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CD13 and ROR2 permit isolation of highly enriched cardiac mesoderm from differentiating human embryonic stem cells

ABSTRACT: The resultant heat map demonstrates the maturation of CD13+/ROR2+ cells as they proceed through cardiac differentiation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE74665 | GEO | 2015/11/05

SECONDARY ACCESSION(S): PRJNA301125

REPOSITORIES: GEO

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CD13 and ROR2 permit isolation of highly enriched cardiac mesoderm from differentiating human embryonic stem cells

Project description:The resultant heat map demonstrates the maturation of CD13+/ROR2+ cells as they proceed through cardiac differentiation. RNA-seq analysis was preformed on RNA samples from undifferentiated hESCs, 13R2+ and 13R2- populations from day 3, 13R2+/NKX2-5+ and 13R2+/NKX2-5- from day 7, and 13R2+/NKX2-5+/Î±-MHC+ and 13R2+/NKX2-5+/MHC- from day 14

2015-11-05 | E-GEOD-74665 | biostudies-arrayexpress

CD13 and ROR2 Permit Isolation of Highly Enriched Cardiac Mesoderm from Differentiating Human Embryonic Stem Cells.

Project description:The generation of tissue-specific cell types from human embryonic stem cells (hESCs) is critical for the development of future stem cell-based regenerative therapies. Here, we identify CD13 and ROR2 as cell-surface markers capable of selecting early cardiac mesoderm emerging during hESC differentiation. We demonstrate that the CD13+/ROR2+ population encompasses pre-cardiac mesoderm, which efficiently differentiates to all major cardiovascular lineages. We determined the engraftment potential of CD13+/ROR2+ in small (murine) and large (porcine) animal models, and demonstrated that CD13+/ROR2+ progenitors have the capacity to differentiate toward cardiomyocytes, fibroblasts, smooth muscle, and endothelial cells in vivo. Collectively, our data show that CD13 and ROR2 identify a cardiac lineage precursor pool that is capable of successful engraftment into the porcine heart. These markers represent valuable tools for further dissection of early human cardiac differentiation, and will enable a detailed assessment of human pluripotent stem cell-derived cardiac lineage cells for potential clinical applications.

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RNA expression profiling of CD13/CD33-positive and CD13/CD33-negative B-ALL patients [miRNA expression]

Project description:To study the effect of expression of CD13/CD33 on the pathogenesis of B-cell acute lymphoblastic (B-ALL), we collected samples from 4 CD13/CD33-positive and 4 CD13/CD33-negative B-ALL patients and performed RNA-seq.

2023-12-31 | GSE197180 | GEO

RNA expression profiling of CD13/CD33-positive and CD13/CD33-negative B-ALL patients [mRNA expression]

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Transcriptomic analysis of primary CD105+CD90+CD13- and CD105+CD90+CD13+ mesenchymal cells in human lung

Project description:Primary mesenchymal CD105+CD90+CD13- and CD105+CD90+CD13+ populations from human lung were isolated and characterized using bulk population mRNA sequencing to understand differences between these populations.

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Comparison of gene expression in CD13 wild type versus Knock out Macrophages

Project description:The robust and consistent expression of the CD13 cell surface marker on very early as well as differentiated myeloid hematopoietic cells has prompted numerous investigations seeking to define roles for CD13 in myeloid cells. To directly address the function of myeloid CD13 we created a CD13 null mouse and assessed the responses of purified primary macrophages or dendritic cells from wild type and CD13 null animals in cell assays and inflammatory disease models where CD13 has been previously implicated. We find that mice lacking CD13 develop normally with normal hematopoietic profiles. Moreover, in in vitro assays, CD13 appears to be largely dispensable for the aspects of phagocytosis, proliferation and antigen presentation that we tested, but may contribute to adhesion to endothelial cells. In vivo assessment of four inflammatory disease models showed that lack of CD13 has little effect on disease onset or progression. Nominal alterations in gene expression levels between CD13 wild type and null macrophages argue against compensatory mechanisms. Analysis of the dataset with Ingenuity Pathway Analysis software did not suggest that loss of CD13 resulted in a purturbation of any specific biological pathways, processes or networks. Therefore, while CD13 is highly expressed on myeloid cells and is a reliable marker of the myeloid lineage of both normal and leukemic cells, it is not a critical regulator of hematopoietic development, hemostasis or myeloid cell function.

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Gene transcript alterations exhibited in luminal and basal epithelial compartments with impaired Ror2 signaling

Project description:Microarray analyses revealed distinct gene expression alterations in the luminal and basal epithelial compartments in the absence of Ror2 with marked alterations observed in genes associated with actin filament-based processes and the actin cytoskeletal network. Given that Ror2 expression resides in both basal and luminal epithelial cells, we wanted to identify compartment-specific functions for Ror2 in coordinating development. Accordingly, luminal and basal epithelial cell populations from shLUC and shRor2 outgrowths were isolated by FACS separation on the basis of CD24 and CD29 surface marker expression and gene expression analysis was subsequently performed using Agilent microarrays.

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Project description:ROR2 is a type I orphan-receptor tyrosine-kinase-like membrane protein. Its expression level is decreased after birth and barely detectable in adulthood. However, it is re-expressed by various cancer cells and is negatively correlated with patients' survival. The role of ROR2 in breast cancer is still unknown.This study demonstrated that ROR2 activates RhoA GTPase, and induces EMT in breast cancer. In addition, ROR2 is enriched in breast CSCs and required for maintaining the stemness features of CSCs. We developed a ROR2 specific antibody that inhibits breast cancer primary tumor growth and metastasis through targeting CSCs.

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Functional expression of membrane alanyl-aminopeptidase (CD13/APN) promotes tumor cell proliferation and neoangiogenesis in malignant gliomas.

Project description:Malignant gliomas are characterized by marked neovascularization and increased tumor cell proliferation. Recently, membrane alanyl-aminopeptidase (CD13/APN) has been identified to play a crucial role in neoangiogenesis. In this study, we show that among various central nervous system tumors, malignant astrocytomas are unique in their high expression levels of functionally active CD13/APN. CD13/APN was found in both tumor cells and tumor vessels of malignant astrocytomas, while in low-grade astrocytomas only endothelial cells of tumor vessels expressed CD13/APN. Inhibitors of the enzymatic activity of CD13/APN significantly reduced the proliferation of U87MG and U138MG malignant glioma cells. Inhibition of CD13/APN mRNA expression by siRNA in glioma cells co-cultured with human umbilical vein endothelial cells (HUVEC) effectively decreased blood vessel formation. Pro-angiogenic factors like bFGF and VEGF induced CD13/APN expression in glioma cells. Treatment of U87MG and U138MG cells with CD13/APN inhibitors resulted in an increased mRNA expression of VEGF and VEGF receptor 2 (VEGF-R2) in these cells. Taken together, these findings provide evidence that CD13/APN promotes tumor cell proliferation and blood vessel formation in malignant astrocytomas. Remarkably, inhibition of CD13/APN induces an angiogenic expression profile via an autocrine feed-back mechanism involving the VEGF/VEGF-R2 system in malignant gliomas.

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