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Molecular and cellular effects of in vitro shockwave treatment on lymphatic endothelial cells

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): Mus musculus Rattus norvegicus Homo sapiens

PROVIDER: GSE62748 | GEO | 2014/10/28

SECONDARY ACCESSION(S): PRJNA265036

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

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

2014-10-20 | GSE62510 | GEO

KSHV vIRF3 promotes angiogenesis of lymphatic endothelial cells (LECs)

Project description:Herein, we report viral interferon regulatory factor 3 (vIRF3) as a pro-angiogenic factor together with HDAC5 that coordinates with LEC transcriptome, thus resulting in hyper-sprouting formation and ultimately leading to abnormal lymphangiogenesis. Overexpression of vIRF3 in LECs but not blood endothelial cells (BECs) exhibited a unique KSHV-associated angiogenic effect, evidenced by elongated spindle shape, sprouting, and tube formation. Furthermore, using vIRF3 knockout recombinant KSHV, we confirmed that vIRF3 is a critical factor of KSHV-mediated lymphangiogenesis in primary LECs.

2017-12-19 | GSE102132 | GEO

Molecular profiling of lymphatic endothelial cells activation in vitro

Project description:The lymphatic vascular system plays a key role in cancer progression. Indeed, the activation of lymphatic endothelial cells (LECs) through the lymphangiogenic process allows the formation of new lymphatic vessels (LVs) that represent the major route for dissemination of solid tumors. This process is governed by a plethora of cancer-derived and microevironmental mediators that strictly activate and control specific molecular pathways in LECs. In this work we used an in vitro model of LEC activation to trigger lymphangiogenesis using a mix of recombinant pro-lymphangiogenic factors (VFS) and a co-culture system with human melanoma cells. Both systems efficiently activated LECs, and under these experimental conditions RNA sequencing was exploited to unveil the transcriptional profile of activated LECs. Our data demonstrate that both recombinant and tumor cell-mediated activation trigger significant molecular pathways associated with endothelial activation, morphogenesis and cytokine-mediated signaling. In addition, this system provides information on new genes to be further investigated in the lymphangiogenesis process and open the possibility for further exploitation in other tumor contexts where lymphatic dissemination plays a relevant role.

2023-12-13 | GSE247178 | GEO

Transcriptional profiling of ex vivo isolated inflammed mouse lymphatic endothelial cells

Project description:Chemokines and adhesion molecules upregulated in lymphatic endothelial cells (LECs) during tissue inflammation are believed to enhance dendritic cell (DC) migration to draining lymph nodes (dLNs), but the in vivo control of this process is not well understood. By performing transcriptional profiling of LECs isolated from murine skin, we found that inflammation induced by a contact hypersensitivity (CHS) response upregulated the adhesion molecules ICAM-1 and VCAM-1 and inflammatory chemokines in LECs. Furthermore, lymphatic lineage markers like Prox-1, VEGFR3 and LYVE-1 were significantly downregulated during CHS. By contrast, skin inflammation induced by Complete FreundM-bM-^@M-^Ys adjuvant (CFA) induced a different pattern of chemokine and lymphatic marker gene expression and almost no ICAM-1 up-regulation in LECs. In FITC painting experiments, DC migration to dLNs was more strongly increased in CFA- as compared to CHS-induced inflammation. Interestingly, DC migration did not correlate with the induction of CCL21 and ICAM-1 in LECs. However, the requirement for CCR7 signaling became further pronounced during inflammation, whereas CCR7-independent signals only had a minor role in enhancing DC migration. Collectively, these findings indicate that inflammation-induced DC migration is stimulus-dependent and only moderately enhanced by LEC-induced genes other than CCL21. Mouse ear skin single-cell suspensions were prepared by a fast protocol that minimizes the RNA degradation. Fluorescence-activated cell sorting (FACS) was used to sort lymphatic endothelial cells (LEC) from CHS inflammed and control skin. 4 pairs (each with one control and one CHS inflammed sample, sorted and extracted on the same day) of LECs were chosen based on the quality of extracted and amplified material. This gave 8 samples to analyze (4 biological replicates in each condition). Each sample was sorted from 3 mice.

