The effects of T-DPSC-conditioned media on human umbilical vein endothelial cell proliferation and migration were examined by MTT, wound healing, and trans-well migration assay.
[Stem Cell Research & Therapy]
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Scientists silenced Syndecan-1 in TNBC cell lines using a 3D human umbilical vein endothelial cell co-culture system to study its role in angiogenesis.
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Nassar, E., Hassan, N., El-Ghonaimy, E. A., Hassan, H., Abdullah, M. S., Rottke, T. V., Kiesel, L., Greve, B., Ibrahim, S. A., & Götte, M. (2021). Syndecan-1 Promotes Angiogenesis in Triple-Negative Breast Cancer through the Prognostically Relevant Tissue Factor Pathway and Additional Angiogenic Routes. Cancers, 13(10), 2318. https://doi.org/10.3390/cancers13102318 Cite
Using three-dimensional structured illumination microscopy, scientists observed that the mitochondrial protein Mitofusin-2 (Mfn2) co-localized at the plasma membrane with VE-cadherin and β-catenin in endothelial cells during homeostasis.
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Kim, Y.-M., Krantz, S., Jambusaria, A., Toth, P. T., Moon, H.-G., Gunarathna, I., Park, G. Y., & Rehman, J. (2021). Mitofusin-2 stabilizes adherens junctions and suppresses endothelial inflammation via modulation of β-catenin signaling. Nature Communications, 12(1), 2736. https://doi.org/10.1038/s41467-021-23047-6 Cite
Scientists found a decrease in endothelial cells and an increase in cells co-expressing CD31 and α-smooth muscle actin at eight weeks in heart tissue of mice subjected to transverse aortic constriction, which implied EndMT.
[Cell Death & Disease]
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Zhang, L., He, J., Wang, J., Liu, J., Chen, Z., Deng, B., Wei, L., Wu, H., Liang, B., Li, H., Huang, Y., Lu, L., Yang, Z., Xian, S., & Wang, L. (2021). Knockout RAGE alleviates cardiac fibrosis through repressing endothelial-to-mesenchymal transition (EndMT) mediated by autophagy. Cell Death & Disease, 12(5), 1–13. https://doi.org/10.1038/s41419-021-03750-4 Cite
Scientists showed that PACSIN2 recruited the trafficking regulators EHD4 and MICAL-L1 to the rear end of asymmetric adherens junctions to form a recycling endosome-like tubular structure.
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Malinova, T. S., Angulo-Urarte, A., Nüchel, J., Tauber, M., van der Stoel, M. M., Janssen, V., de Haan, A., Groenen, A. G., Tebbens, M., Graupera, M., Plomann, M., & Huveneers, S. (2021). A junctional PACSIN2/EHD4/MICAL-L1 complex coordinates VE-cadherin trafficking for endothelial migration and angiogenesis. Nature Communications, 12(1), 2610. https://doi.org/10.1038/s41467-021-22873-y Cite
Researchers determined the contributions of FUNDC1-mediated MAMs to angiogenesis in vitro and in vivo. In cultured endothelial cells, VEGF significantly increased the formation of MAMs and MAM-related proteins, including FUNDC1.
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Scientists consider a gamut of attractive possibilities for modifying inflammation in atherosclerosis, including targeting pivotal inflammatory pathways such as the inflammasomes, inhibiting cytokines, manipulating adaptive immunity and promoting pro-resolution mechanisms.
[Nature Reviews Drug Discovery]
Vascularized dental pulp stem cells (DPSC) constructs were fabricated by inducing endothelial differentiation, and then scientist investigated the behavior of differentiated DPSCs, the internal structure of cell constructs, and their pulp regenerative ability in vivo.
[Journal of Dental Research]
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Scientists measured the susceptibility to infection, immune response, and expression of adhesion molecules, in human pulmonary microvascular endothelial cells exposed to conditioned medium from infected epithelial cells.
[Clinical Infectious Diseases]
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Researchers identified trafficking pathways that regulated collagen type IV (Col IV) deposition during angiogenic blood vessel development. They have identified the GTPase Rab10 as a major regulator of Col IV vesicular trafficking during vascular development using both in vitro imaging and biochemistry as well as in vivo models.
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Gross, S. J., Webb, A. M., Peterlin, A. D., Durrant, J. R., Judson, R. J., Raza, Q., Kitajewski, J. K., & Kushner, E. J. (2021). Notch regulates vascular collagen IV basement membrane through modulation of lysyl hydroxylase 3 trafficking. Angiogenesis. https://doi.org/10.1007/s10456-021-09791-9 Cite
Researchers investigated the involvement of histone deacetylases (HDACs) in the regulation of Robo4 expression. An HDAC inhibitor, MS-275, which inhibits HDAC1, HDAC2, and HDAC3, was found to suppress Robo4 expression in endothelial cells.
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Kashio, T., Shirakura, K., Kinoshita, M., Morita, M., Ishiba, R., Muraoka, K., Kanbara, T., Tanaka, M., Funatsu, R., Hino, N., Koyama, S., Suzuki, R., Yoshioka, Y., Aoshi, T., Doi, T., & Okada, Y. (2021). HDAC inhibitor, MS-275, increases vascular permeability by suppressing Robo4 expression in endothelial cells. Tissue Barriers, 0(0), 1911195. https://doi.org/10.1080/21688370.2021.1911195 Cite