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vegfc (show VEGFC ELISA Kits) 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 ELISA Kits) also redundantly drive artery hyperbranching phenotypes observed upon depletion of Flt1 (show FLT1 ELISA Kits) or Dll4 (show DLL4 ELISA Kits).
Vegfd can compensate for loss of Vegfc (show VEGFC ELISA Kits) 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 ELISA Kits) activation by ADAMTS3 (show Adamts2 ELISA Kits) and CCBE1 (show CCBE1 ELISA Kits) 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 ELISA Kits) 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 ELISA Kits) and VEGF-D play critical roles in this process.
Results provided evidence that IL-7 (show IL7 ELISA Kits)/IL-7R induce VEGF-D upregulation and promote lymphangiogenesis via c-Fos/c-Jun (show JUN ELISA Kits) pathway in lung cancer.
Epidermal keratinocyte proliferation in vitro was not affected by VEGF-C (show VEGFC ELISA Kits) or VEGF-D.
Neutrophils contribute to lymphangiogenesis primarily by modulating VEGF-A (show VEGFA ELISA Kits) bioavailability and bioactivity and, to a lesser extent, secreting VEGF-D. Neutrophils increased VEGF-A (show VEGFA ELISA Kits) bioavailability and bioactivity via the secretion of MMP9 (show MMP9 ELISA Kits) and heparanase (show HPSE ELISA Kits).
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 ELISA Kits), VEGF-D, and VEGFR-3 (show FLT4 ELISA Kits) 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 ELISA Kits) 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 ELISA Kits)) may help to determine the prognosis and management of colorectal cancer (CRC (show CALR ELISA Kits)).
Taken together, our data suggest that TNF-alpha (show TNF ELISA Kits) can promote lymphangiogenesis and lymphatic metastasis of GBC through the ERK1/2 (show MAPK1/3 ELISA Kits)/AP-1 (show FOSB ELISA Kits)/VEGF-D pathway.
VEGF-D may play an important role in the process of lymphatic metastasis of epithelial ovarian cancer
CCL21 (show CCL21 ELISA Kits)/CCR7 (show CCR7 ELISA Kits) induce VEGF-D up-regulation and promote lymphangiogenesis via ERK (show EPHB2 ELISA Kits)/Akt (show AKT1 ELISA Kits) 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