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

Profiling of filarial induced genes in lymphatic endothelial cells

Project description:To observe the global changes in the lymphatic endothelial cells upon exposure to filarial antigens or parasites, LECs were stimulated for 24, 48, and 72hrs and the expression profiles were carried out. Human filarial parasites Brugia malayi and Wuchereria bancrofti habitat the lymphatics and cause lymphatic dilatation and lymphedema. In order to evaluate the effect of various stage specific effects on the lymphatic endothelial cells (LEC) and understand how they modulate the lymphatic dysfunction, LECs were stimulated in antigens derived from the Brugia malayi. These are preliminary time course data towards understanding how the filarial antigens induce lymphangiogenesis.

2010-05-19 | E-GEOD-15454 | biostudies-arrayexpress

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.

2022-07-13 | GSE189084 | GEO

Atlas of lymphangiogenesis [scRNA-Seq]

Project description:During development, lymphatic vasculature forms as a second and distinct network that derives from embryonic blood vessels. Transdifferentiation of venous endothelial cells into specified lymphatic endothelial cells (LECs) is the first step in this process. Transdifferentiation and specification of LEC fate requires Prox1, but how Prox1 regulates transdifferentiation and differentiation is not fully understood. We present a single cell transcriptomic atlas of lymphangiogenesis spanning four key developmental stages that reveals new markers and functional regulators of lymphatic development. We extend this to comprehensively profile single cell transcriptomic and chromatin changes controlled by Prox1 using zygotic prox1a mutants, which form lymphatics that then dedifferentiate. Combining this with single cell analysis of Prox1-null, double prox1a/prox1b maternal zygotic mutants, we reveal in depth the role of Prox1 in control of LEC fate specification and differentiation. This resource reveals dual and progressive functions for Prox1, blocking blood vascular and hematopoietic fate while simultaneously up-regulating a small number of early acting genes that include tspan18a/b and lgals3a/b which are essential for lymphangiogenesis. This embryonic developmental resource will serve as a baseline to better understand both developmental and pathological lymphangiogenesis in the future. [Citations in sample metadata correspond to reference numbers in the associated publication.]

2023-04-27 | GSE188341 | GEO

Atlas of lymphangiogenesis [scATAC-Seq]

2023-04-27 | GSE188340 | GEO

Transcriptional profiling of ex vivo isolated inflammed mouse lymphatic endothelial cells

Project description:Chemokines and adhesion molecules upregulated in lymphatic endothelial cells (LECs) during tissue inflammation are believed to enhance dendritic cell (DC) migration to draining lymph nodes (dLNs), but the in vivo control of this process is not well understood. By performing transcriptional profiling of LECs isolated from murine skin, we found that inflammation induced by a contact hypersensitivity (CHS) response upregulated the adhesion molecules ICAM-1 and VCAM-1 and inflammatory chemokines in LECs. Furthermore, lymphatic lineage markers like Prox-1, VEGFR3 and LYVE-1 were significantly downregulated during CHS. By contrast, skin inflammation induced by Complete Freund’s adjuvant (CFA) induced a different pattern of chemokine and lymphatic marker gene expression and almost no ICAM-1 up-regulation in LECs. In FITC painting experiments, DC migration to dLNs was more strongly increased in CFA- as compared to CHS-induced inflammation. Interestingly, DC migration did not correlate with the induction of CCL21 and ICAM-1 in LECs. However, the requirement for CCR7 signaling became further pronounced during inflammation, whereas CCR7-independent signals only had a minor role in enhancing DC migration. Collectively, these findings indicate that inflammation-induced DC migration is stimulus-dependent and only moderately enhanced by LEC-induced genes other than CCL21.

2011-05-20 | GSE26229 | GEO

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