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Expression data from two sorted lymphatic endothelial cell (LEC) populations, podoplanin-high versus podoplanin low

ABSTRACT: Extracorporeal shockwave treatment was shown to improve orthopaedic diseases, wound healing and to stimulate lymphangiogenesis in vivo. The aim of this study was to investigate in vitro shockwave treatment (IVSWT) effects on lymphatic endothelial cell (LEC) behavior and lymphangiogenesis. We analyzed migration, proliferation, vascular tube forming capability and marker expression changes of LECs after IVSWT compared with HUVECs. Finally, transcriptome- and miRNA analyses were conducted to gain deeper insight into the IVSWT-induced molecular mechanisms in LECs. The results indicate that IVSWT-mediated proliferation changes of LECs are highly energy flux density-dependent and LEC 2D as well as 3D migration was enhanced through IVSWT. IVSWT suppressed HUVEC 3D migration but enhanced vasculogenesis. Furthermore, we identified podoplaninhigh and podoplaninlow cell subpopulations, whose ratios changed upon IVSWT treatment. Transcriptome- and miRNA analyses on these populations showed differences in genes specific for signaling and vascular tissue. Our findings help to understand the cellular and molecular mechanisms underlying shockwave-induced lymphangiogenesis in vivo.

ORGANISM(S): Homo sapiens

PROVIDER: GSE62510 | GEO | 2014/10/20

SECONDARY ACCESSION(S): PRJNA264309

REPOSITORIES: GEO

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Expression data from two sorted lymphatic endothelial cell (LEC) populations, podoplanin-high versus podoplanin low

Project description:Extracorporeal shockwave treatment was shown to improve orthopaedic diseases, wound healing and to stimulate lymphangiogenesis in vivo. The aim of this study was to investigate in vitro shockwave treatment (IVSWT) effects on lymphatic endothelial cell (LEC) behavior and lymphangiogenesis. We analyzed migration, proliferation, vascular tube forming capability and marker expression changes of LECs after IVSWT compared with HUVECs. Finally, transcriptome- and miRNA analyses were conducted to gain deeper insight into the IVSWT-induced molecular mechanisms in LECs. The results indicate that IVSWT-mediated proliferation changes of LECs are highly energy flux density-dependent and LEC 2D as well as 3D migration was enhanced through IVSWT. IVSWT suppressed HUVEC 3D migration but enhanced vasculogenesis. Furthermore, we identified podoplaninhigh and podoplaninlow cell subpopulations, whose ratios changed upon IVSWT treatment. Transcriptome- and miRNA analyses on these populations showed differences in genes specific for signaling and vascular tissue. Our findings help to understand the cellular and molecular mechanisms underlying shockwave-induced lymphangiogenesis in vivo. Immortalized lymphatic endothelial cells were flow-sorted in two populations according to their differences in FSC and SSC values and subjected to Affymetrix analysis in triplicate samples

2014-10-20 | E-GEOD-62510 | biostudies-arrayexpress

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Transcription profiling of lymphatic endothelial cell subtypes expressing high and low levels of podoplanin

Project description:We microprepared native mammary skin resections from healthy female donors (breast size reduction) by a combination of enzymatic and mechanical treatment. The resulting suspensions of single dermal cells were then subjected to FACSorting using antibodies against the lymphovascular marker protein podoplanin and the panendothelial protein CD31 as positive and the leukocytic protein CD45 as negative markers. We aimed at separating lymphatic vascular endothelial cells (LECs) from blood vascular endothelial cells (BECs) in order to characterize their moelcular and functional phenotypes in health and disease. We found that lymphatic endothelial cells consisted of two instead of only one cell population. Their discrimination marker was high versus low expression of podoplanin surface protein, respectively. Especially, the low-podoplanin expressors were undescribed. Thus, we screened for their transcription profile using U133A. We identified specific marker genes and finally have assigned a specific function to the novel LEC subpopulation unknown up to now. Importantly, we did not use lysates from cell culture, but from ex vivo cells. Thus, there was no treatment of cells except processing the samples on ice.

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MCF-7 Cell Derived Soluble Factors Define Growth of Vascular and Lymphatic Endothelial Cells: Modulatory Role of miR193a

Project description:Angiogenesis and Lymphangiogenesis plays a key role in promoting tumor growth and breast cancer progression as well as metastasis. Active angiogenic process within the tumor tissue is known to promote cancer/tumor growth via nutrient supply, moreover, soluble molecules secreted by lymphatic endothelial cells (ECs) promotes tumor growth. Hence is feasible that paracrine factors generated by breast cancer cells play a role in regulating tumor neovascularization by lymphatic and vascular ECs. Here using cultured VECs and LECs assessed the paracrine impact of MCF-7 breast cancer derived soluble factors on LEC and VEC growth (cell number), gene expression (micro array) and angiogenic proteins (protein array). Moreover, we explored the modulatory actions of miR193 on LEC and VEC growth driven by MCF-7 derived conditioned medium (MCF7-CM). We demonstrate that MCF7-CM differentially modulates VEC and LEC growth, i.e. induces VEC growth and inhibits LEC growth. Moreover, the growth actions of MCF7-CM were accompanied with differential modulation VEC and LEC growth regulatory genes, that were further altered by miR193 a pretreatment of MCF7 cells. Our findings provide in-depth analysis of MCF7-CM altered genes relevant for angiogenesis and lymphogenesis. The fact that vascular capillaries support growth and lymphatic capillaries play a role counteracting cancer growth (kill cancer cells), together with our observation in VECs and LECs, suggests that MCF-7 breast cancer cells differentially modulate vascular and lymphatic growth to facilitate their survival and growth. Since miR193a abrogates the effects of MCF7-CM, it may be an effective therapeutic tool against breast cancer.

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2011-05-19 | E-GEOD-26229 | biostudies-arrayexpress

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