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A Novel Population of Human Cardiac Resident Mesenchymal Stem Cells

ABSTRACT: We describe a novel population of human adult cardiac resident stem cells (CRSCs), which are positive for W8B2 antigen, originating from human adult atrial appendages. W8B2+ CRSCs exhibit a spindle-shaped morphology, are clonogenic and able to self-renew. W8B2+ CRSCs show high expression of mesenchymal but not hematopoietic nor endothelial markers. W8B2+ CRSCs expressed GATA4, HAND2, and TBX5, but not C-KIT, SCA-1, NKX2.5, PDGFRα, ISL1 or Wilm’s tumor gene-1 (WT1). W8B2+ CRSCs can differentiate into the cardiovascular lineages and secrete various cytokines.

ORGANISM(S): Homo sapiens

PROVIDER: GSE62288 | GEO | 2014/10/15

SECONDARY ACCESSION(S): PRJNA263766

REPOSITORIES: GEO

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A Novel Population of Human Cardiac Resident Mesenchymal Stem Cells

Project description:We describe a novel population of human adult cardiac resident stem cells (CRSCs), which are positive for W8B2 antigen, originating from human adult atrial appendages. W8B2+ CRSCs exhibit a spindle-shaped morphology, are clonogenic and able to self-renew. W8B2+ CRSCs show high expression of mesenchymal but not hematopoietic nor endothelial markers. W8B2+ CRSCs expressed GATA4, HAND2, and TBX5, but not C-KIT, SCA-1, NKX2.5, PDGFR?, ISL1 or Wilm’s tumor gene-1 (WT1). W8B2+ CRSCs can differentiate into the cardiovascular lineages and secrete various cytokines. Comparative RNA sequencing was performed using W8B2+ cell from human atrial appendages (passage 2 from 3 different patients), c-Kit+ cell from human atrial appendages (passage 2 from 3 different patients) and W8B2+ cell from bone marrow (passage 3 from 2 different patients, from PromoCell, Heidelberg, Germany).

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Project description:We show that cardiac-specific RNA-sequencing studies reveal a disrupted embryonic Nkx2.5 transcriptional profile despite histologically normal, Nkx2.5 loss-of-function adult myocardium. Yet, adult nkx2.5-/- fish exhibit an impaired ability to recover following ventricular apex amputation as illustrated by retention of fibrin and collagen in the injured area. Complex network analyses illuminate that Nkx2.5 is required to mount a proliferative response for cardiomyocyte renewal and to provoke proteolytic pathways necessary for sarcomere disassembly. Moreover, direct Nkx2.5 targets embedded in these distinct gene regulatory modules coordinate appropriate, multi-faceted injury responses. Altogether, our findings support a previously unrecognized, Nkx2.5-dependent regenerative circuit that invokes myocardial proliferation and dedifferentiation to ensure effective regeneration in the teleost heart.

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