Pannexin1 channels regulate mechanically stimulated but not spontaneous adenosine release

Lee, Scott T.; Chang, Yuanyu; Venton, B. Jill

doi:10.1007/s00216-022-04047-x

Cited by 6 publications

(4 citation statements)

References 46 publications

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“…Other rapidly signaling neurochemicals, including guanosine’s sister purine adenosine, have been demonstrated to release following local mechanical stimulation in a wide range of brain regions. ,,, However, we suspect that if guanosine is responding to mechanical stimulation, it is following a separate pathway than adenosine. Previous studies documenting adenosine release following electrode implantation show singular large, long events immediately after application of the stimulus. ,, We do not observe similar events. Rather, elevated guanosine release begins several seconds to 2 min following implantation and is not characterized by high concentrations or prolonged release.…”

Section: Resultscontrasting

confidence: 80%

“…Previous studies documenting adenosine release following electrode implantation show singular large, long events immediately after application of the stimulus. 40,50,51 We do not observe similar events. Rather, elevated guanosine release begins several seconds to 2 min following implantation and is not characterized by high concentrations or prolonged release.…”

Section: ■ Results and Discussioncontrasting

confidence: 51%

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Dynamic and Rapid Detection of Guanosine during Ischemia

Weese-Myers

Cryan

Witt

et al. 2023

ACS Chem. Neurosci.

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Guanosine acts in both neuroprotective and neurosignaling pathways in the central nervous system; in this paper, we present the first fast voltammetric measurements of endogenous guanosine release during pre-and post-ischemic conditions. We discuss the metric of our measurements via analysis of event concentration, duration, and interevent time of rapid guanosine release. We observe changes across all three metrics from our normoxic to ischemic conditions. Pharmacological studies were performed to confirm that guanosine release is a calcium-dependent process and that the signaling observed is purinergic. Finally, we show the validity of our ischemic model via staining and fluorescent imaging. Overall, this paper sets the tone for rapid monitoring of guanosine and provides a platform to investigate the extent to which guanosine accumulates at the site of brain injury, i.e., ischemia.

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Section: Resultscontrasting

confidence: 80%

Section: ■ Results and Discussioncontrasting

confidence: 51%

Dynamic and Rapid Detection of Guanosine during Ischemia

Weese-Myers

Cryan

Witt

et al. 2023

ACS Chem. Neurosci.

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“…Previous studies showed that among various processes implicated in sleep homeostasis, adenosine—a critical component of the cell metabolic pathway—was a prominent physiological mediator of sleep homeostasis ( 64 ). Pannexin-1 is a release mechanism for mechanically stimulated adenosine release, pannexin channels can regulate rapid adenosine release and be targeted to differentially affect mechanically stimulated adenosine due to brain damage ( 65 ). Our previous studies have shown that the concentration of adenosine in CID patients was reduced and was associated with poor sleep quality ( 66 ).…”

Section: Discussionmentioning

confidence: 99%

Serum levels of neurotensin, pannexin-1, and sestrin-2 and the correlations with sleep quality or/and cognitive function in the patients with chronic insomnia disorder

Su,

Ma,

et al. 2024

Front. Psychiatry

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ObjectivesTo examine serum concentrations of neurotensin, pannexin-1 and sestrin-2, and their correlations with subjective and objective sleep quality and cognitive function in the patients with chronic insomnia disorder (CID).MethodsSixty-five CID patients were enrolled continuously and fifty-six good sleepers in the same period were served as healthy controls (HCs). Serum levels of neurotensin, pannexin-1 and sestrin-2 were measured by enzyme-linked immunosorbent assays. Sleep quality was assessed with the Pittsburgh Sleep Quality Index (PSQI) and polysomnography, and mood was evaluated by 17-item Hamilton Depression Rating Scale. General cognitive function was assessed with the Chinese-Beijing Version of Montreal Cognitive Assessment and spatial memory was evaluated by Blue Velvet Arena Test (BVAT).ResultsRelative to the HCs, the CID sufferers had higher levels of neurotensin (t=5.210, p<0.001) and pannexin-1 (Z=−4.169, p<0.001), and lower level of sestrin-2 (Z=−2.438, p=0.015). In terms of objective sleep measures, pannexin-1 was positively associated with total sleep time (r=0.562, p=0.002) and sleep efficiency (r=0.588, p=0.001), and negatively with wake time after sleep onset (r=−0.590, p=0.001) and wake time (r=−0.590, p=0.001); sestrin-2 was positively associated with percentage of rapid eye movement sleep (r=0.442, p=0.016) and negatively with non-rapid eye movement sleep stage 2 in the percentage (r=−0.394, p=0.034). Adjusted for sex, age and HAMD, pannexin-1 was still associated with the above objective sleep measures, but sestrin-2 was only negatively with wake time (r=−0.446, p=0.022). However, these biomarkers showed no significant correlations with subjective sleep quality (PSQI score). Serum concentrations of neurotensin and pannexin-1 were positively associated with the mean erroneous distance in the BVAT. Adjusted for sex, age and depression, neurotensin was negatively associated with MoCA score (r=−0.257, p=0.044), pannexin-1 was positively associated with the mean erroneous distance in the BVAT (r=0.270, p=0.033).ConclusionsThe CID patients had increased neurotensin and pannexin-1 and decreased sestrin-2 in the serum levels, indicating neuron dysfunction, which could be related to poor sleep quality and cognitive dysfunction measured objectively.

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“…Cell plasma membrane-associated Panx1 proteins exhibit a fixed expression profile, i.e., their cell surface localization is steady for at least 8 h, after which they are internalized and subjected to lysosomal degradation (Penuela et al, 2007;Boassa et al, 2008;Bhalla-Gehi et al, 2010;Gehi et al, 2011). At the cell plasma membrane surface, Panx1 channels are activated by various triggers, including mechanical stress, intracellular calcium ions, extracellular ATP molecules and potassium ions (Qiu and Dahl, 2009;Suadicani et al, 2012;Diem et al, 2020;Lee et al, 2022). Furthermore, Panx1 channels are modulated by post-translational modifications of Panx1 proteins, including phosphorylation, deacetylation and proteolysis (Figure 2).…”

Section: Regulationmentioning

confidence: 99%

Pannexin1 channels in the liver: an open enemy

Van Campenhout,

Caufriez,

Tabernilla

et al. 2023

Front. Cell Dev. Biol.

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Pannexin1 proteins form communication channels at the cell plasma membrane surface, which allow the transfer of small molecules and ions between the intracellular compartment and extracellular environment. In this way, pannexin1 channels play an important role in various cellular processes and diseases. Indeed, a plethora of human pathologies is associated with the activation of pannexin1 channels. The present paper reviews and summarizes the structure, life cycle, regulation and (patho)physiological roles of pannexin1 channels, with a particular focus on the relevance of pannexin1 channels in liver diseases.

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Pannexin1 channels regulate mechanically stimulated but not spontaneous adenosine release

Cited by 6 publications

References 46 publications

Dynamic and Rapid Detection of Guanosine during Ischemia

Dynamic and Rapid Detection of Guanosine during Ischemia

Serum levels of neurotensin, pannexin-1, and sestrin-2 and the correlations with sleep quality or/and cognitive function in the patients with chronic insomnia disorder

Pannexin1 channels in the liver: an open enemy

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