Respiratory mechanics following chronic cigarette smoke exposure in the Apoe$$^{-/-}$$ mouse model

Matz, Jacob; Farra, Yasmeen M; Cotto, Héctor Millán; Bellini, Chiara; Oakes, Jessica M.

doi:10.1007/s10237-022-01644-8

Cited by 5 publications

(6 citation statements)

References 75 publications

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“…42 JUUL Labs, Inc.© was dominating the e-cigarette market at the time of this study and remains nowadays among the five top-selling brands. 43 Similar to cigarette smoke 31, 44 and prior generation (tank-style) e-cigarette aerosol, 24, 25, 28, 45 particulates and gases produced by pod-mod devices access the body primarily through the respiratory system yet retain the ability to modulate biological processes in other organs. 46, 47 Related to the cardiovascular system, acute inhalation of pod-mod e-cigarette aerosol increases the augmentation index (arterial stiffness), reduces the reactive hyperemia index (endothelial vasodilator function), and raises peripheral blood pressure in occasional users.…”

Section: Discussionmentioning

confidence: 99%

Chronic Pod-Mod E-Cigarette Aerosol Exposure Induces Aortic Dysfunction in Hypercholesterolemic Mice: Role of Oxidative Stress and Inflammation

Farra,

Matz,

Wilker

et al. 2024

Preprint

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ObjectiveElectronic (e-)cigarettes are the most used tobacco product amongst youth, and adult smokers favor e-cigarettes over approved cessations aids. Despite the lower perceived harm of vaping compared to smoking, inhalation of e-cigarette aerosol elicits cardiovascular responses that may lead to permanent injury when repeated over time. We thus aimed to infer the long-term outcomes of vaping on the function and structure of the aorta and shed light on the underlying cellular and molecular mechanisms.Approach and ResultsWe exposed female hypercholesterolemic mice to either pod-mod e-cigarette aerosol or room air daily for 24 weeks. Chronic inhalation of e-cigarette aerosol triggered accumulation of inflam-matory signals systemically and within aortic tissues, as well as T lymphocyte accrual in the aortic wall. Reduced eNOS expression and enhanced ROS production following eNOS uncoupling and NADPH oxi-dase activation curbed nitric oxide availability in the aorta of mice exposed to e-cigarette aerosol, impairing the endothelium-dependent vasodilatation that regulates blood flow distribution. Inhalation of e-cigarette aerosol thickened and stiffened aortic tissues via collagen deposition and remodeling, hindering the storage of elastic energy and limiting the cyclic distensibility that enables the aorta to function as a pressure reservoir. These effects combined contributed to raising systolic and pulse pressure above control levels.ConclusionsChronic inhalation of aerosol from pod-mod e-cigarettes promotes oxidative stress, inflammation, and fibrosis within aortic tissues, significantly impairing passive and vasoactive aortic functions. This evidence provides new insights on the biological processes that increase the risk for adverse cardio-vascular events as a result of pod-mod e-cigarette vaping.

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Section: Discussionmentioning

confidence: 99%

Chronic Pod-Mod E-Cigarette Aerosol Exposure Induces Aortic Dysfunction in Hypercholesterolemic Mice: Role of Oxidative Stress and Inflammation

Farra,

Matz,

Wilker

et al. 2024

Preprint

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“…Apoe −/− mice naturally exhibit elevated lipid and cholesterol profiles [95,298]. On account of this feature, we showed that Apoe −/− mice chronically exposed to cigarette smoke experience the same cardiovascular and respiratory ailments of habitual smokers [222,1]. These findings motivated the use of Apoe −/− mice as a preclinical model to study the cardiopulmonary occupational risk associated with WFS inhalation.…”

Section: Animalsmentioning

confidence: 73%

“…Following application of broadband frequency perturbations between 1 and 20.5 Hz, lung impedance (Z) was calculated as the ratio of measured pressure and applied volume at each frequency. MATLAB (MathWorks, Natick, MA) builtin fmincon algorithm was used to fit the parameters of the constant phase model [137] from lung impedance data, by minimization of an objective function [222]. Anesthetized mice were sacrificed by exsanguination following mechanical ventilation.…”

Section: A1 Materials and Methodsmentioning

confidence: 99%

“…Upon completion of functional testing, lungs were perfusion fixed with 3% glutaraldehyde at 20 cmH 2 O tracheal pressure for 40 minutes [222]. Lobes and trachea were dissected en bloc and stored in fixative solution at 4 • C for at least 24 hours, then transferred to 70% ethanol.…”

Section: A1 Materials and Methodsmentioning

confidence: 99%

“…This chapter has been adapted from the publication [222]. With grateful acknowledgment for Yasmeen M. Farra, without your diligence and organization these daily cigarette exposures would not have come to fruition.…”

