Cellular interactions between endothelial cell (EC) and vascular smooth muscle cell (VSMC)/macrophages seem to be greatly changed under inflammatory conditions. Although simvastatin could regulate inflammatory transcription factors in EC and VSMC and also could inhibit leukocyte-endothelium interaction, whether it could modulate VSMC/macrophage functions that are induced by tumor necrosis factor-α (TNF-α)-activated EC remained unclear. The purpose of this study was to investigate the effects of simvastatin on VSMC/macrophage functions, which are induced by TNF-α-activated EC in coculture system in vitro. The results showed that under noncontacting conditions, simvastatin could reduce the proliferation, apoptosis, and TNF-α, IL-6, and vascular endothelial growth factor secretion both in VSMC and macrophage, which is induced by TNF-α-activated EC. And a hypothesis that simvastatin regulates the interactions and the soluble factors between EC and VSMC/macrophages could be drawn. And that might be a potential anti-atherosclerosis mechanism of simvastatin.
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http://dx.doi.org/10.1097/FJC.0000000000000567 | DOI Listing |
Trends Mol Med
December 2024
Department of Endocrinology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, China; Anhui Provincial Key Laboratory of Metabolic Health and Panvascular Diseases, Hefei, 23001, China. Electronic address:
Most patients with Hutchinson-Gilford progeria syndrome (HGPS) succumb to cardiovascular disease. Recent studies by Barettino et al., Cardoso et al.
View Article and Find Full Text PDFPLoS One
December 2024
Division of Medical Biochemistry, Tohoku Medical and Pharmaceutical University, Sendai, Japan.
The vascular endothelium is vital for cardio-pulmonary homeostasis and, thus, plays a crucial role in preventing life-threatening lung diseases. The transcription factor GATA2 is essential for hematopoiesis and maintaining vascular integrity. Heterozygous mutations in GATA2 can lead to a primary immunodeficiency syndrome with pulmonary manifestations.
View Article and Find Full Text PDFCardiovasc Res
December 2024
Baker Heart and Diabetes Institute, Melbourne, VIC, Australia.
Oxidation of lipids, excessive cell death and iron deposition are prominent features of human atherosclerotic plaques. While extensive research has established the detrimental roles of lipid oxidation and apoptosis in atherosclerosis development, the involvement of iron in atherogenesis is not yet fully understood. With the emergence of an iron-dependent form of cell death termed ferroptosis, new attention has been brought to the complex interplay among iron, ferroptosis and atherosclerosis.
View Article and Find Full Text PDFNat Commun
December 2024
Whitehead Institute for Biomedical Research, Cambridge, MA, 02142, USA.
Although respiratory symptoms are the most prevalent disease manifestation of infection by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), nearly 20% of hospitalized patients are at risk for thromboembolic events. This prothrombotic state is considered a key factor in the increased risk of stroke, which is observed clinically during both acute infection and long after symptoms clear. Here, we develop a model of SARS-CoV-2 infection using human-induced pluripotent stem cell-derived endothelial cells (ECs), pericytes (PCs), and smooth muscle cells (SMCs) to recapitulate the vascular pathology associated with SARS-CoV-2 exposure.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Psychology, University of Bath, Bath, UK.
Introduction: White matter hyperintensity volumes (WMHVs) are disproportionally prevalent in individuals with Alzheimer's disease (AD), potentially reflecting neurovascular injury. We quantify the association between AD polygenic risk score (AD-PRS) and WMHV, exploring single-nucleotide polymorphisms (SNPs) that are proximal to genes overexpressed in cerebrovascular cell species.
Methods: In a UK-Biobank sub-sample (mean age = 64, range = 45-81 years), we associate WMHV with (1) AD-PRS estimated via SNPs across the genome (minus apolipoprotein E [APOE] locus) and (2) AD-PRS estimated with SNPs proximal to specific genes that are overexpressed in cerebrovascular cell species.
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