 -driven terminal differentiation of the stomach epithelium is induced by an autocrine Bmp2 positive feedback loop and inhibited by H. pylori via Interferon gamma signaling [RNA-seq]

ABSTRACT: Bmp2 -driven terminal differentiation of the stomach epithelium is induced by an autocrine Bmp2 positive feedback loop and inhibited by H. pylori via Interferon gamma signaling [RNA-seq]

PROVIDER: PRJNA562930 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10044351_1.fastq.gz	Fastqsanger.gz
	SRR10044351_2.fastq.gz	Fastqsanger.gz
	SRR10044352_1.fastq.gz	Fastqsanger.gz
	SRR10044352_2.fastq.gz	Fastqsanger.gz
	SRR10044353_1.fastq.gz	Fastqsanger.gz

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Bmp2 -driven terminal differentiation of the stomach epithelium is induced by an autocrine Bmp2 positive feedback loop and inhibited by H. pylori via Interferon gamma signaling

Project description:Bmp2 -driven terminal differentiation of the stomach epithelium is induced by an autocrine Bmp2 positive feedback loop and inhibited by H. pylori via Interferon gamma signaling

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Bmp2 -driven terminal differentiation of the stomach epithelium is induced by an autocrine Bmp2 positive feedback loop and inhibited by H. pylori via Interferon gamma signaling [microarray]

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Bmp2 -driven terminal differentiation of the stomach epithelium is induced by an autocrine Bmp2 positive feedback loop and inhibited by H. pylori via Interferon gamma signaling [microarray]

Project description:We find that Bmp2 expression in the surface epithelium of the stomach provides a decisive, dominant fate-determining signal in the gland resulting in terminal differentiation. Terminal differentiation is induced by Bmp2 expression controlled by Bmp2 itself, creating an auto- and paracrine loop that maintains the cells in the differentiated state. Infection with H. pylori leads to a loss of stromal and epithelial Bmp2 expression resulting in gland hyperplasia and impaired differentiation. We demonstrate that Interferon gamma blocks endogenous Bmp2 expression and therefore Bmp2 signaling. Its effect on differentiated cells via Bmp2 inhibition maintains plasticity in this compartment, allowing for recruitment of differentiated cells to the stem cell pool, accounting for the rearrangement of stem cell compartment and increased plasticity in the epithelium in the context of epithelial damage in the gastrointestinal tract.

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Bmp2 -driven terminal differentiation of the stomach epithelium is induced by an autocrine Bmp2 positive feedback loop and inhibited by H. pylori via Interferon gamma signaling [RNA-seq]

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Project description:Liver sinusoidal endothelial cells (LSEC) represent a unique, organ-specific type of discontinuous endothelial cells. LSEC instruct the hepatic vascular niche by paracrine-acting angiocrine factors. Recently, we have shown that LSEC-specific transcriptional regulator GATA4 induces expression of BMP2 in cultured endothelial cells (EC) in vitro. Furthermore, angiocrine Bmp2 signaling in the liver in vivo was demonstrated to control iron homeostasis. Here, we investigated GATA4-dependent autocrine BMP2 signaling in endothelial cells by gene expression profiling. GATA4 induced a large cluster of inflammatory endothelial response genes in cultured EC, which is similar to previously identified virus-induced and interferon-associated responses. Treating the cells with the BMP2 inhibitor Noggin counter-regulated the GATA4-dependent inflammatory phenotype of EC, indicating that BMP2 is indeed the major driver. In contrast to continuous EC, LSEC were less prone to activation by BMP2. Notably, GATA4-dependent induction of the inflammatory EC response gene cluster was attenuated by over-expression of the LSEC-specific transcriptional modifier LMO3 while hepatocyte activation was fully preserved, indicating conserved BMP2 synthesis. In summary, our data suggest that transcriptional counter-regulation by GATA4 and LMO3 in LSEC prevents autocrine induction of an inflammatory phenotype, while maintaining angiocrine BMP2-mediated cell communication in the liver vascular niche.

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Bmp2 -driven terminal differentiation of the stomach epithelium is induced by an autocrine Bmp2 positive feedback loop and inhibited by H. pylori via Interferon gamma signaling

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