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Specification of endothelial cell (EC) fate during vascular development is controlled by distinct key regulators. While Notch plays an essential role in induction of arterial phenotypes, COUP-TFII is required to maintain the venous EC identity. Homeodomain transcription factor Prox1 functions to reprogram venous ECs to lymphatic endothelial cells (LECs). Here, we report that the venous EC fate regulator COUP-TFII is expressed in LECs throughout development and physically interacts with Prox1 to form a stable complex in various cell types including LECs. We found that COUP-TFII functions as a coregulator of Prox1 to control several lineage-specific genes including VEGFR-3, FGFR-3, and neuropilin-1 and is required along with Prox1 to maintain LEC phenotype. Together, we propose that the physical and functional interactions of the 2 proteins constitute an essential part in the program specifying LEC fate and may provide the molecular basis for the hypothesis of venous EC identity being the prerequisite for LEC specification.
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http://dx.doi.org/10.1182/blood-2008-03-145789 | DOI Listing |
Diagn Pathol
September 2025
Department of Gastrointestinal Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Background: Gastric cancer is one of the most common cancers worldwide, with its prognosis influenced by factors such as tumor clinical stage, histological type, and the patient's overall health. Recent studies highlight the critical role of lymphatic endothelial cells (LECs) in the tumor microenvironment. Perturbations in LEC function in gastric cancer, marked by aberrant activation or damage, disrupt lymphatic fluid dynamics and impede immune cell infiltration, thereby modulating tumor progression and patient prognosis.
View Article and Find Full Text PDFFront Mol Neurosci
August 2025
Department of Cardiovascular Sciences, Lewis Katz School of Medicine, Lemole Center for Integrated Lymphatics and Vascular Research, Temple University, Philadelphia, PA, United States.
Introduction: Endothelial-to-mesenchymal transition (EndoMT), cell death, and fibrosis are increasingly recognized as contributing factors to Alzheimer's disease (AD) pathology, but the underlying transcriptomic mechanisms remain poorly defined. This study aims to elucidate transcriptomic changes associated with EndoMT, diverse cell death pathways, and fibrosis in AD using the 3xTg-AD mouse model.
Methods: Using RNA-seq data and knowledge-based transcriptomic analysis on brain tissues from the 3xTg-AD mouse model of AD.
Adv Sci (Weinh)
September 2025
Department of Pharmaceutics, Shandong Key Laboratory of Targeted Drug Delivery and Advanced Pharmaceutics, NMPA Key Laboratory for Technology Research and Evaluation of Drug Products, Key Laboratory of Chemical Biology (Ministry of Education), State Key Laboratory of Discovery and Utilization of Fun
The effectiveness of antitumor immunotherapy is limited to immune cell infiltration into solid tumors, primarily via T-cell migration through tumor blood vessels. This study introduces a multifunctional nitric oxide (NO)-driven hollow gold Janus nanomotor (HAM) designed to promote tumor blood vessel normalization and increase T-cell infiltration, thereby enhancing the immune response against tumors. It is revealed that self-generated NO facilitates the penetration of HAM into tumors and increases pericyte coverage of blood vessels, thereby enhancing intratumoral T-cell infiltration.
View Article and Find Full Text PDFEcotoxicol Environ Saf
September 2025
School of Public Health, Anhui University of Science and Technology, Huainan, China; Key Laboratory of Industrial Dust Control and Occupational Health of the Ministry of Education, Anhui University of Science and Technology, Huainan, China; Key Laboratory of Industrial Dust Deep Reduction and Occupa
Pulmonary endothelial injury is a critical factor in the pathogenesis and progression of coal pneumoconiosis. However, the precise mechanisms underlying this injury remain poorly understood. To address this, we established a coal pneumoconiosis mouse model by chronic intranasal coal dust exposure over 9 months.
View Article and Find Full Text PDFFront Immunol
September 2025
Wound Healing Center, Peking University Third Hospital, Beijing, China.
Background And Objective: Melanoma exhibits profound biological complexity, driven by immune evasion, phenotypic plasticity, and resistance to therapy. While programmed cell death (PCD) shapes tumor-immune interactions, its mechanistic landscape in melanoma remains incompletely defined. This study aims to comprehensively characterize PCD-related signatures and their associations with tumor heterogeneity, prognosis, and immunotherapeutic outcomes.
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