Section: Respiratory Mechanics Followingmentioning

confidence: 99%

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Cardiovascular outcomes of wildland fire smoke inhalation: a robust preclinical exposure paradigm to infer the occupational risk of wildland firefighting

Matz

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I want to thank my research advisor, Chiara Bellini. Thank you for your unwavering support, guidance, and collaboration throughout my PhD journey. I will always be grateful for the chance you took on me and the kindness you have shown me. Your work ethic and commitment to producing high-quality research is incredibly inspiring; I cannot wait to see where the lab goes next and what research you will do in the future.To my committee, Rouzbeh Amini, Luke Montrose, and Lee Makowski, as well as my co-advisor Jessica Oakes, thank you all for your support, guidance, and insight. It has been a pleasure to learn from you all. I appreciate all the kindness you have shown me. To all my mentors, teachers, and professors over the years, thank you for always encouraging my curiosity, for your probing to ask deeper questions, and for valuing my contributions; your support and guidance has been instrumental for me both personally and professionally.Thank you to all my lab mates, both past and present. Matt and Yasmeen, thank you for being the best supporters throughout all our exposure projects. Without you two, I would not have survived or completed even a fraction of my research; I am immensely grateful for how you two were always willing to go out of your way to lend a hand. I look up to you both and can't wait to see everything you accomplish going forward. Samar, thank you for answering all my questions, for lending a supportive ear in good times and in bad, and for giving me recipe and restaurant inspiration. This final year of our PhD has been a big push to the finish, and I am so grateful we have been able to do it together. Ana, thank you for being the best distraction and for keeping things fun. On a more serious note, it has been so wonderful to be reminded to take a deep breath and remember to take time for excitement; thank you for the levity, and thank you for the support. Ashley, thank you for making lab work entertaining; we've spent many long hours in the lab together, and it has always been a pleasure to work alongside you. I know life has not been easy, but I admire your grit and determination; I wish the very best for you. Nick, thank you for not taking life too seriously, I appreciate that you always have a smile on your face and are quick to laugh; research can be very trying and exceptionally difficult at times, and I am so appreciative of the levity you bring to the lab. Simone, Victoria, Cindy, and Serena, I wish you all the best of luck; I can't wait to see what you each accomplish, it has been my pleasure meeting all of you and imparting as much wisdom as I could before leaving.To all the undergraduate researchers and co-ops I've had the pleasure to work with, thank you for all your hard work and your contributions to our research. Namely, I would like to thank our co-ops, Alex and Kathrine, who ran our long-term wildland fire exposures; this research truly would not have been feasible without your rigorous efforts and organization. Hannah, thank you for helping me finish my research and for your effor...

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Mapping the unicellular transcriptome of the ascending thoracic aorta to changes in mechanosensing and mechanoadaptation during aging

Farra

Rivera

Silvestro

et al. 2022

Preprint

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Aortic stiffening is an inevitable manifestation of chronological aging, yet the mechano-molecular programs that orchestrate region- and layer-specific adaptations along the length and through the wall of the aorta are incompletely defined. Here, we show that the decline in passive cyclic distensibility is more pronounced in the ascending thoracic (ATA) compared to distal segments of the aorta and that tissues in both the medial and adventitial compartments of the ATA stiffen during aging. Single-cell RNA sequencing of aged ATA tissues reveals altered cellular senescence, remodeling, and inflammatory responses accompanied by enrichment of T-lymphocytes and rarefaction of vascular smooth muscle cells, compared to young samples. T-lymphocytes accumulate in the adventitia and likely promote fibrosis, while activation of mechanosensitive piezo-1 enhances medial vasoconstriction. These results portray the immuno-mechanical aging of the ATA as a process that culminates in a stiffer conduit permissive to the accrual of multi-gerogenic signals priming to disease development.

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Respiratory mechanics following chronic cigarette smoke exposure in the Apoe$$^{-/-}$$ mouse model

Cited by 5 publications

References 75 publications

Chronic Pod-Mod E-Cigarette Aerosol Exposure Induces Aortic Dysfunction in Hypercholesterolemic Mice: Role of Oxidative Stress and Inflammation

Chronic Pod-Mod E-Cigarette Aerosol Exposure Induces Aortic Dysfunction in Hypercholesterolemic Mice: Role of Oxidative Stress and Inflammation

Cardiovascular outcomes of wildland fire smoke inhalation: a robust preclinical exposure paradigm to infer the occupational risk of wildland firefighting

Mapping the unicellular transcriptome of the ascending thoracic aorta to changes in mechanosensing and mechanoadaptation during aging

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