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vegfc (show VEGFC Proteins) and vegfd cooperatively control lymphangiogenesis throughout the embryo, including during the formation of the trunk lymphatic vasculature. Interestingly, we find that vegfd and vegfc (show VEGFC Proteins) also redundantly drive artery hyperbranching phenotypes observed upon depletion of Flt1 (show FLT1 Proteins) or Dll4 (show DLL4 Proteins).
Vegfd can compensate for loss of Vegfc (show VEGFC Proteins) in zebrafish facial lymphatic sprouting.
VEGFD-mediated pathologies include or involve an underlying dysregulation of SOXF-mediated transcriptional networks.
Our studies therefore identified the first non-mammalian VEGF-D and established its in vivo role for vascular system development during vertebrate embryogenesis and provided an alternative animal model to further reveal functions of VEGF-D.
lymphangiogenesis is regulated by two distinct proteolytic mechanisms of ligand activation: one in which VEGFC (show VEGFC Proteins) activation by ADAMTS3 (show Adamts2 Proteins) and CCBE1 (show CCBE1 Proteins) spatially and temporally patterns developing lymphatics, and one in which VEGFD activation by a distinct proteolytic mechanism may be stimulated during inflammatory lymphatic growth
This study uncovers a reciprocal relationship between dendrite geometry, the ability to generate nuclear calcium transients in response to synaptic inputs, and the subsequent induction of expression of plasticity-related and dendritic structure-preserving genes. Insufficient nuclear calcium signaling in CA1 (show CA1 Proteins) hippocampal neurons and, consequently, reduced expression of the nuclear calcium target gene VEGFD.
Overexpression of VEGFD causes lymphatic hyperplasia in lung, kidney, and brown adipose tissue. Overexpression of VEGFD in white adipose tissue causes a de novo lymphatic network.
Vegf-d promotes oedema in response to hyperoxia in mice and support the hypothesis that VEGF-D signalling promotes vascular leak in human hyperoxic acute lung injury (HALI).
VEGF-D may be beneficial in early-stage tumors since it suppresses the pro-tumorigenic inflammation, while at later stages VEGF-D-induced tumor lymphatics provide a route for metastasis.
These results suggest that lymph node lymphangiogenesis occurs before metastasis in OSCC. VEGF-A (show VEGFA Proteins) and VEGF-D play critical roles in this process.
Results provided evidence that IL-7 (show IL7 Proteins)/IL-7R induce VEGF-D upregulation and promote lymphangiogenesis via c-Fos/c-Jun (show JUN Proteins) pathway in lung cancer.
Epidermal keratinocyte proliferation in vitro was not affected by VEGF-C (show VEGFC Proteins) or VEGF-D.
Neutrophils contribute to lymphangiogenesis primarily by modulating VEGF-A (show VEGFA Proteins) bioavailability and bioactivity and, to a lesser extent, secreting VEGF-D. Neutrophils increased VEGF-A (show VEGFA Proteins) bioavailability and bioactivity via the secretion of MMP9 (show MMP9 Proteins) and heparanase (show HPSE Proteins).
Vegf-d deficiency alters the caliber of initial lymphatics in the dermis leading to reduced functional capacity.
High VEGFD expression is associated with lymphangioleiomyomatosis.
Data show that VEGF-C (show VEGFC Proteins), VEGF-D, and VEGFR-3 (show FLT4 Proteins) were expressed in a substantial percentage of breast carcinomas.
High VEGFD expression is associated with angiogenesis and lymphangiogenesis.
VEGF-D and its receptors were co-localized on blood vessels in clinical samples of human lungs exposed to hyperoxia; hence, VEGF-D may act directly on blood vessels to promote fluid leak.
VEGF-D-enhanced metastasis was evidently reversed by MP. MP significantly reduced the invasion of VEGFD-SK cells, tumor volume, lymphatic metastasis rates and lymphatic vessel density compared with control groups
Sulf2 (show SULF2 Proteins) facilitated lymphangiogenesis in breast cancer cells by regulating VEGF-D and that the AKT1related signaling pathway was involved.
Data indicate that vascular endothelial growth factor D (VEGF-D) was the best indicator of metastasis and vascular endothelial growth factors and receptor-3 (VEGFR-3 (show FLT4 Proteins)) may help to determine the prognosis and management of colorectal cancer (CRC (show CALR Proteins)).
Taken together, our data suggest that TNF-alpha (show TNF Proteins) can promote lymphangiogenesis and lymphatic metastasis of GBC through the ERK1/2/AP-1 (show FOSB Proteins)/VEGF-D pathway.
VEGF-D may play an important role in the process of lymphatic metastasis of epithelial ovarian cancer
CCL21 (show CCL21 Proteins)/CCR7 (show CCR7 Proteins) induce VEGF-D up-regulation and promote lymphangiogenesis via ERK (show EPHB2 Proteins)/Akt (show AKT1 Proteins) pathway in lung cancer.
The protein encoded by this gene is a member of the platelet-derived growth factor/vascular endothelial growth factor (PDGF/VEGF) family and is active in angiogenesis, lymphangiogenesis, and endothelial cell growth. This secreted protein undergoes a complex proteolytic maturation, generating multiple processed forms which bind and activate VEGFR-2 and VEGFR-3 receptors. This protein is structurally and functionally similar to vascular endothelial growth factor C. Read-through transcription has been observed between this locus and the upstream PIR (GeneID 8544) locus.
c-fos induced growth factor (vascular endothelial growth factor D)
, vascular endothelial growth factor D
, vascular enthelial growth factor D
, vegf d
, Vascular endothelial growth factor D
, c-fos-induced growth factor