In this study we investigate the effects of nanotubular titanium oxide (TiO(2)) surfaces on vascular cells. EC and VSMC response to nanotubes was investigated through immunofluorescence staining, scanning electron microscopy, 5-ethynyl-2'-deoxyuridine proliferation assays, and prostaglandin I(2) (PGI(2)) enzyme immunoassays. We found that the nanotubular surface significantly enhances EC proliferation and secretion of PGI(2). The surface also results in a decrease in VSMC proliferation and increased expression of smooth muscle alpha-actin. These data suggest that engineered nanotopographical cues may influence both EC and VSMC behavior in a manner that may be useful for stent or other vascular applications.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.biomaterials.2008.11.012 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Oxylipin Profiling of Airway Structural Cells Is Unique and Modified by Relevant Stimuli.
J Proteome Res
January 2025
Department of Physiology and Pathophysiology, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg R3E0J9, Canada.
Oxylipins, diverse lipid mediators derived from fatty acids, play key roles in respiratory physiology, but the contribution of lung structural cells to this diverse profile is not well understood. This study aimed to characterize the oxylipin profiles of airway smooth muscle (ASM), lung fibroblasts (HLF), and epithelial (HBE) cells and define how they shift when they are exposed to stimuli related to contractility, fibrosis, and inflammation. Using HPLC-MS/MS, 162 oxylipins were measured in baseline media from cultured human ASM, HLF, and HBE cells as well as after stimulation with modulators of contractility and central regulators of fibrosis/inflammation.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Eli Lilly and Company, Indianapolis, IN, USA.
Background: Anti-amyloid-β (Aβ) immunotherapy trials have shown amyloid-related imaging abnormalities (ARIA) as the most common and serious adverse events linked to pathological changes in cerebral vasculature. Nevertheless, the mechanisms underlying how amyloid immunotherapy triggers vascular damage, increases vascular permeability, and results in microhemorrhages remains unclear. Notably, activation of perivascular macrophages and infiltration of peripheral immune cells have been implicated in regulating cerebrovascular damage.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of Arizona, Tucson, AZ, USA.
Background: Cerebral microvascular dysfunction and nitro-oxidative stress are present in patients with Alzheimer's disease (AD) and may contribute to disease progression and severity. A pro-nitro-oxidative environment can lead to post-translational modifications of ion channels central to microvascular regulation in the brain, including the large conductance Ca-activated K channels (BK). Nitro-oxidative modulation of BK can resulting in decreased activity and vascular hyper-contractility, thus compromising neurovascular regulation.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Massachusetts Alzheimer's Disease Research Center, Charlestown, MA, USA.
Background: In cerebral amyloid angiopathy, amyloid beta accumulates within the walls of blood vessels and contributes to impaired vascular integrity and function. In this work, we observe that tau protein similarly builds up along blood vessels in Alzheimer's disease brain.
Method: We obtained frozen inferior temporal cortex from the Massachusetts Alzheimer's Disease Research Center from n = 7 neuropathological confirmed Alzheimer's disease donors and n = 6 normal aging controls.
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
Alzheimer's Center at Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.
Background: Alzheimer's disease (AD) is characterized- at both early and late stages- by neurovascular impairment. In AD, dysfunctional cerebral microvasculature is accompanied by an inflammatory response, contributing to Aβ and tau accumulation, brain cell stress and death, impaired clearance of metabolic waste, BBB permeability, and ultimately leading to neuronal demise and cognitive impairment. We previously showed that Aβ peptides induce mitochondrial dysregulation and caspase-mediated apoptosis in brain cells, including endothelial, glial, and smooth muscle cells.
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!