Effect of long-term maternal smoking on the offspring's lung health.
- Publisher:
- American Physiological Society
- Publication Type:
- Journal Article
- Citation:
- American Journal of Physiology - Lung Cellular and Molecular Physiology, 2017, 313 (2), pp. L416 - L423
- Issue Date:
- 2017-08-01
Embargoed
Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author | Sukjamnong, S | en_US |
dc.contributor.author | Chan, YL | en_US |
dc.contributor.author | Zakarya, R | en_US |
dc.contributor.author | Saad, S | en_US |
dc.contributor.author | Sharma, P | en_US |
dc.contributor.author | Santiyanont, R | en_US |
dc.contributor.author | Chen, H | en_US |
dc.contributor.author | Oliver, BG | en_US |
dc.date.available | 2017-05-11 | en_US |
dc.date.issued | 2017-08-01 | en_US |
dc.identifier.citation | American Journal of Physiology - Lung Cellular and Molecular Physiology, 2017, 313 (2), pp. L416 - L423 | en_US |
dc.identifier.issn | 1040-0605 | en_US |
dc.identifier.uri | http://hdl.handle.net/10453/115193 | |
dc.description.abstract | Maternal smoking during pregnancy contributes to long-term health problems in offspring, especially respiratory disorders that can manifest in either childhood or adulthood. Receptors for advanced glycation end products (RAGE) are multiligand receptors abundantly localized in the lung, capable of responding to by-products of reactive oxygen species and proinflammatory responses. RAGE signaling is a key regulator of inflammation in cigarette smoking-related pulmonary diseases. However, the impact of maternal cigarette smoke exposure on lung RAGE signaling in the offspring is unclear. This study aims to investigate the effect of maternal cigarette smoke exposure (SE), as well as mitochondria-targeted antioxidant [mitoquinone mesylate (MitoQ)] treatment, during pregnancy on the RAGE-mediated signaling pathway in the lung of male offspring. Female Balb/c mice (8 wk) were divided into a sham group (exposed to air), an SE group (exposed to cigarette smoke), and an SE + MQ group (exposed to cigarette smoke with MitoQ supplement from mating). The lungs from male offspring were collected at 13 wk. RAGE and its downstream signaling, including nuclear factor-κB and mitogen-activated protein kinase family consisting of extracellular signal-regulated kinase 1, ERK2, c-JUN NH2-terminal kinase (JNK), and phosphorylated JNK, in the lung were significantly increased in the SE offspring. Mitochondrial antioxidant manganese superoxide dismutase was reduced, whereas IL-1β and oxidative stress response nuclear factor (erythroid-derived 2)-like 2 were significantly increased in the SE offspring. Maternal MitoQ treatment normalized RAGE, IL-1β, and Nrf-2 levels in the SE + MQ offspring. Maternal SE increased RAGE and its signaling elements associated with increased oxidative stress and inflammatory cytokines in offspring lungs, whereas maternal MitoQ treatment can partially normalize these changes. | en_US |
dc.language | eng | en_US |
dc.publisher | American Physiological Society | en_US |
dc.relation | http://purl.org/au-research/grants/nhmrc/APP1110368 | |
dc.relation.ispartof | American Journal of Physiology - Lung Cellular and Molecular Physiology | en_US |
dc.relation.isbasedon | 10.1152/ajplung.00134.2017 | en_US |
dc.subject.classification | Respiratory System | en_US |
dc.subject.mesh | Lung | en_US |
dc.subject.mesh | Mitochondria | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Mice, Inbred BALB C | en_US |
dc.subject.mesh | Mice | en_US |
dc.subject.mesh | Tobacco | en_US |
dc.subject.mesh | Prenatal Exposure Delayed Effects | en_US |
dc.subject.mesh | Inflammation | en_US |
dc.subject.mesh | Smoking | en_US |
dc.subject.mesh | Smoke | en_US |
dc.subject.mesh | Maternal Exposure | en_US |
dc.subject.mesh | Signal Transduction | en_US |
dc.subject.mesh | Oxidative Stress | en_US |
dc.subject.mesh | Pregnancy | en_US |
dc.subject.mesh | Female | en_US |
