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Global gene expression profile of human placental pericytes

ABSTRACT: The objective of this array was to determine the global gene expression profile of human placental pericytes for comparison with other publicly available arrays of pericytes and mesenchymal stromal cells isolated from various human tissues. Pericytes are critical cellular components of the microvasculature that play a major role in vascular development and pathologies, yet their study has been hindered by lack of a standardized method for their isolation and growth. Here we report a method for culturing human pericytes from a readily available tissue source, placenta, and provide a thorough characterization of resultant cell populations. We developed an optimized protocol for obtaining pericytes by outgrowth from microvessel fragments recovered after enzymatic digestion of human placental tissue. We characterized outgrowth populations by immunostaining, by gene expression analysis, and by functional evaluation of cells implanted in vivo. Our approach yields human pericytes that may be serially expanded in culture and that uniformly express the cellular markers NG2, CD90, CD146, α-SMA, and PDGFR-β, but lack markers of smooth muscle cells, endothelial cells, and leukocytes. When co-implanted with human endothelial cells into C.B-17 SCID/bg mice, human pericytes invest and stabilize developing human endothelial cell-lined microvessels. We conclude that our method for culturing pericytes from human placenta results in the expansion of functional pericytes that may be used to study a variety of questions related to vascular biology.

ORGANISM(S): Homo sapiens

PROVIDER: GSE21332 | GEO | 2010/04/14

SECONDARY ACCESSION(S): PRJNA126161

REPOSITORIES: GEO

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Global gene expression profile of human placental pericytes

Project description:The objective of this array was to determine the global gene expression profile of human placental pericytes for comparison with other publicly available arrays of pericytes and mesenchymal stromal cells isolated from various human tissues. Pericytes are critical cellular components of the microvasculature that play a major role in vascular development and pathologies, yet their study has been hindered by lack of a standardized method for their isolation and growth. Here we report a method for culturing human pericytes from a readily available tissue source, placenta, and provide a thorough characterization of resultant cell populations. We developed an optimized protocol for obtaining pericytes by outgrowth from microvessel fragments recovered after enzymatic digestion of human placental tissue. We characterized outgrowth populations by immunostaining, by gene expression analysis, and by functional evaluation of cells implanted in vivo. Our approach yields human pericytes that may be serially expanded in culture and that uniformly express the cellular markers NG2, CD90, CD146, α-SMA, and PDGFR-β, but lack markers of smooth muscle cells, endothelial cells, and leukocytes. When co-implanted with human endothelial cells into C.B-17 SCID/bg mice, human pericytes invest and stabilize developing human endothelial cell-lined microvessels. We conclude that our method for culturing pericytes from human placenta results in the expansion of functional pericytes that may be used to study a variety of questions related to vascular biology. Total RNA from three different pericyte isolations at subculture 1 was collected and examined for relative gene expression.

2010-04-14 | E-GEOD-21332 | biostudies-arrayexpress

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Project description:alpha2-adrenoceptors are essential presynaptic regulators of norepinephrine release from sympathetic nerves. Previous studies in mice with targeted deletions in the three alpha2-adrenoceptor genes have indicated that these receptors are essential for embryonic development. In the present study, we searched for the alpha2-adrenoceptor subtype(s) involved in placental development and its molecular mechanism using mice carrying targeted deletions in alpha2-adrenoceptor genes. Congenic alpha2B-adrenoceptor-deficient mice (Adra2b-/-) developed a defect in fetal and maternal vessel formation in the placenta labyrinth at embryonic day E10.5. This defect was accompanied by reduced endothelial cell proliferation and decreased ERK1/2 phosphorylation levels in Adra2b-/- as compared with Adra2b+/+ placenta. Microarray analysis of wild-type and mutant placentae (maternal genotype Adra2b+/-) revealed 179 genes which were significantly up- or downregulated >1.5-fold in alpha2B-deficient placenta. The type 1 receptor for vascular endothelial growth factor (Flt1), which is coexpressed with alpha2B-adrenoceptors in spongiotrophoblast and giant cells of the placenta, was found to be 2.3-fold upregulated in alpha2B-deficient placenta. Neutralization of Flt1 and its soluble splice variant sFlt1 by a specific antibody in vivo prevented the vascular defect in alpha2B-deficient placenta at E10.5. Thus, alpha2B-adrenoceptors are essential to suppress antiangiogenic (s)Flt1 in spongiotrophoblasts to control the coordinated formation of a vascular labyrinth of fetal and maternal blood vessels in the murine placenta during development. Experiment Overall Design: Comparative transcriptome analysis was determined using the GeneChip Mouse Genome 430 2.0 Array (Affymetrix, Santa Clara, CA, USA). Six microarrays from three wild-type and three adra2b deficient mice were performed.

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Imatinib Disrupts Lymphoma Angiogenesis by Targeting Vascular Pericytes

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