CO metabolism, sensing, and signaling

Abstract

Abstract.CO is a colorless and odorless gas produced by the incomplete combustion of hydrocarbons, both of natural and anthropogenic origin. Several microorganisms, including aerobic and anaerobic bacteria and anaerobic archaea, use exogenous CO as a source of carbon and energy for growth. On the other hand, eukaryotic organisms use endogenous CO, produced during heme degradation, as a neurotransmitter and as a signal molecule. CO sensors act as signal transducers by coupling a ''regulatory'' heme-binding domain to a ''functional'' signal transmitter. Although high CO concentrations inhibit generally heme-protein actions, low CO levels can influence several signaling pathways, including those regulated by soluble guanylate cyclase and/or mitogenactivated protein kinases. This review summarizes recent insights into CO metabolism, sensing, and signaling.

Changes in the deep subsurface microbial biosphere resulting from a field-scale CO2 geosequestration experiment

“…(Svetlitchnyi et al, 2001; Ragsdale, 2004; Oelgeschläger and Rother, 2008; Sokolova et al, 2009; Gullotta et al, 2011; Techtmann et al, 2011; Wilkins and Atiyeh, 2011). …”

CO-independent modification of K + channels by tricarbonyldichlororuthenium(II) dimer (CORM-2)

“…Gullotta et al 2012; Wegiel et al, 2013). For example, it is generally accepted that activation of large-conductance, Ca 2+ - and voltage-activated K + (K Ca 1.1) channels contributes to the CO-dependent vasorelaxation (Wang et al, 1997; Williams et al, 2004).…”

Effect of carbon monoxide on gene expression in cerebrocortical astrocytes: Validation of reference genes for quantitative real-time PCR

“…Exogenous administration of CO is beneficial in several pathologies [3][4][5][6][7][16][17][18][19][20] by acting as metabolic modulator [20], anti-apoptotic molecule [21], anti-inflammatory agent [22], stemness regulator [23], vasodilator [24], modulator of proliferation [25] and anti-rejection agent in organ transplantation [26]. The effects of CO, either from exogenous or endogenous sources, are mediated by multiple pathways, including mitogen-activated protein kinases (MAPKs), nitric oxide (NO), soluble guanylyl cyclase (sGC), peroxisome proliferator-activated receptor gamma (PPARɣ) [3][4][5]27] and mitochondrial function (cell death control and cell metabolism) [28]. In the Central Nervous System (CNS) CO limits neuroinflammation [29,30] and promotes cytoprotection in in vivo cerebral ischemia [11,31].…”

“…Several studies have addressed the molecular mechanisms underlying the effects of CO in the treatment of pathologies as diverse as vascular and cerebral diseases, cancer and inflammation [3][4][5][6][7][8][9][10][11][12][13][14][15]. Exogenous administration of CO is beneficial in several pathologies [3][4][5][6][7][16][17][18][19][20] by acting as metabolic modulator [20], anti-apoptotic molecule [21], anti-inflammatory agent [22], stemness regulator [23], vasodilator [24], modulator of proliferation [25] and anti-rejection agent in organ transplantation [26].…”