A novel model of senile lung: senescence-accelerated mouse (SAM).

Teramoto, Shinji; Fukuchi, Yoshinosuke; Uejima, Yoji; Teramoto, Kazuko; Oka, Teruaki; Orimo, Hajime

doi:10.1164/ajrccm.150.1.8025756

Cited by 55 publications

(56 citation statements)

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“…The AKR/J strain is relatively short-lived compared with other inbred strains (Teramoto et al, 1994). The mean life span for the AKR/J strain in our facilities is 319 ± 14 days with a range between 197 and 548 days (Tankersley et al, 2003).…”

Section: Animalsmentioning

confidence: 79%

Particle Effects on Heart-Rate Regulation in Senescent Mice

Tankersley

Campen

Bierman

et al. 2004

Inhalation Toxicology

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Because epidemiology studies consistently identify the elderly at risk for air pollution-related morbidity and mortality, we developed a model of senescent-dependent susceptibility based on indices of physiological aging. In the current study, we hypothesized that heart-rate regulation during particulate matter (PM) exposure differs with senescence-dependent susceptibility owing to variation in autonomic nervous control. Heart rate (HR) and heart-rate variability (HRV) parameters were measured from 162 samples of 2-min electrocardiograph (ECG) recordings in age-matched healthy (n = 5) and terminally senescent (n = 3) AKR mice during 3-h exposures to filtered-air (FA, day 1) and carbon black (CB, day 4; <200 µg/m 3 ). On day 1, HR was significantly (p < .01) depressed during FA in terminally senescent mice. By day 4, HR was further slowed significantly (p < .01) due to the effects of CB exposure for 3 days. The combined effects of terminal senescence and CB exposure acted to depress HR to an average (±SEM) 445 ± 40 bpm, or ∼80 bpm lower compared to healthy HR responses. The change in rMSSD, an HRV parameter corresponding to relative influences of parasympathetic tone on HR, was significantly (p < .01) greater on day 1 and day 4 in terminally senescent mice compared to healthy mice. In contrast, the LF/HF ratio, an HRV parameter derived from spectral analysis indicating relative changes in cardiac sympathetic tone, was significantly (p < .01) depressed in terminally senescent mice on day 1. By day 4, significant increases in LF/HF were evident in healthy mice during CB exposure, suggesting that HR regulation was associated with an increase in sympathetic tone. Alternatively, terminally senescent mice appeared to modulate a lower HR without change in LF/HF ratio during CB exposure, suggesting an absence of sympathetic tone. In conclusion, older healthy mice increase cardiac sympathetic tone during PM exposure while terminally senescent mice show a greater PM-induced parasympathetic tone in regulating HR. The significance of the current results suggest that PM-induced HR regulatory changes may ultimately depend on the degree of physiological aging.

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Section: Animalsmentioning

confidence: 79%

Particle Effects on Heart-Rate Regulation in Senescent Mice

Tankersley

Campen

Bierman

et al. 2004

Inhalation Toxicology

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“…Como consecuencia de ello se produce una disminución de la relación ventilación/perfusión (V'/Q') y de los flujos espiratorios. Es interesante señalar que en la cepa de ratones SAM P2 que sufren un envejecimiento acelerado, se ha encontrado que la curva presión-volumen de los pulmones aislados se desplaza hacia la izquierda en relación a los controles y aumenta significativamente la constante experimental "k" que describe la forma de la curva presión-volumen de los pulmones aislados 6 . b) Disminución de la distensibilidad del tórax.…”

Section: Artículo De Revisiónunclassified

Función respiratoria en la senectud

2009

Rev. méd. Chile

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“…Indeed, lungs of aged rodents show similar "senile" changes when compared with lungs of young animals [35]. However, premature ageing in mouse models does not always recapitulate senile emphysema: senescence-accelerated mice (SAM), Klotho-, and senescence-marker protein-30 deficient mice show air space enlargement without airway wall destruction [36][37][38][39]. In contrast, no functional and structural changes in the lungs were observed in prematurely aged telomerase RNA knock-out mice [40].…”

Section: Introductionmentioning

confidence: 99%

Hallmarks of the ageing lung

2015

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Ageing is the main risk factor for major non-communicable chronic lung diseases, including chronic obstructive pulmonary disease, most forms of lung cancer and idiopathic pulmonary fibrosis. While the prevalence of these diseases continually increases with age, their respective incidence peaks at different times during the lifespan, suggesting specific effects of ageing on the onset and/or pathogenesis of chronic obstructive pulmonary disease, lung cancer and idiopathic pulmonary fibrosis. Recently, the nine hallmarks of ageing have been defined as cell-autonomous and non-autonomous pathways involved in ageing. Here, we review the available evidence for the involvement of each of these hallmarks in the pathogenesis of chronic obstructive pulmonary disease, lung cancer, or idiopathic pulmonary fibrosis. Importantly, we propose an additional hallmark, "dysregulation of the extracellular matrix", which we argue acts as a crucial modifier of cell-autonomous changes and functions, and as a key feature of the above-mentioned lung diseases. @ERSpublications Hallmarks of ageing are selecting factors for the pathogenesis of COPD, lung cancer and IPF

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A novel model of senile lung: senescence-accelerated mouse (SAM).

Cited by 55 publications

References 0 publications

Particle Effects on Heart-Rate Regulation in Senescent Mice

Particle Effects on Heart-Rate Regulation in Senescent Mice

Función respiratoria en la senectud

Hallmarks of the ageing lung

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