Ask about this productRelated genes to: VEGFC protein (Rat)
- Gene:
- VEGFC NIH gene
- Name:
- vascular endothelial growth factor C
- Previous symbol:
- -
- Synonyms:
- VRP
- Chromosome:
- 4q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-26
- Date modifiied:
- 2015-08-26
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- Cancer cell-derived exosomal microRNAs (miRNAs) are crucial mediators of intercellular communication within the tumor microenvironment, including with lymphatic endothelial cells (LECs). Hypoxia, a key driver of tumor aggressiveness, modulates exosome release and cargo. However, the specific functions of exosomal miRNAs derived from hypoxic oral squamous cell carcinoma (OSCC) cells are not well defined. - Source: PubMed
Publication date: 2026/05/20
You TengchaoMao FurongZhang KeshengZhang XulinHu Xiaohua - Atrial fibrillation represents a prevalent cardiac arrhythmia whose pathogenic mechanisms remain incompletely understood. Here, we identify impaired atrial lymphangiogenesis as a critical determinant in atrial fibrillation pathogenesis. Analysis of human left atrial appendage specimens reveals decreased lymphatic vessel density in atrial fibrillation patients compared to those in sinus rhythm. Mechanistically, we demonstrate that epicardial adipose tissues from atrial fibrillation patients secrete kynurenic acid, which acts via GPR35 to disrupt lymphatic endothelial cell metabolism and mitochondrial homeostasis, ultimately promoting endothelial-to-mesenchymal transition. Using an organotypic culture system, we show that epicardial adipose tissue -derived factors directly impair lymphatic vessel formation. In vivo studies utilizing angiotensin II-induced and high-fat diet male mouse models confirm the critical role of lymphatic dysfunction in atrial fibrillation susceptibility. Therapeutic interventions promoting lymphangiogenesis, either through VEGFC administration or weight loss intervention by LY3437943 (the novel triple GIP, GLP-1, and glucagon receptor agonist), significantly attenuate atrial fibrillation inducibility. These findings establish lymphatic dysfunction as a novel pathogenic mechanism in atrial fibrillation and highlight lymphatic vessel formation as a promising therapeutic target. - Source: PubMed
Publication date: 2026/05/19
Takahashi MasakiAbe IchitaroYoshida NaofumiKatoh DaisukeFujita DaishiGoto ShunsukeYamasaki HirochikaKo ToshiyukiJiang YueHe YuIto ShinjiHarada TaisukeTakano MasayukiSato HirokiKondo HidekazuFukui AkiraTeshima YasushiSako HidenoriOhta KeisukeMiyamoto ShinjiYamauchi ToshimasaNomura SeitaroTakeda NorihikoKomuro IsseiTakahashi Naohiko - Rheumatoid arthritis (RA) is a complex autoimmune joint disease characterized by persistent synovial inflammation and hyperplasia. The TNF-α/NF-κB signaling pathway is one of the most important inflammatory pathways involved in the onset and progression of RA. In addition, impaired lymphatic drainage plays a critical role in disease exacerbation. Iguratimod (IGU), a novel disease-modifying antirheumatic drug, has been shown to exert immunomodulatory effects. However, the precise mechanisms underlying its anti-inflammatory function remain unclear. Furthermore, whether IGU could restore lymphatic reflux function in inflammatory arthritis has yet to be determined. Therefore, the study aimed to elucidate the mechanisms underlying the therapeutic effects of IGU in RA. The therapeutic efficacy of IGU was evaluated in a collagen-induced arthritis (CIA) mouse model, with methotrexate used as a positive control. Histopathological analyses of footpad and ankle tissues were performed to asses of disease onset and progression. Levels of inflammatory cytokines (e.g., TNF-α, IFN-γ, IL-4, and IL-6) and IgG autoantibody (such as anti-CCP antibody) were determined using ELISA. Lymphangiogenic markers, including VEGF-C, VEGFR-3, and LYVE-1, were assessed in