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Strategies for Cardiovascular Risk Reduction in Smokers

For American Heart Month, we want to highlight the importance of advancing cardiovascular research to better understand vascular health, heart function, disease mechanisms, and to develop new therapies for disease treatment. Cardiovascular disease (CVD) remains the leading cause of death in the United States, claiming the lives of approximately 695,000 Americans in 2021 alone.

Cigarette smoking is one of the leading risk factors for CVD, compromising the normal repair mechanisms necessary for vascular endothelium homeostasis, such as the inhibition of endothelial cell migration. This can cause damage to the vascular system and is an early precursor to the development of pathologies such as hypertension and arteriosclerosis. Understanding the full impact of risk factors on CVD can support public health initiatives aimed at CVD risk reduction and prevention.

Role of HUVEC Cells in Cardiovascular Research

Human Umbilical Vein Endothelial Cells (HUVECs) are often used as a model system in cardiovascular research. By mimicking physiological and pathological conditions in vitro, HUVEC-based studies provide a robust platform to investigate disease mechanisms, screen potential therapeutic compounds, and advance our understanding of cardiovascular pathophysiology.

Lifeline Cell Technology’s characterized and quality-tested HUVEC cells have been extensively utilized as in vitro cellular tools in numerous vascular research studies related to angiogenesis, endothelial dysfunction, inflammation, thrombosis, and vascular permeability. Lifeline’s HUVEC cells offer superior performance characteristics, including robust growth, high viability, and physiological functionality, making them an ideal model system for studying vascular endothelial biology and pathology.

The Lifeline® catalog has a variety of high-quality endothelial and cardiac cells to enable cardiovascular research and more including:

REPLICA Project: Ring Study Using Lifeline HUVECs

In a new publication, Caruso and Colleagues conducted a multi-center replication study as part of the REPLICA project to verify the data robustness and replicability of Taylor et al’s original 2017 findings on the reduced effect of electronic cigarette (EC) aerosol on endothelial cell migration compared with cigarette smoke. Endothelial cells exposed to EC aerosol maintained their wound healing ability compared to those exposed to cigarette smoke.

The study utilized an in vitro endothelial cell model (HUVECs) exposed to aqueous aerosol extracts (AqE) from tobacco smoke, EC aerosols, or heated tobacco products (HTPs) to mimic in vivo toxicant exposure. Normal Human Umbilical Vein Endothelial Cells (HUVECs) obtained from Lifeline Cell Technology and cultured in complete VascuLife VEGF Medium were utilized in both the original and replication studies. A network of independent laboratories using harmonized protocols (from cell exposure to smoke/aerosols to the assessment of biological parameters such as wound width) executed endothelial cell scratch wound assays to compare the effects of three commercial electronic nicotine delivery systems to conventional cigarettes on endothelial cell wound-healing capabilities.

Linear scratch wounds were created manually on the cells’ surface prior to their exposure to cigarette smoke and AqE generated from the three electronic nicotine delivery systems at different exposure concentrations. At established timepoints between 0 to 48 h (T0–T48), images of the wound area were taken and measured using the open-source software imageJ/Fiji®. For each scratch wound assay, a negative control with AqE capture media and a positive control with cytochalasin D (2 μM) were used to determine the baseline and the maximal inhibition of HUVEC migration, respectively. A pre-determined formula was used to calculate endothelial cell migration over time across conditions.

Consistently with the original study, four independent laboratories observed a substantial reduction in EC and HTPs aerosol effects on endothelial cell migration compared with cigarette smoke. Cigarette smoke notably impaired endothelial wound healing and wound area closure even at low concentrations (12.5%), with its effects increasing in a concentration-dependent manner. In contrast, aerosols from electronic cigarettes (EC) and heated tobacco products (HTPs) did not exhibit any significant impact on endothelial cell migration and wound closure rate until concentrations reached 80%–100%.

Both the original study and the Caruso et al. replica study conclude that the harm caused by electronic nicotine delivery systems is significantly less than the harm caused by cigarette smoke. These alternatives reduce vascular damage and onset of smoking-related diseases, which could be viable harm reduction strategy for tobacco smokers. The data from these studies can help shape human health prevention policymaking in the regulation of these products.

At Lifeline, we are always excited to share the latest research with the community on our blog. If you have used Lifeline cells and/or media in your research, we would love to hear from you!

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