dc.subject.mesh | Male | en_US |
dc.subject.mesh | Advanced Glycosylation End Product-Specific Receptor | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Female | en_US |
dc.subject.mesh | Inflammation | en_US |
dc.subject.mesh | Lung | en_US |
dc.subject.mesh | Male | en_US |
dc.subject.mesh | Maternal Exposure | en_US |
dc.subject.mesh | Mice | en_US |
dc.subject.mesh | Mice, Inbred BALB C | en_US |
dc.subject.mesh | Mitochondria | en_US |
dc.subject.mesh | Oxidative Stress | en_US |
dc.subject.mesh | Pregnancy | en_US |
dc.subject.mesh | Prenatal Exposure Delayed Effects | en_US |
dc.subject.mesh | Receptor for Advanced Glycation End Products | en_US |
dc.subject.mesh | Signal Transduction | en_US |
dc.subject.mesh | Smoke | en_US |
dc.subject.mesh | Smoking | en_US |
dc.subject.mesh | Tobacco | en_US |
dc.title | Effect of long-term maternal smoking on the offspring's lung health. | en_US |
dc.type | Journal Article | |
utslib.description.version | Published | en_US |
utslib.citation.volume | 2 | en_US |
utslib.citation.volume | 313 | en_US |
utslib.location.activity | United States | en_US |
utslib.for | 0606 Physiology | en_US |
utslib.for | 1116 Medical Physiology | en_US |
pubs.embargo.period | Not known | en_US |
pubs.organisational-group | /University of Technology Sydney | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science/School of Life Sciences | |
pubs.organisational-group | /University of Technology Sydney/Strength - CHT - Health Technologies | |
utslib.copyright.status | embargoed | |
pubs.consider-herdc | false | en_US |
utslib.copyright.embargo | 2018-08-02T00:00:00+1000 | |
pubs.issue | 2 | en_US |
pubs.publication-status | Published | en_US |
pubs.volume | 313 | en_US |
Files in This Item:
Filename | Description | Size | |||
---|---|---|---|---|---|
ajplung.00134.2017.full.pdf | Accepted Manuscript | 773.86 kB | Adobe PDF |
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Abstract:
Maternal smoking during pregnancy contributes to long-term health problems in offspring, especially respiratory disorders that can manifest in either childhood or adulthood. Receptors for advanced glycation end products (RAGE) are multiligand receptors abundantly localized in the lung, capable of responding to by-products of reactive oxygen species and proinflammatory responses. RAGE signaling is a key regulator of inflammation in cigarette smoking-related pulmonary diseases. However, the impact of maternal cigarette smoke exposure on lung RAGE signaling in the offspring is unclear. This study aims to investigate the effect of maternal cigarette smoke exposure (SE), as well as mitochondria-targeted antioxidant [mitoquinone mesylate (MitoQ)] treatment, during pregnancy on the RAGE-mediated signaling pathway in the lung of male offspring. Female Balb/c mice (8 wk) were divided into a sham group (exposed to air), an SE group (exposed to cigarette smoke), and an SE + MQ group (exposed to cigarette smoke with MitoQ supplement from mating). The lungs from male offspring were collected at 13 wk. RAGE and its downstream signaling, including nuclear factor-κB and mitogen-activated protein kinase family consisting of extracellular signal-regulated kinase 1, ERK2, c-JUN NH2-terminal kinase (JNK), and phosphorylated JNK, in the lung were significantly increased in the SE offspring. Mitochondrial antioxidant manganese superoxide dismutase was reduced, whereas IL-1β and oxidative stress response nuclear factor (erythroid-derived 2)-like 2 were significantly increased in the SE offspring. Maternal MitoQ treatment normalized RAGE, IL-1β, and Nrf-2 levels in the SE + MQ offspring. Maternal SE increased RAGE and its signaling elements associated with increased oxidative stress and inflammatory cytokines in offspring lungs, whereas maternal MitoQ treatment can partially normalize these changes.
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