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Variation in senescent-dependent lung changes in inbred mouse strains.

Variation in senescent-dependent lung changes in inbred mouse strains. Research Abstract Details 

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  • Variation in senescent-dependent lung changes in inbred mouse strains. Abstract Text:

    kewu huangKewu Huang,wayne mitznerWayne Mitzner,richard raboldRichard Rabold,brian schofieldBrian Schofield,hannah leeHannah Lee,shyam biswalShyam Biswal,clarke g tankersleyClarke G Tankersley,

    Previous studies from our laboratories showed lung development differences between inbred strains of mice. In the present study, the C57BL/6J (B6) and DBA/2J (D2) strains were examined for senescent-dependent differences with respect to the lung structure and function. Specifically, we hypothesize that senescent changes in lung vary between strains due to identifiable gene expression differences. Quasi-static pressure-volume curves and respiratory impedance measurements were performed on 2- and 20-mo-old B6 and D2 mice. Lung volume at 30 cm H(2)O (V(30)) pressure was significantly (P < 0.01) increased with age in both strains, but the increase was proportionally greater in D2 (68%) than in B6 (40%) mice. In addition, decreased elastic recoil pressure at 50% of V(30) and a reduction in airway resistance as a function of positive end-expiratory pressure were observed in 20-mo-old D2 mice but not in B6 mice. Morphometric analysis of lung parenchyma showed significant decreases in elastic fiber content with age in both strains, but the collagen content was significantly (P < 0.01) increased with age in D2 but not B6 mice at 20 mo. Furthermore, using quantitative RT-PCR methods, gene expression differences between strains suggested that D2 mice significantly (P < 0.05) downregulated the expressions of elastin (Eln) and procollagen I, III, and VI (Col1a1, Col3a1, and Col6a3) in lung tissue at 20 mo of age. These age-dependent changes were accompanied by an increased gene expression in matrix metalloproteinase 9 (Mmp9) in D2 and an increase in tissue inhibitor of matrix metalloproteinase (Timp1 and Timp4) in B6 mice. In conclusion, the results from the present study demonstrate that lung mechanics of both strains show significant age-dependent changes. However, changes in D2 mice are accelerated relative to B6 mice. Moreover, gene expression differences appear to be involved in the strain-specific changes of lung mechanic properties.

    Variation in senescent-dependent lung changes in inbred mouse strains. Publishing Authors By Initials

    k huangK Huang,w mitznerW Mitzner,r raboldR Rabold,b schofieldB Schofield,h leeH Lee,s biswalS Biswal,cg tankersleyCG Tankersley,

    For similar biological phenomena, cell phenomena, and immunity: immunity: antibody specificity: species specificity research abstracts see: biological phenomena, cell phenomena, and immunity: immunity: antibody specificity: species specificity research

    PUBMED ID PMID:

    MEDLINE DATE:

    Variation in senescent-dependent lung changes in inbred mouse strains. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: Journal of applied physiology (Bethesda, Md. : 198

    VOLUME: 102

    Page Numbers: 1632-9

    Journal Abbreviation:

    ISSN: 8750-7587

    DAY: 11

    MONTH: 01

    YEAR: 2007

    Variation in senescent-dependent lung changes in inbred mouse strains. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 8502536

    Variation in senescent-dependent lung changes in inbred mouse strains. Keywords Mesh Terms:

    KEYWORDS: Species Specificity

    MESH TERMS: physiology

    Chemical & Substance for Abstract: Variation in senescent-dependent lung changes in inbred mouse strains. Information

    Substance Name: Extracellular Matrix Proteins

    Registry Number: 0

    Grant and Affiliation Information for Variation in senescent-dependent lung changes in inbred mouse strains.

    AFFILIATION: Johns Hopkins Bloomberg School of Public Health, Department of Environmental Health Sciences, Baltimore, Maryland 21205, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NHLBI

    GRANT: HL-081205

    ACRONYM: HL

    MEDLINETA: J Appl Physiol

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

    Number Hits: 0

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