The role of interleukin-4 (IL-4) in the inflammatory process has emerged recently. In this study, we investigated the effect of IL-4 on the angiogenic process in an in vitro experimental system. IL-4 significantly inhibited the proliferation of human umbilical vein endothelial cells (HUVEC) that was induced by the vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF). VEGF- or bFGF-induced HUVEC chemotaxis was abrogated by the IL-4 treatment. In addition, the formation of tube-like structures by HUVEC in the presence of VEGF or bFGF was also severely down-regulated by IL-4. The inhibitory effects on the critical steps of angiogenesis were not observed with IL-6 that is abundantly found in the inflamed tissue. Our results suggest that IL-4 may play a regulatory role in normal physiology and provide the potential possibility for IL-4 as a therapeutic agent in the intervention of angiogenesis-related diseases.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Dysregulation of neural tube vascular development as an aetiological factor in autism spectrum disorder: Insights from valproic acid exposure.
J Physiol
January 2025
Instituto de Investigaciones Cerebrales, Universidad Veracruzana, Xalapa Ver, México.
Autism spectrum disorder (ASD) is a prevalent neurodevelopmental condition affecting a substantial number of children globally, characterized by diverse aetiologies, including genetic and environmental factors. Emerging research suggests that neurovascular dysregulation during development could significantly contribute to autism. This review synthesizes the potential role of vascular abnormalities in the pathogenesis of ASD and explores insights from studies on valproic acid (VPA) exposure during neural tube development.
View Article and Find Full Text PDFLocal tissue response to a C-X-C motif chemokine ligand 12 therapy for fecal incontinence in a rabbit model.
Am J Physiol Gastrointest Liver Physiol
January 2025
Wake Forest Institute for Regenerative Medicine, Wake Forest Baptist Medical Center, Winston-Salem, North Carolina, USA.
This study aimed to determine if local injection of CXCL12 reduces sphincter fibrosis, restores sphincter muscle content, vascularization, and innervation, and recruits progenitor cells in a rabbit model of anal sphincter injury and incontinence. Adult female rabbits were assigned to 3 groups: uninjured/no treatment (control), injured/treated (treated), and injured/no treatment (untreated) (n=4 each). Injured groups were anesthetized and a section of external anal sphincter was removed at the 9:00 o'clock position.
View Article and Find Full Text PDFInduction of PD-1 and CD44 in CD4 T cells by circulatory extracellular vesicles from severe dengue patients drives endothelial damage via the NF-kB signaling pathway.
J Virol
December 2024
Laboratory of Virology, Regional Centre for Biotechnology, National Capital Region Biotechnology Science Cluster, Faridabad, Haryana, India.
Extracellular vesicles (EVs) emerged as critical contributors to the pathogenesis of vascular endothelial barrier dysfunction during the inflammatory response to infection. However, the contribution of circulating EVs to modifying endothelial function during dengue virus infection remains unclear. In this study, we showed that severe dengue patients' plasma-derived EV (SD-EV) were found to carry elevated levels of different protein cargos, e.
View Article and Find Full Text PDFDemonstration of Enhancement of Tumor Intravasation by Dicarbonyl Stress Using a Microfluidic Organ-on-chip.
Small
January 2025
Department of Bioengineering, Indian Institute of Science, Bengaluru, 560012, India.
Cancer metastasis involves cell migration from their primary organ foci into vascular channels, followed by dissemination to prospective colonization sites. Vascular entry of tumor cells or intravasation involves their breaching stromal and endothelial extracellular matrix (ECM) and the endothelial barriers. How the kinetics of this breach are confounded by chronic inflammatory stresses seen in diabetes and aging remains ill-investigated.
View Article and Find Full Text PDFInvestigating the Role of TRPV4 and GPR35 Interaction in Endothelial Dysfunction in Aging Mice.
Aging Cell
January 2025
Wuxi School of Medicine, Jiangnan University, Wuxi, China.
Endothelial dysfunction, characterized by a decline in endothelial physiological functions, is a significant aspect of cardiovascular aging, contributing notably to arterial stiffness, atherosclerosis, and hypertension. Transient receptor potential channel V4 (TRPV4), a key member of Ca-permeable channels, plays a crucial role in maintaining vascular functions. However, the role and mechanisms of TRPV4 in aging-related endothelial dysfunction remain incompletely understood.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!