Reactive oxygen species and respiratory plasticity following intermittent hypoxia

Abstract

The neural network controlling breathing exhibits plasticity in response to environmental or physiological challenges. For example, while hypoxia initiates rapid and robust increases in respiratory motor output to defend against hypoxemia, it also triggers persistent changes, or plasticity, in chemosensory neurons and integrative pathways that transmit brainstem respiratory activity to respiratory motor neurons. Frequently studied models of hypoxia-induced respiratory plasticity include: 1) carotid chemosensory plasticity and metaplasticity induced by chronic intermittent hypoxia (CIH), and 2) acute intermittent hypoxia (AIH) induced phrenic long-term facilitation (pLTF) in naïve and CIH preconditioned rats. These forms of plasticity share some mechanistic elements, although they differ in anatomical location and the requirement for CIH preconditioning. Both forms of plasticity require serotonin receptor activation and formation of reactive oxygen species (ROS). While the cellular sources and targets of ROS are not well known, recent evidence suggests that ROS modify the balance of protein phosphatase and kinase activities, shifting the balance towards net phosphorylation and favoring cellular reactions that induce and/or maintain plasticity. Here, we review possible sources of ROS, and the impact of ROS on phosphorylation events relevant to respiratory plasticity.

Canonical Transient Receptor Potential 6 Channel: A New Target of Reactive Oxygen Species in Renal Physiology and Pathology

“…Because chronic hypoxia is usually accompanied with oxidative stress (124,143,155,157), the results from the Liao et al study seem to contradict with ours. However, multiple signaling pathways, such as Ang II signaling, are activated by chronic hypoxia (35, 54, 128, 129, 159).…”

Distinct physiological strategies are used to cope with constant hypoxia and intermittent hypoxia in killifish (Fundulus heteroclitus)

“…Acclimation to intermittent hypoxia increases hypoxia tolerance in killifish, and the mechanisms involved appear to be distinct from those for constant hypoxia. Intermittent hypoxia is also known to have different effects than constant hypoxia on the control of ventilation and circulation in mammals (MacFarlane et al, 2008;Prabhakar and Semenza, 2012). On the one hand, it is possible that comparable changes occur in fish and mammals in response to intermittent hypoxia.…”

Lipid Raft Redox Signaling: Molecular Mechanisms in Health and Disease

“…Introduction R edox signaling is increasingly regarded as an important cellular process in a variety of cellular activities, including cell proliferation (50,52,275), differentiation (72,153,219,337,338), and apoptosis (162,242,254,304,413). Redox injury, as a pathological mechanism, is also involved in a wide range of pathophysiological processes such as senescence (65), inflammation (17,264,421), hypoxia (32,148,200,245), and ischemia/reperfusion (126,379,384), which contribute to the progression of almost all diseases, from cardiovascular ones such as shock (94,116,117), hypertension (73,167,288,294,316,440), atherosclerosis (208,297), to metabolic ones such as diabetes mellitus (20,217), neurodegenerative ones such as Alzheimer's disease (AD) (55,305), infectious diseases (184,252,285,375), and cancer (16,…”