Dataset Information

Extracellular vesicles from Notch activated cardiac mesenchymal stem cell promote myocyte proliferation and neo-vasculogenesis

ABSTRACT: Cardiac mesenchymal stem cells (C-MSC) are a novel mesenchymal stem cell subpopulation derived from cardiac tissue, whichi are reported to be responsible for cardiac regeneration. Notch siganling is believed to aid in cardiac repair following myocardial injury.Here, we investigated the difference of protein cargo content among extracellular vesicles from wild type C-MSC, Notch1 knock out C-MSC and Notch1 activated C-MSC.

INSTRUMENT(S): Orbitrap Fusion

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Mesenchymal Cell

SUBMITTER: Wanling Xuan

LAB HEAD: Muhammad Ashraf

PROVIDER: PXD016578 | Pride | 2020-05-27

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	Exo_S1-EV-C-MSCNotch1FF.raw	Raw
	Exo_S1-EV-C-MSCNotch1FF.xlsx	Xlsx
	Exo_S1.msf	Msf
	Exo_S2-EV-C-MSCNotch1FF.raw	Raw
	Exo_S2-EV-C-MSCNotch1FF.xlsx	Xlsx

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Extracellular Vesicles From Notch Activated Cardiac Mesenchymal Stem Cells Promote Myocyte Proliferation and Neovasculogenesis.

Xuan Wanling W Khan Mahmood M Ashraf Muhammad M

Frontiers in cell and developmental biology 20200221

Cardiac mesenchymal stem cells (C-MSCs) are a novel mesenchymal stem cell (MSC) subpopulation derived from cardiac tissue, which are reported to be responsible for cardiac regeneration. Notch signaling is believed to aid in cardiac repair following myocardial injury. In this study, we have investigated the role of extracellular vesicles (EVs) from Notch1 engineered C-MSCs on angiogenesis and cardiomyocyte (CM) proliferation in ischemic myocardium. C-MSCs were isolated from Notch1<sup>flox</sup> ...[more]

PMID: 32154243

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Project description:In this study, we explored the transcriptomic consequences of strong activation of the Notch pathway in embryonic human neural stem cells and in gliomas. For this we used a forced expression of the Notch intracellular domain (NICD). Glioblastoma multiforms (GBMs) are highly vascularized brain tumors containing a subpopulation of multipotent cancer stem cells. These cells closely interact with endothelial cells in neurovascular niches. In this study we have uncovered a close link between the Notch1 pathway and the tumoral vascularization process of GBM stem cells. We observed that although the Notch1 receptor was activated, the typical target proteins (HES5, HEY1, HEY2) were not or barely expressed in two explored GBM stem cell cultures. Notch1 signalling activation by expression of the intracellular form (NICD) in these cells was found to reduce their growth rate and migration which was accompanied by the sharp reduction of neural stem cell transcription factor expression (ASCL1, OLIG2, SOX2) while HEY1/2, KLF9, SNAI2 transcription factors were upregulated. Expression of OLIG2 and growth were restored after termination of Notch1 stimulation. Remarkably, NICD expression induced the expression of pericyte cell markers (NG2, PDGFRb and a-smooth muscle actin (aSMA)) in GBM stem cells. This was paralleled with the induction of several angiogenesis-related factors most notably cytokines (HB-EGF, IL8, PLGF), metalloprotease (MMP9) and adhesion proteins (VCAM-1, ICAM-1, ITGA9). In xenotransplantation experiments, contrasting with the infiltrative and poorly-vascularized tumors obtained with control GBM stem cells, Notch1 stimulation resulted in poorly-disseminating but highly-vascularized grafts containing large vessels with lumen. Notch1-stimulated GBM cells expressed pericyte cell markers and closely associated with endothelial cells. These results reveal an important role for the Notch1 pathway in regulating GBM stem cell plasticity and angiogenic properties. Embryonic human neural progenitors obtained from Lonza, the U87 glioma cell line, and glioma cancer stem cells (Gb4 and Gb7) characterized in Guichet et al. (Glia, 2013, 61(2), 225-39) were infected with lentiviruses expressing YFP or YFP-IRES-NICD (activated form of Notch receptor). After 48h, RNA were extracted for Affymetrix microarray analysis.