EXPOSURE TO AIR POLLUTION FINE PARTICULATE MATTER (PM2.5) PROMOTES ADIPOSE TISSUE INFLAMMATION AND OBESITY BY IMPAIRING THERMOGENESIS

JORGE A. NARVAÉZ PARDO; BENJAMÍN BARRALES; BRUNO BUCHHOLZ; DOMINICI, FERNANDO PABLO; SANTIAGO DE LA FUENTE; MARIELA GIRONACCI; PABLO A EVELSON; AGUSTINA FREIRE; MARINA C MUÑOZ; NATALIA MAGNANI

Mar del Plata

Congreso; LXVII Reunión anual de la Sociedad Argentina de Investigación Clínica (SAIC); 2023

REUNIÓN ANUAL DE LA SOCIEDAD ARGENTINA DE INVESTIGACIÓN CLÍNICA (SAIC)

EXPOSURE TO AIR POLLUTION FINE PARTICULATE MATTER (PM2.5) ALTERS EXPRESSION OF SYS-TEMIC AND TISSUE-SPECIFIC COMPONENTS OF THE RENIN-ANGIOTENSIN SYSTEMPrevious studies have implicated air pollution fine particulate matter (PM2.5) in various cardiovascular and cardiometabolic disease states. However, the molecular mechanisms by which these pollutants mediate these comorbidities have not been fully elucidated. Dysregulation of the renin-angiotensin system (RAS) may be one potential mechanism. To study the impact of PM2.5 on systemic and tissue components of the RAS, male 8-week-old Balb/C mice were exposed to filtered air (FA) or urban air (UA) from Buenos Aires City, in whole-body exposure chambers for 14 weeks. Levels of main RAS components including angiotensin converting enzyme (ACE) and ACE2, as well as AT1, AT2 and Mas receptors (R) abundance were determined in kidney, heart and lung tissue by Western Blotting (WB) and their corresponding mRNA expression was detected by RT-qPCR. Circulating angiotensin (Ang) II levels were determined by radioimmunoassay. Exposure to air pollution resulted in increased mRNA levels of ACE and MasR, and increased protein levels of ACE in the kidney; upregulated mRNA and protein abundance of cardiac and pulmonary AT2R and MasR, together with increased levels of proteins nitrated at Tyr residues in both kidney and lung homogenates, indicative of nitrosative stress in these tissues. In addition, exposure to PM2.5 was associated with increased levels of circulating Ang II, indicative of an exacerbation of the RAS. Our findings indicate that chronic exposure to air pollution induces an altered expression of both tissue and systemic components of the RAS. Given that both the AT2R and the MasR have been ascribedto participate in tissue-repair mechanisms, the upregulation of thesereceptors detected in mice hearts and lungs after chronic exposureto polluted air could represent a mechanism of tissue protectionagainst damage induced by PM2.5.