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Objective: This study aims to explore the possible role of fenofibrate in inhibiting choroidal neovascularization (CNV) in Brown Norway (BN) rats.
Methods: BN rats underwent binocular retinal laser photocoagulation to induce CNV. On day one, fenofibrate was injected into the vitreous cavity of rats in the control and experimental groups. Fundus fluorescein angiography (FFA), isolectin B4-FITC staining, immunofluorescence staining, qRT-PCR and western blot were performed at 1, 2, 3 and 4 weeks to observe the morphological changes of CNV and the expression of the vascular endothelial growth factor C (VEGF-C) and the vascular endothelial growth factor receptor-3 (VEGFR-3).
Results: CNV with the spontaneous gradual regression and scarring phenomenon appeared in BN rats. In neovascularization, VEGF-C was mainly distributed in the ganglion cell layer, while VEGFR-3 was mainly expressed in the choroid. In the control group, choroidal VEGF-C initially increased, and subsequently decreased, while VEGFR-3 level maintained a constant level after the decrease. Both had a decreasing expression in the retina. The early formation of CNV was significantly weakened in the experimental group, but there was no difference in the later period. VEGF-C and VEGFR-3 expression in the choroid and retina were lower than in the control group. Furthermore, VEGFR-3 protein was not expressed in the retina. However, this gradually increased in the early period and declined in the terminal stage in the choroid.
Conclusion: VEGF-C and VEGFR-3 participated in the laser-induced CNV formation in BN rats. Fenofibrate could inhibit CNV formation.
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http://dx.doi.org/10.1016/j.exer.2018.05.030 | DOI Listing |
Mediators Inflamm
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Department of Anesthesiology, Jiangsu Province Hospital, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
The role of meningeal lymphatic vessels (mLVs) in neurodegenerative diseases has been increasingly recognized. However, their involvement in lipopolysaccharide (LPS)-induced neuroinflammation and associated depression-like behaviors remains poorly understood. Given that impaired clearance of neurotoxic substances can prolong central nervous system (CNS) inflammation, investigating the function of mLVs in this context may offer new insights into the mechanisms underlying acute neuroinflammation and provide potential therapeutic targets.
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July 2025
Department of Cell Biology and Medical Genetics, College of Basic Medical Sciences, Jilin University, Changchun, Jilin, China.
Lymphedema is a chronic inflammatory disease without an effective treatment method, and it results in a high disease burden and psychological distress in patients. Although there have been significant advances in targeted therapies, there are still no effective options to treat this refractory disease. In recent years, new advances and breakthroughs have been made in signaling pathways, including RAS/MAPK, PI3K/AKT, VEGF-C/VEGFR-3, HGF/MET, and TGF-β1, which are important for understanding the pathogenesis and disease progression of lymphedema.
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Division of Hepatobiliary Surgery, Department of Surgical Education and Research, The Second Affiliated Hospital of Kunming Medical University, Kunming 650101, Yunnan Province, China.
This letter comments on the recently published article in the , in which the authors demonstrated a strong link between lymphangiogenesis and the process of platelet adherence, aggregation, and activation by employing a rat model of liver cirrhosis caused by bile duct ligation (BDL). The authors applied both gain and loss of function approach by using platelet-rich plasma and vascular endothelial growth factor 3 receptor inhibitor MAZ-51 to activate and inhibit angiogenetic signaling in BDL rat model, respectively, to verify the crucial function of lymphangiogenesis in the development of liver cirrhosis and portal hypertension (PHT). In clinical practice, platelet transfusion has been applied to improve liver function in patients suffering from chronic liver disease and cirrhosis.
View Article and Find Full Text PDFAnn Vasc Surg
May 2025
School of Clinical Medicine, Shandong Second Medical University, Weifang, Shandong, P.R. China; Laboratory of Translational Medicine in Microvascular Regulation, Medical Research Center, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jin
Lymphatic malformation (LM) is a lymphatic system tumor caused by abnormal development during the embryonic period, which leads to structural defects in the lymphatic vessels. It originates from lymphatic endothelial cells (LECs) and is prone to occur in the lymphatic vessels of the head, neck and axilla. It is characterized by abnormal proliferation and cystic expansion of LECs.
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May 2025
Cancer Biology Program, Mitchell Cancer Institute, University of South Alabama, Mobile, Alabama, USA.
Despite the recent advances in treatment, breast cancer (BCa) remains a leading cause of cancer-related mortality worldwide, and metastasis accounts for the most significant number of BCa deaths. Lymphangiogenesis, the process by which new lymphatic vessels develop from pre-existing ones, is a major driver of BCa metastasis. High lymphatic vessel density is linked to lymph node metastasis and poor prognosis in BCa.
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