Role of cystathionine-γ-lyase in hypoxia-induced changes in TASK activity, intracellular [Ca 2+ ] and ventilation in mice

Wang, Jiaju; Hogan, James O.; Wang, Rui; White, Carl; Kim, Dong‐Hee

doi:10.1016/j.resp.2017.08.009

Cited by 26 publications

(25 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As with hypoxia ( Buckler and Vaughan-Jones, 1994 ; Urena et al, 1994 ), the increases in [Ca 2+ ] i are dependent on cellular depolarization and extracellular Ca 2+ influx through voltage gated Ca 2+ channels ( Wyatt and Buckler, 2004 ). TASK1/3, TREK-1, BK Ca , K v 4.1, and K v 4.3, have all been shown to be expressed in the CB and inhibited by hypoxia ( Buckler et al, 2000 ; Sanchez et al, 2002 ; Williams et al, 2004 ; Yamamoto and Taniguchi, 2006 ; Kim et al, 2009 ; Kreneisz et al, 2009 ; Turner and Buckler, 2013 ; Wang et al, 2017b ). Of these, TASK1/3 and TASK-like K + currents are diminished by a multitude of mitochondrial inhibitors leading to membrane depolarization ( Barbe et al, 2002 ; Wyatt and Buckler, 2004 ; Buckler, 2011 ; Turner and Buckler, 2013 ; Kim D. et al, 2015 ).…”

Section: Mitochondrial Inhibitors Mimic All Aspects Of the Carotid Bomentioning

confidence: 99%

Is Carotid Body Physiological O2 Sensitivity Determined by a Unique Mitochondrial Phenotype?

et al. 2018

View full text Add to dashboard Cite

The mammalian carotid body (CB) is the primary arterial chemoreceptor that responds to acute hypoxia, initiating systemic protective reflex responses that act to maintain O2 delivery to the brain and vital organs. The CB is unique in that it is stimulated at O2 levels above those that begin to impact on the metabolism of most other cell types. Whilst a large proportion of the CB chemotransduction cascade is well defined, the identity of the O2 sensor remains highly controversial. This short review evaluates whether the mitochondria can adequately function as acute O2 sensors in the CB. We consider the similarities between mitochondrial poisons and hypoxic stimuli in their ability to activate the CB chemotransduction cascade and initiate rapid cardiorespiratory reflexes. We evaluate whether the mitochondria are required for the CB to respond to hypoxia. We also discuss if the CB mitochondria are different to those located in other non-O2 sensitive cells, and what might cause them to have an unusually low O2 binding affinity. In particular we look at the potential roles of competitive inhibitors of mitochondrial complex IV such as nitric oxide in establishing mitochondrial and CB O2-sensitivity. Finally, we discuss novel signaling mechanisms proposed to take place within and downstream of mitochondria that link mitochondrial metabolism with cellular depolarization.

show abstract

Section: Mitochondrial Inhibitors Mimic All Aspects Of the Carotid Bomentioning

confidence: 99%

Is Carotid Body Physiological O2 Sensitivity Determined by a Unique Mitochondrial Phenotype?

et al. 2018

View full text Add to dashboard Cite

show abstract

“…In the carotid body, the mechanism involves a reduced activity of HO-2 which in turn increases CSE activity and thus H 2 S production; however, the role of CSE and H 2 S in the hypoxia sensing is not universally accepted. Recently, Wang et al ( 2017 ) reported that in glomus cells from CSE −/− mice, hypoxia-dependent effects on TASK-like channels, intracellular calcium, and ventilation were not modified. Even if the study does not provide a role for CSE in acute hypoxia sensing, this cannot be excluded (Wang et al, 2017 ), also considering that CSE inhibition affects the hypoxia response in chronic pathological states (Yuan et al, 2016 ).…”

Section: Three Hypotheses For Oxygen-sensing and Downstream Responsesmentioning

confidence: 99%

Hypoxia Tolerance in Teleosts: Implications of Cardiac Nitrosative Signals

Gattuso¹,

Garofalo²,

Cerra³

et al. 2018

Front. Physiol.

View full text Add to dashboard Cite

Changes in environmental oxygen (O2) are naturally occurring phenomena which ectotherms have to face on. Many species exhibit a striking capacity to survive and remain active for long periods under hypoxia, even tolerating anoxia. Some fundamental adaptations contribute to this capacity: metabolic suppression, tolerance of pH and ionic unbalance, avoidance and/or repair of free-radical-induced cell injury during reoxygenation. A remarkable feature of these species is their ability to preserve a normal cardiovascular performance during hypoxia/anoxia to match peripheral (tissue pO2) requirements. In this review, we will refer to paradigms of hypoxia- and anoxia-tolerant teleost fish to illustrate cardiac physiological strategies that, by involving nitric oxide and its metabolites, play a critical role in the adaptive responses to O2 limitation. The information here reported may contribute to clarify the molecular and cellular mechanisms underlying heart vulnerability vs. resistance in relation to O2 availability.

show abstract

“…However, as with the majority of hypotheses of acute oxygen sensing there are now conflicting data to temper any enthusiasm. Recent studies have indicated that an increase in H 2 S does not modulate ion channels (Kim et al 2015) and knockout of the enzymes that produce H 2 S has no effect on acute oxygen sensing in the carotid body (Wang et al 2017). These contradictory data will need to be addressed before we can fully understand the role of H 2 S in acute oxygen sensing.…”

Section: Hydrogen Sulphide Hypothesismentioning

confidence: 99%

“…) and knockout of the enzymes that produce H 2 S has no effect on acute oxygen sensing in the carotid body (Wang et al . ). These contradictory data will need to be addressed before we can fully understand the role of H 2 S in acute oxygen sensing.…”

Section: Introductionmentioning

confidence: 97%

Acute oxygen sensing by the carotid body: a rattlebag of molecular mechanisms

Rakoczy

Wyatt

2017

The Journal of Physiology

View full text Add to dashboard Cite

The molecular underpinnings of the oxygen sensitivity of the carotid body Type I cells are becoming better defined as research begins to identify potential interactions between previously separate theories. Nevertheless, the field of oxygen chemoreception still presents the general observer with a bewildering array of potential signalling pathways by which a fall in oxygen levels might initiate Type I cell activation. The purpose of this brief review is to address five of the current oxygen sensing hypotheses: the lactate-Olfr 78 hypothesis of oxygen chemotransduction; the role mitochondrial ATP and metabolism may have in chemotransduction; the AMP-activated protein kinase hypothesis and its current role in oxygen sensing by the carotid body; reactive oxygen species as key transducers in the oxygen sensing cascade; and the mechanisms by which H S, reactive oxygen species and haem oxygenase may integrate to provide a rapid oxygen sensing transduction system. Over the previous 15 years several lines of research into acute hypoxic chemotransduction mechanisms have focused on the integration of mitochondrial and membrane signalling. This review places an emphasis on the subplasmalemmal-mitochondrial microenvironment in Type I cells and how theories of acute oxygen sensing are increasingly dependent on functional interaction within this microenvironment.

show abstract

Role of cystathionine-γ-lyase in hypoxia-induced changes in TASK activity, intracellular [Ca 2+ ] and ventilation in mice

Cited by 26 publications

References 44 publications

Is Carotid Body Physiological O2 Sensitivity Determined by a Unique Mitochondrial Phenotype?

Is Carotid Body Physiological O2 Sensitivity Determined by a Unique Mitochondrial Phenotype?

Hypoxia Tolerance in Teleosts: Implications of Cardiac Nitrosative Signals

Acute oxygen sensing by the carotid body: a rattlebag of molecular mechanisms

Contact Info

Product

Resources

About