Apoetm1Unc mice have impaired alveologenesis, low lung function, and rapid loss of lung function
Autor: | Donald Massaro, Gloria DeCarlo Massaro |
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Rok vydání: | 2008 |
Předmět: |
Male
Pulmonary and Respiratory Medicine Aging medicine.medical_specialty Physiology Biology Body size Body weight Short stature Mice Apolipoproteins E Physiology (medical) Internal medicine medicine Animals Body Size Respiratory system Lung Lung function Vascular disease Body Weight Lung volume measurement Cell Biology Atherosclerosis medicine.disease biology.organism_classification Respiratory Function Tests respiratory tract diseases Mice Inbred C57BL Pulmonary Alveoli Disease Models Animal Smok Immunology Cardiology medicine.symptom Lung Volume Measurements |
Zdroj: | American Journal of Physiology-Lung Cellular and Molecular Physiology. 294:L991-L997 |
ISSN: | 1522-1504 1040-0605 |
DOI: | 10.1152/ajplung.00013.2008 |
Popis: | Diminished lung function, indicated by a low forced expiratory volume in one second (FEV1), and short physical stature, predict early mortality from all causes, including cardiovascular, among smokers and never smokers. The basis for these associations is unclear, and, it is not known if there is a pulmonary morphological component to the relationship between low FEV1 and early death in a general population. Some apolipoprotein E genotypes also predict atherosclerosis and early mortality. These considerations led us to examine the Apoe tm1Unc (Apoe) mouse, in which the apolipoprotein E gene is deleted, and that develops dyslipidemia, atherosclerosis at an early age, and has a shorter life span than the founder wild-type (wt) strain. We asked if Apoe mice have a morphological or functional pulmonary phenotype. We measured the size, number, and surface area of pulmonary gas-exchange units (alveoli) and mechanical properties of the lung. Compared with wt mice, Apoe mice had: 1) diminished developmental alveologenesis, 2) increased airway resistance in early adulthood, 3) high lung volume and high dynamic and static compliance in later adulthood, 4) more rapid loss of lung recoil with age, and 5) were less long than wt mice. These findings in mice indicate the association of a low FEV1 with early death in humans may have developmental, and accelerated ageing, related pulmonary components, and that dietary, genetic, or dietary and genetic influences, on lipid metabolism may be an upstream cause of inflammation and oxidative stress, currently considered to be major risk factors for COPD. |
Databáze: | OpenAIRE |
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