ankle joint tissues. The protein and mRNA expression levels of TNF-α and NF-κB in joint tissues were also evaluated. In addition, an in vitro tube formation assay was performed to examine the direct effects of IGU on lymphangiogenesis. IGU treatment significantly alleviated arthritis severity in CIA mice by reducing joint inflammation, minimizing tissue damage, and preserving bone integrity. Beyond its established anti-inflammatory properties, IGU could enhance lymphangiogenesis in inflamed joints. Mechanistically, IGU suppressed the TNF-α/NF-κB signaling pathway, thereby attenuating immune responses and inflammatory cytokine production. Furthermore, IGU directly promoted lymphatic vessel formation by upregulating LYVE-1, Prox-1, VEGF-C, and VEGFR-3 in lymphatic endothelial cells. The effect might contribute to the restoration of lymphatic drainage function. The study suggests that IGU exerts a dual therapeutic action by modulating inflammation and promoting lymphatic vessel formation, which might facilitate the restoration of lymphatic drainage and contribute to improved outcomes in RA. - Source: PubMed
Publication date: 2026/05/20
Du MinminXu XiaofenCui XiaohuiChen YilinZhao PengHu QingqingWang CaifengZhang JidaHao GuifengHu Changfeng - Glial tumors are the most common malignant brain tumors, and IDH1 serves as an important diagnostic and prognostic molecular marker in gliomas. The mutation status of IDH1 influences prognosis, patient survival, and treatment response in glial tumors. However, the effects of the IDH1 mutation on the angiogenic potential of glial tumors have yet to be thoroughly elucidated. Our aim was to investigate the impact of the IDH1 mutation on the angiogenic potential of glial tumors by overexpressing both mutant and wild-type IDH1 genes in these tumors. Furthermore, we examined how the signaling pathways affecting the angiogenic behavior of glial tumors differ based on IDH1 mutation status by evaluating the mRNA expressions of VEGF, EGF, PDGF, and FGF signaling pathways in the U87MG cell line as well as in patient-derived tumor samples. The IDH1 mutation induced proliferation and tube-formation potential in U87MG cells while suppressing these activities in HUVEC cells. Considering angiogenesis-associated signaling pathways, we found that mutant IDH1 expression indirectly upregulates angiogenesis-associated pathways via HIF1A. The genes VEGFC, ERBB3, PDGFB, and PDGFC may serve as potential markers for the prognosis of glial tumors and for anti-angiogenic therapy. - Source: PubMed
Publication date: 2026/05/13
Oksal Muhammed DenizKilic TurkerAvsar Timucin - Lymphatic vessels are essential for tissue homoeostasis and their growth is regulated by vascular endothelial growth factor C (VEGF-C) signalling through VEGFR3. However, how VEGF-C balances lymphatic endothelial cells (LECs) proliferation versus sprouting to ensure functional vessel formation has remained unclear. Using high-fidelity conditional genetics and receptor-specific ligands, we uncover a requirement for the alternative receptor VEGFR2 in VEGF-C-VEGFR3-driven lymphatic vessel sprouting. While activation of VEGFR2 alone fails to induce lymphangiogenesis, VEGFR2 loss abolishes LEC sprouting, but not proliferation, in response to VEGF-C. In contrast, deletion of the VEGFR3 downstream effector PI3Kα completely abrogates lymphangiogenesis. VEGFR2 is activated and found in proximity to VEGFR3 in LECs in vivo, with PI3Kα controlling their relative cell-surface availability and VEGF-C increasing VEGFR2 relative to VEGFR3, thereby priming LECs for sprouting. This receptor coordination balances VEGF-C-driven proliferative and sprouting responses, coupling LEC expansion to vessel growth, ensuring the formation of functional lymphatic networks. - Source: PubMed
Publication date: 2026/05/15
Schoofs HansZhang YanOrtsäter HenrikLytvyn MariyaBenedito RuiMäkinen Taija