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In Utero PM 2.5 Exposure Contributes to Adult Cardiac Dysfunction
Author(s) -
Tanwar Vineeta,
Gorr Matthew,
Eichenseer Clayton,
Wold Loren
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.1043.14
Subject(s) - in utero , cardiac function curve , western blot , endocrinology , medicine , andrology , biology , chemistry , pregnancy , fetus , heart failure , biochemistry , gene , genetics
The present study was designed to investigate the effects of in utero exposure to PM 2.5 on the adult cardiac functions. Female FVB mice were exposed either to filtered air (FA) or particulate matter (PM 2.5 ) at concentration of 51.69 μg/m 3 for 6 h/day, 7 days/wk throughout pregnancy. To examine cardiac function, male offsprings at 12 weeks of age underwent a baseline echocardiographic assessment. Following sacrifice, cardiomyocytes were isolated to assess cardiac dysfunction at cellular level using IonOptix. LV tissue from separate group of mice was used to isolate mRNA and protein to study underlying mechanisms. Mice exposed to PM 2.5 in utero demonstrated increased LVESd and LVEDd dimensions and reduced PWTs. Morphological alterations were associated with lower systolic function as indicated by reduced FS in PM 2.5 exposed mice compared to FA controls. Cardiomyocytes isolated from PM 2.5 exposed hearts showed reduced %PS compared to FA exposed hearts. ‐dL/dt was significantly reduced whereas +dL/dt, TR90 and TPS90 remain unchanged between the groups. qPCR analyses revealed decreased TNF‐α, increased IL‐1ß, collagen I and MMP9 expression in one‐day‐old mice exposed to PM 2.5 in utero compared to FA. Western blot analyses demonstrated modified NCX, SERCA and PLN expression in PM 2.5 compared to FA exposed hearts. Mass spectrometry revealed differential expression of proteins involved in maintaining cardiac physiological functions in PM 2.5 compared to FA exposed hearts. Conclusions In utero PM 2.5 exposure triggers an inflammatory and profibrotic response and alters Ca 2+ homeostasis (through NCX, SERCA and PLN hypophosphorylation) thereby promoting adult cardiac dysfunction.