Inhibition of lymphangiogenesis with resulting lymphedema in transgenic mice expressing soluble VEGF receptor-3
By Taija Mäkinen, L. Jussila, Tanja Veikkola, Terhi Karpanen, M. Kettunen, K. Pulkkanen, R. Kauppinen, D. Jackson, H. Kubo, S. Nishikawa and 2 more. Nature Medicine, 2001
816 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology, Physiology
View Paper: https://www.semanticscholar.org/paper/15ea19aab9c0ccb27b9010b20b43a1e3c9384b54
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Citations in the corpus
- CCBE1 Enhances Lymphangiogenesis via A Disintegrin and Metalloprotease With Thrombospondin Motifs-3–Mediated Vascular Endothelial Growth Factor-C Activation (2014, methodology): “Ba/F3-VEGFR/EpoR Assays The Ba/F3-hVEGFR-3/EpoR,(13) Ba/F3-mVEGFR-2/EpoR(14) and Ba/ F3-hVEGFR-2/EpoR bioassays were performed with conditioned cell culture medium as described.(15) Stimulation of VEGFR-3 Phosphorylation”
- Pathogenesis of persistent lymphatic vessel hyperplasia in chronic airway inflammation. (2005, neutral): “More recent studies show that lymphangiogenesis can be stimulated or inhibited by agonists or antagonists of VEGFR-3 signaling independent of angiogenesis (32, 33).”
- Interstitial fluid and lymph formation and transport: physiological regulation and roles in inflammation and cancer. (2012, background): “Wiig, unpublished data), another model of primary lymphedema (281).”
- Biology of vascular endothelial growth factors (2006, background): “2) Transgenic mice overexpressing a soluble VEGFR-3-Ig fusion protein in the skin lack dermal lymphatic vessels [46].”
- Lymphangiogenesis: Molecular mechanisms and future promise. (2010, background): “5 onward in mouse embryos results in severe hypoplasia of the lymphatic vessels (Makinen et al., 2001), indicating that VEGF-C/VEGFR-3 signaling plays a key role in further development of the lymphatic vascular tree following formation of the lymph sacs.”