Unlabelled: Vascular adhesion and endothelial transmigration are critical steps in the establishment of distant metastasis by circulating tumor cells (CTCs). Also, vascular inflammation plays a pivotal role in steering CTCs out of the blood stream. Here, long circulating lipid-polymer nanoparticles encapsulating curcumin (NANOCurc) are proposed for modulating the vascular deposition of CTCs. Upon treatment with NANOCurc, the adhesion propensity of highly metastatic breast cancer cells (MDA-MB-231) onto TNF-α stimulated endothelial cells (HUVECs) reduces by ~70%, in a capillary flow. Remarkably, the CTCs vascular deposition already reduces up to ~50% by treating solely the inflamed HUVECs. The CTCs arrest is mediated by the interaction between ICAM-1 on HUVECs and MUC-1 on cancer cells, and moderate doses of curcumin down-regulate the expression of both molecules. This suggests that NANOCurc could prevent metastasis and limit the progression of the disease by modulating vascular inflammation and impairing the CTCs arrest.
From The Clinical Editor: In this novel study, lipid nanoparticles encapsulating curcumin were able to prevent metastasis formation and limited the progression of the disease by modulating vascular inflammation and impairing the circulating tumor cells' arrest as a result of down-regulation of ICAM1 and MUC1 in a highly metastatic breast cancer cell line model.
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http://dx.doi.org/10.1016/j.nano.2014.02.004 | DOI Listing |
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 PDFJ Cell Biochem
January 2025
Division of Cell Biology and Physiology, CSIR-Indian Institute of Chemical Biology, Kolkata, India.
Cellular prion protein (PRNP) has been implicated in various physiological processes in different cell types, for decades. Little has been known how PRNP functions in multiple, yet related processes within a particular system. In our current study, with the aid of high-throughput RNA-sequencing technique, we have presented an overall transcriptome profile of rat vascular smooth muscle cells (VSMCs) with Prnp knockdown.
View Article and Find Full Text PDFAging 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 PDFFront Physiol
December 2024
NextGen Precision Health, University of Missouri, Columbia, MO, United States.
The Lim Kinase (LIMK) family of serine/threonine kinases is comprised of LIMK1 and LIMK2, which are central regulators of cytoskeletal dynamics via their well-characterized roles in promoting actin polymerization and destabilizing the cellular microtubular network. The LIMKs have been demonstrated to modulate several fundamental physiological processes, including cell cycle progression, cell motility and migration, and cell differentiation. These processes play important roles in maintaining cardiovascular health.
View Article and Find Full Text PDFInt J Med Sci
January 2025
Department of Cardiology, Jiangbin Hospital of Guangxi Zhuang Autonomous Region, Nanning 530021, Guangxi, People's Republic of China.
Coronary microembolization (CME) is defined as atherosclerotic plaque erosion, spontaneous rupture, or rupture of the plaque while undergoing interventional therapy resulting in the formation of tiny emboli that obstruct the coronary microcirculatory system. For percutaneous coronary intervention, CME is a major complication, with a periprocedural incidence of up to 25%. Recent studies have demonstrated that regulatory cell death (RCD) exerts a profound influence on CME through its modulation of inflammatory responses, oxidative stress, cell death, and angiogenesis.
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