Gestational chronic intermittent hypoxia triggers maternal inflammation and disrupts placental stress responses.

Gestational hypoxia is associated with placental cellular responses, including oxidative stress and inflammation. Circulating cell-free mitochondrial DNA (ccf-mtDNA) is a marker of cell stress that can be transported within extracellular vehicles (EVs), eliciting proinflammatory responses. We hypothesized that systemic exposure to chronic intermittent hypoxia (CIH) during late pregnancy would increase maternal inflammation, alter circulating EV characteristics, and disrupt placental stress responses.

Evidence of postnatal neglect-dependent resiliency in thymic, gut, and behavioral outcomes in a mouse model of early life stress.

Background: Early life is an impressionable period often regarded as the window of opportunity. Environmental exposures, such as stress, in the early postnatal period can influence developmental trajectory and long-term health. The brain and immune systems continue to develop after birth and are shaped by postnatal exposures.

Gestational Chronic Intermittent Hypoxia Triggers Maternal Inflammation and Disrupts Placental Stress Responses.

Gestational hypoxia is associated with placental cellular responses, including oxidative stress and inflammation. Circulating cell-free mitochondrial DNA (ccf-mtDNA) is a marker of cell stress, that can be transported within extracellular vehicles (EVs), eliciting proinflammatory responses. We hypothesized that systemic exposure to chronic intermittent hypoxia (CIH) during late pregnancy would increase maternal inflammation, alter circulating EV characteristics, and disrupt placental stress responses.

Oxidative stress induces release of mitochondrial DNA into the extracellular space in human placental villous trophoblast BeWo cells.

Circulating cell-free mitochondrial DNA (ccf-mtDNA) is an indicator of cell death, inflammation, and oxidative stress. ccf-mtDNA in pregnancies with placental dysfunction differs from that in healthy pregnancies, and the direction of this difference depends on gestational age and method of mtDNA quantification. Reactive oxygen species (ROS) trigger release of mtDNA, yet it is unknown whether trophoblast cells release mtDNA in response to oxidative stress, a common feature of pregnancies with placental pathology.

Oxidative stress induces release of mitochondrial DNA into the extracellular space in human placental villous trophoblast BeWo cells.

Unlabelled: Circulating cell-free mitochondrial DNA (ccf-mtDNA) is an indicator of cell death, inflammation, and oxidative stress. ccf-mtDNA differs in pregnancies with placental dysfunction from healthy pregnancies and the direction of this difference depends on gestational age and method of mtDNA quantification. Reactive oxygen species (ROS) trigger release of mtDNA from non-placental cells; yet it is unknown whether trophoblast cells release mtDNA in response to oxidative stress, a common feature of pregnancies with placental pathology.

Blood-Based mtDNA Quantification Indicates Population-Specific Differences Associated with Alzheimer's Disease-Related Risk.

Background: Age is known to be the biggest risk factor for Alzheimer's disease (AD), and Mexican Americans (MAs), who are one of the fastest-aging populations in the United States, are at a uniquely elevated risk. Mitochondrial stress and dysfunction are key players in the progression of AD and are also known to be impacted by lifestyle and environmental exposures/stressors.

Objective: This study aimed to identify population-specific differences in indicators of mitochondrial stress and dysfunction associated with AD risk that are detectable in the blood.

Mitochondrial SOS: how mtDNA may act as a stress signal in Alzheimer's disease.

Background: Alterations in mitochondrial DNA (mtDNA) levels have been observed in Alzheimer's disease and are an area of research that shows promise as a useful biomarker. It is well known that not only are the mitochondria a key player in producing energy for the cell, but they also are known to interact in other important intracellular processes as well as extracellular signaling and communication. BODY: This mini review explores how cells use mtDNA as a stress signal, particularly in Alzheimer's disease.