Abstract
Aging and smoking are major risk factors for cardiovascular diseases (CVD). Our in vitro study compared, in the context of aging, the effects of the aerosol of Tobacco Heating System 2.2 (THS; an electrically heated tobacco product) and 3R4F reference cigarette smoke (CS) on processes that contribute to vascular pathomechanisms leading to CVD. Young and old human aortic smooth muscle cells (HAoSMC) were exposed to various concentrations of aqueous extracts (AE) from 3R4F CS [0.014–0.22 puffs/mL] or THS aerosol [0.11–1.76 puffs/mL] for 24 h. Key markers were measured by high-content imaging, transcriptomics profiling and multianalyte profiling. In our study, in vitro aging increased senescence, DNA damage, and inflammation and decreased proliferation in the HAoSMCs. At higher concentrations of 3R4F AE, young HAoSMCs behaved similarly to aged cells, while old HAoSMCs showed additional DNA damage and apoptosis effects. At 3R4F AE concentrations with the maximum effect, the THS AE showed no significant effect in young or old HAoSMCs. It required an approximately ten-fold higher concentration of THS AE to induce effects similar to those observed with 3R4F. These effects were independent of nicotine, which did not show a significant effect on HAoSMCs at any tested concentration. Our results show that 3R4F AE accelerates aging in young HAoSMCs and exacerbates the aging effect in old HAoSMCs in vitro, consistent with CS-related contributions to the risk of CVD. Relative to 3R4F AE, the THS AE showed a significantly reduced impact on HAoSMCs, suggesting its lower risk for vascular SMC-associated pathomechanisms leading to CVD.
Highlights
Age, independent of other conventional risk factors, constitutes a major risk factor for the development of cardiovascular diseases (CVD), such as atherosclerosis and abdominal aneurysms (Forsdahl et al 2009; Kent et al 2010; Office of the Surgeon General (US) 2010; Messner and Bernhard 2014)
We investigated the biological impact of cigarette smoke (CS) and Tobacco Heating System 2.2 (THS) 2.2 aerosol in the form of aqueous extracts (AE) as well as the impact of nicotine in “young” and “old/aged” primary human aortic vascular smooth muscle cells (HAoSMC) using the replicative senescence approach for aging cells in vitro
We investigated and compared the functional and molecular changes that occurred at baseline between young and old human aortic smooth muscle cells (HAoSMC), respectively
Summary
Independent of other conventional risk factors, constitutes a major risk factor for the development of cardiovascular diseases (CVD), such as atherosclerosis and abdominal aneurysms (Forsdahl et al 2009; Kent et al 2010; Office of the Surgeon General (US) 2010; Messner and Bernhard 2014). One characteristic of aging is the accumulation of senescent cells Aging-triggered senescence (replicative senescence) occurs normally because of the limited number of replication cycles per cell, which is controlled by telomere shortening (Harley et al 1990; Chi et al 2019). Premature cell senescence can occur by environmental or extrinsic insults that induce stressors, such as oxidative stress, inflammation, and DNA damage (Chi et al 2019)
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