CD13 and ROR2 permit isolation of highly enriched cardiac mesoderm from differentiating human embryonic stem cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE74665 | GEO | 2015/11/05
SECONDARY ACCESSION(S): PRJNA301125
REPOSITORIES: GEO
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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+/α-MHC+ and 13R2+/NKX2-5+/MHC- from day 14
2015-11-05 | E-GEOD-74665 | biostudies-arrayexpress
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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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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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. Method: RNA was isolated from resting peritoneal or bone marrow derived macrophages from wild type or CD13 null mice using Trizol according to the manufacturer’s protocol. For quality control, RNA purity and integrity was evaluated by denaturing gel electrophoresis, OD 260/280 ratio and analysis on an Agilent 2100 Bioanalyzer (Agilent Technologies, Palo Alto, CA). Total RNA was amplified and purified using the Ambion Ilumina RNA amplification kit (Ambion, www.ambion.com). Briefly, 300 ng of total RNA was reverse transcribed to cDNA using a T7 oligo(dT) primer. Second-strand cDNA was synthesized, in vitro transcribed and labeled with biotin-16-UTP. The labeled cRNA was analyzed on the Agilent 2100 Bioanalyzer and quantitated by Nanodrop analysis (www.nanodrop.com). The labeled cRNAs were hybridized to the Mouse WholeGenome- 6 BeadChip (Illumina Inc.,) for 16 hours at 58°C, as per manufacturer's instructions. The BeadChips were washed, stained with streptavidin-Cy3 and scanned on the Illumina BeadArray Reader. Analysis: Microarray data was extracted, normalized and analyzed using Illumina GenomeStudio software. Illumina MouseWG-6 v 2.0 Expression BeadChip (Illumina, San Diego, CA) contains 50-mer gene specific oligonucleotide probes corresponding to 45,281 mouse transcript variants. There is on average a 30-fold redundancy for each transcript per array. Intensity data were normalized using the Quantile algorithm in GenomeStudio. Differential expression of each gene, relative to the respective control was evaluated using the Illumina custom error model that calculates a p value as a function of intensity, differential and biological, technical and nonspecific variation. Those samples with p values less than 0.05 were deleted, the relative expression of CD13 null vs. wild type calculated and expressed as fold wild type, and the data ranked from low to high expression relative to wild type values. The dataset was further analyzed using the Ingenuity Pathway Analysis software (Ingenuity Systems, http://www.ingenuity.com).
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