Effect of long-term maternal smoking on the offspring's lung health.
Surpon SukjamnongYik Lung ChanRazia ZakaryaSonia SaadPawan SharmaRachana SantiyanontHui ChenBrian Gregory George OliverPublished in: American journal of physiology. Lung cellular and molecular physiology (2017)
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.
Keyphrases
- oxidative stress
- high fat diet
- nuclear factor
- signaling pathway
- birth weight
- pregnancy outcomes
- reactive oxygen species
- public health
- toll like receptor
- healthcare
- induced apoptosis
- cell death
- adipose tissue
- weight gain
- epithelial mesenchymal transition
- pi k akt
- clinical trial
- hydrogen peroxide
- inflammatory response
- pulmonary hypertension
- depressive symptoms
- risk assessment
- gestational age
- young adults
- anti inflammatory
- nitric oxide
- tyrosine kinase
- health information
- room temperature
- preterm birth
- transcription factor
- smoking cessation
- climate change
- diabetic rats
- cell proliferation
- type diabetes
- ionic liquid
- high fat diet induced
- double blind
- endoplasmic reticulum stress
- human health
- replacement therapy
- health promotion