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Bmp2 and Notch cooperate to pattern the embryonic endocardium

ABSTRACT: Bmp2 and Notch cooperate to pattern the embryonic endocardium

PROVIDER: PRJNA413427 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6134450.fastq.gz	Fastqsanger.gz
	SRR6134451.fastq.gz	Fastqsanger.gz
	SRR6134452.fastq.gz	Fastqsanger.gz
	SRR6134453.fastq.gz	Fastqsanger.gz
	SRR6134454.fastq.gz	Fastqsanger.gz

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Bmp2 and Notch cooperate to pattern the embryonic endocardium

Project description:Our study describes in detail the role of Bmp2 during cardiac valve developmnent and its implication in Notch pathway activation.

2018-06-14 | GSE104670 | GEO

Transcriptional regulation in the embryonic endocardium after NOTCH pathway manipulation

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Injury-activated endocardium plays structural and signalling roles in zebrafish heart regeneration

Project description:The zebrafish heart remarkably regenerates after a severe ventricular damage followed by inflammation, fibrotic tissue deposition and removal concomitant with cardiac muscle replacement. We have investigated the role of the endocardium in this regeneration process. 3D-whole mount imaging in injured hearts revealed that GFP-labelled endocardial cells in ET33mi-60A transgenic fish become rapidly activated and highly proliferative at 3 days post cryoinjury (dpci). Endocardial cells extensively expand within the injury site and organize to form a coherent structure at 9 dpci that persists throughout the regeneration process. Upon injury, endocardial cells strongly up-regulate the Notch pathway ligand delta like4 (dll4) and the Notch receptors notch1b, notch2 and notch3. Expression profiling showed that Notch signalling inhibition affects endocardial gene expression and genes related to extracellular matrix remodelling and inflammation. Gain- and loss-of-function experiments revealed that Notch is required for the organization of the endocardium, attenuation of the inflammatory response and cardiomyocyte proliferation. These results demonstrate a novel structural and signalling role for the endocardium during heart regeneration.

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Endocardium-to-coronary artery differentiation during heart development and regeneration involves sequential roles of Bmp2 and Cxcl12/Cxcr4.

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Myocardial Bmp2 overexpression leads to ectopic cardiac EMT and promotes chamber cardiomyocyte proliferation and immaturity

Project description:Defective valve and septa formation constitute a substantial part of congenital heart defects affecting the neonate or the adult. During cardiac development, restricted myocardial Bmp2 expression is a key signal for the specification and patterning of the valve-forming field in the atrio-ventricular canal (AVC) region and the initiation of the epithelial-mesenchyme transition (EMT) that gives rise to the valve primordia. We have generated a mouse transgenic line conditionally expressing Bmp2. Nkx2.5Cre-driven Bmp2 overexpression in the myocardium leads to foetal lethality, due to valve and chamber dysmorphogenesis, and rescue of the AVC specification defect of Bmp2-null embryos. Nkx2.5Cre/+;Bmp2tg/+ transgenic embryos show ventricular septal defect, thickened valves, enlarged trabeculae and dilated ventricles, whose endocardium is able to undergo EMT when explanted onto collagen gels. Gene profile and marker analysis indicates that cellular proliferation is increased and chamber differentiation and patterning is impaired in Nkx2.5Cre/+;Bmp2tg/+ embryos, but the ventricular-specific gene expression program is not abolished. We obtained similar results using a second myocardial driver (cTnTCre) to activate Bmp2 expression, but not with an endothelial-specific one (Tie2Cre), as Tie2Cre/+;Bmp2tg/+ mice are normal and survive to adulthood, indicating that Bmp2 must emanate from the myocardium to exert its EMT-driving and cardiomyocyte maturation blocking effect. Forced Bmp2 expression in vitro stimulates EBs proliferation and blocks their progression into cardiomyogenesis, an effect partially rescued by Noggin. These data show that widespread myocardial Bmp2 expression directs ectopic valve primordium formation and maintains chamber myocardium and early cardiac progenitors in a primitive, proliferative state, identifying Bmp2 as a potential factor for the expansion of immature cardiomyocytes.

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Effect of BMP2 on B16F10 melanoma cells

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Notch

Project description:Notch

| PRJNA988118 | ENA