The interaction between vascular endothelial cells (VECs) and osteoblasts (OBs) is the focus of this recent research. Vascular endothelial cells secrete bone morphogenetic protein, which promotes OB differentiation and stimulates OBs and their precursor cells to secrete vascular endothelial growth factor. Vascular endothelial growth factor is important in angiogenesis and angiopoiesis. Cloning studies have shown that adipose-derived stem cells (ADSCs) have the potential to differentiate into fat, bone, cartilage, and skeletal and smooth muscle cells, among others. Adipose-derived stem cells can express multiple growth factors, including vascular endothelial growth factor and hepatocyte growth factor. Our study examined the influence of coculturing VECs and ADSCs on osteogenic differentiation. Cord blood-derived VECs and ADSCs were isolated from rats and characterized with immunofluorescence staining and morphological observation. Coculture of third-generation ADSCs and VECs was induced for 6 weeks. Cell growth was analyzed using a modified MTT assay. Alkaline phosphatase (ALP) and osteocalcin (OC) was analyzed using immunofluorescence staining. When ADSCs and VECs were cocultured, the absorbance of cells gradually increased, reaching a peak on day 12. The highest absorbance was seen in a coculture system with a ratio of ADSCs and VECs of 1:1. The secretion of ALP and OC gradually increased in these cells and was significantly higher than controls (P < 0.01). Coculturing of ADSCs and VECs at a 1:1 ratio gave the highest secretion of ALP and OC at every time point, and was significantly higher than other groups (P < 0.01). Our results indicated that ADSCs can be induced to osteogenic differentiation by VECs in vitro, suggesting a coculture system of VECs and ADSC as a novel source of cells for bone engineering.
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http://dx.doi.org/10.1097/SAP.0b013e3182583eb9 | DOI Listing |
Annual epidemics of influenza result in 3-5 million cases of severe illness and more than 600 000 deaths. Severe forms of influenza are usually characterized by vascular endothelial cells damage. Thus, influenza A viruses, including subtypes A(H1N1)pdm09, A(H3N2), as well as highly pathogenic avian influenza viruses, can infect the vascular endothelium, leading to activation and subsequent dysfunction of these cells.
View Article and Find Full Text PDFCardiovasc Toxicol
January 2025
Department of Physiology, Pharmacology and Toxicology, West Virginia University School of Medicine, Morgantown, WV, USA.
Pregnancy is a vulnerable time with significant cardiovascular changes that can lead to adverse outcomes, which can extend into the postpartum window. Exposure to emissions from electronic cigarettes (Ecig), commonly known as "vaping," has an adverse impact on cardiovascular function during pregnancy and post-natal life of offspring, but the postpartum effects on maternal health are poorly understood. We used a Sprague Dawley rat model, where pregnant dams are exposed to Ecigs between gestational day (GD)2-GD21 to examine postpartum consequences.
View Article and Find Full Text PDFCurr Atheroscler Rep
January 2025
Houston Methodist DeBakey Heart and Vascular Center, Houston, TX, USA.
Purpose Of Review: The exposome refers to the total environmental exposures a person encounters throughout life, and its relationship with human health is increasingly studied. This non-systematic review focuses on recent research investigating the effects of environmental factors-such as air pollution, noise, greenspace, neighborhood walkability, and metallic pollutants-on atherosclerosis, a major cause of cardiovascular disease.
Recent Findings: Studies show that long-term exposure to airborne particulate matter can impair endothelial function and elevate adhesion molecule levels, leading to vascular damage.
While key for pathogen immobilization, neutrophil extracellular traps (NETs) often cause severe bystander cell/tissue damage. This was hypothesized to depend on their prolonged presence in the vasculature, leading to cytotoxicity. Imaging of NETs (histones, neutrophil elastase, extracellular DNA) with intravital microscopy in blood vessels of mouse livers in a pathogen-replicative-free environment (endotoxemia) led to detection of NET proteins attached to the endothelium for months despite the early disappearance of extracellular DNA.
View Article and Find Full Text PDFBiomark Med
January 2025
Department of Clinical Laboratory, Gansu Provincial Clinical Research Center for Laboratory Medicine, Lanzhou, China.
Raftlin (raft-linking) protein is an essential component of the lipid raft structure and plays a crucial role in B and T cell signaling pathways. It facilitates B cell receptor (BCR) signaling by promoting calcium mobilization and tyrosine phosphorylation in the cells while colocalizing with BCR on the cell membrane. Interestingly, Raftlin is internalized in lipopolysaccharide-stimulated T cells by colocalization with Toll-like receptor 4 (TLR4), wherein it exerts a similar role as in B cells.
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