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New Advances in Hypercapnia
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New Advances in Hypercapnia

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 30 June 2024 | Viewed by 1655

Special Issue Editor

Dr. Masahiko Shigemura

E-Mail Website
Guest Editor
Feinberg School of Medicine, Northwestern University, Chicago, IL, USA
Interests: hypercapnia; CO2 sensing/signaling; airway smooth muscle cells; monocytes; airway diseases; lung transplant

Special Issue Information

Dear Colleagues,

Cells sense changes in the concentration of gaseous molecules through conserved pathways to elicit adaptive responses and maintain cell homeostasis. Carbon dioxide (CO2), an atmospheric and physiological gas, is a product of cellular oxidative respiration. The physiological levels of CO2 in mammals are significantly higher than atmospheric levels (approx. 5% versus approx. 0.04%, respectively) and are linked to physiological conditions. Recent accumulating evidence suggests that the elevation of CO2 (hypercapnia) is detected by various cells and organisms via as-yet-undescribed mechanisms that lead to specific signaling pathways, many of which are detrimental to cellular and organismal homeostasis. Importantly, these effects of hypercapnia are not limited to mammals.

This Special Issue of IJMS will focus on recent advances in molecular, cellular, and organismal mechanisms of hypercapnia sensing and signaling. We welcome original research and review articles that focus on (but are not limited to) the following topics:

  • The molecular mechanisms of CO2 sensing and signaling;
  • The effects of hypercapnia on cellular and organismal functions (humans, animals, flies, nematodes, plants, etc.);
  • Potentially advantageous versus disadvantageous effects of hypercapnia;
  • Implications on these aspects in human health and diseases.

Dr. Masahiko Shigemura
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • carbon dioxide (CO2)
  • hypercapnia
  • CO2 sensing mechanisms
  • hypercapnia-mediated signal
  • transduction pathways
  • beneficial effects of hypercapnia
  • detrimental effects of hypercapnia
  • humans
  • mammals
  • flies
  • nematodes
  • plants
  • marine animals

Published Papers (2 papers)

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Research

17 pages, 3248 KiB  
Article
Orphan Nuclear Receptor Family 4A (NR4A) Members NR4A2 and NR4A3 Selectively Modulate Elements of the Monocyte Response to Buffered Hypercapnia
by David E. Phelan, Ben Reddan, Masahiko Shigemura, Jacob I. Sznajder, Daniel Crean and Eoin P. Cummins
Int. J. Mol. Sci. 2024, 25(5), 2852; https://doi.org/10.3390/ijms25052852 - 01 Mar 2024
Viewed by 708
Abstract
Hypercapnia occurs when the partial pressure of carbon dioxide (CO2) in the blood exceeds 45 mmHg. Hypercapnia is associated with several lung pathologies and is transcriptionally linked to suppression of immune and inflammatory signalling through poorly understood mechanisms. Here we propose [...] Read more.
Hypercapnia occurs when the partial pressure of carbon dioxide (CO2) in the blood exceeds 45 mmHg. Hypercapnia is associated with several lung pathologies and is transcriptionally linked to suppression of immune and inflammatory signalling through poorly understood mechanisms. Here we propose Orphan Nuclear Receptor Family 4A (NR4A) family members NR4A2 and NR4A3 as potential transcriptional regulators of the cellular response to hypercapnia in monocytes. Using a THP-1 monocyte model, we investigated the sensitivity of NR4A family members to CO2 and the impact of depleting NR4A2 and NR4A3 on the monocyte response to buffered hypercapnia (10% CO2) using RNA-sequencing. We observed that NR4A2 and NR4A3 are CO2-sensitive transcription factors and that depletion of NR4A2 and NR4A3 led to reduced CO2-sensitivity of mitochondrial and heat shock protein (Hsp)-related genes, respectively. Several CO2-sensitive genes were, however, refractory to depletion of NR4A2 and NR4A3, indicating that NR4As regulate certain elements of the cellular response to buffered hypercapnia but that other transcription factors also contribute. Bioinformatic analysis of conserved CO2-sensitive genes implicated several novel putative CO2-sensitive transcription factors, of which the ETS Proto-Oncogene 1 Transcription Factor (ETS-1) was validated to show increased nuclear expression in buffered hypercapnia. These data give significant insights into the understanding of immune responses in patients experiencing hypercapnia. Full article
(This article belongs to the Special Issue New Advances in Hypercapnia)
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15 pages, 1816 KiB  
Article
A Non-Functional Carbon Dioxide-Mediated Post-Translational Modification on Nucleoside Diphosphate Kinase of Arabidopsis thaliana
by Harry G. Gannon, Amber Riaz-Bradley and Martin J. Cann
Int. J. Mol. Sci. 2024, 25(2), 898; https://doi.org/10.3390/ijms25020898 - 11 Jan 2024
Viewed by 558
Abstract
The carbamate post-translational modification (PTM), formed by the nucleophilic attack of carbon dioxide by a dissociated lysine epsilon-amino group, is proposed as a widespread mechanism for sensing this biologically important bioactive gas. Here, we demonstrate the discovery and in vitro characterization of a [...] Read more.
The carbamate post-translational modification (PTM), formed by the nucleophilic attack of carbon dioxide by a dissociated lysine epsilon-amino group, is proposed as a widespread mechanism for sensing this biologically important bioactive gas. Here, we demonstrate the discovery and in vitro characterization of a carbamate PTM on K9 of Arabidopsis nucleoside diphosphate kinase (AtNDK1). We demonstrate that altered side chain reactivity at K9 is deleterious for AtNDK1 structure and catalytic function, but that CO2 does not impact catalysis. We show that nucleotide substrate removes CO2 from AtNDK1, and the carbamate PTM is functionless within the detection limits of our experiments. The AtNDK1 K9 PTM is the first demonstration of a functionless carbamate. In light of this finding, we speculate that non-functionality is a possible feature of the many newly identified carbamate PTMs. Full article
(This article belongs to the Special Issue New Advances in Hypercapnia)
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