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Cellular and Molecular Signaling Meet the Space Environment
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Cellular and Molecular Signaling Meet the Space Environment

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: closed (30 September 2022) | Viewed by 21681

Special Issue Editors

Prof. Dr. John Lawler

E-Mail Website
Guest Editor
Department of Health and Kinesiology, Graduate Faculty of Nutrition, Texas A&M University, College Station, TX, USA
Interests: nitric oxide; free radicals; skeletal muscle function; oxidative stress
Special Issues, Collections and Topics in MDPI journals
Dr. Khaled Kamal

E-Mail Website
Guest Editor
Department of Health and Kinesiology, Graduate Faculty of Nutrition, Texas A&M University, College Station, TX, USA
Interests: microgravity environments; cell biology; oxidative stress; skeletal muscle
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The future of spaceflight missions to the Moon and extended human presence on the Martian surface necessitates seeking answers to the mysteries of organismal adaptation during spaceflight when exposed to microgravity and radiation. In particular, the cellular and molecular adaptations to the microgravitational environments of space travel are critical areas of microgravitational research. Gravity has been a constant stressor throughout evolutionary history on Earth. Therefore, it would be expected that sudden changes in gravitational forces directly catalyze alterations and adaptations in normal biological morphology and function. An important focus of this research topic is:

  1. What are the underlying mechanisms by which a wide range of living organisms can adapt themselves to the space environment without the normal, essential cues for their existence and survival on our planet Earth?
  2. What happens to microorganisms, plants, and zoological life at the cellular level?
  3. What mechanisms are essential to the health, well-being, and performance of astronauts during spaceflight and the gravitational alterations?
  4. What type of molecular mechanisms are important: DNA damage, cell cycle regulation, mechanotransduction, cell signaling protein expression, and post-translational alterations?
  5. Is the genome responding in a concerted way by means of epigenetics, chromatin re-organization or via other genome stabilization mechanisms?

Prof. Dr. John Lawler
Dr. Khaled Kamal
Guest Editors

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

  • Space exploration
  • Microgravity
  • Space Radiation
  • Cellular Mechanism
  • Astronaut health

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Related Special Issue

Published Papers (6 papers)

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Editorial

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3 pages, 189 KiB  
Editorial
Cellular and Molecular Signaling Meet the Space Environment
by Khaled Y. Kamal and John M. Lawler
Int. J. Mol. Sci. 2023, 24(6), 5955; https://doi.org/10.3390/ijms24065955 - 22 Mar 2023
Viewed by 1234
Abstract
During space missions that travel beyond the cocoon of the Earth’s magnetosphere, astronauts are subjected to the microgravity and radiation stressors of outer space [...] Full article
(This article belongs to the Special Issue Cellular and Molecular Signaling Meet the Space Environment)

Research

Jump to: Editorial, Review

21 pages, 1968 KiB  
Article
Chronic Hypergravity Induces a Modification of Histone H3 Lysine 27 Trimethylation at TCRβ Locus in Murine Thymocytes
by Gaetano Calcagno, Nassima Ouzren, Sandra Kaminski, Stéphanie Ghislin and Jean-Pol Frippiat
Int. J. Mol. Sci. 2022, 23(13), 7133; https://doi.org/10.3390/ijms23137133 - 27 Jun 2022
Cited by 5 | Viewed by 2034
Abstract
Gravity changes are major stressors encountered during spaceflight that affect the immune system. We previously evidenced that hypergravity exposure during gestation affects the TCRβ repertoire of newborn pups. To identify the mechanisms underlying this observation, we studied post-translational histone modifications. We first showed [...] Read more.
Gravity changes are major stressors encountered during spaceflight that affect the immune system. We previously evidenced that hypergravity exposure during gestation affects the TCRβ repertoire of newborn pups. To identify the mechanisms underlying this observation, we studied post-translational histone modifications. We first showed that among the four studied post-translational histone H3 modifications, only lysine 27 trimethylation (H3K27me3) is downregulated in the thymus of mice exposed to 2× g for 21 days. We then asked whether the TCRβ locus chromatin structure is altered by hypergravity exposure. ChIP studies performed on four Vβ segments of the murine double-negative SCIET27 thymic cell line, which corresponds to the last maturation stage before V(D)J recombination, revealed increases in H3K27me3 after 2× g exposure. Finally, we evaluated the implication for the EZH2 methyltransferase in the regulation of the H3K27me3 level at these Vβ segments by treating SCIET27 cells with the GSK126-specific inhibitor. These experiments showed that the downregulation of H3K27me3 contributes to the regulation of the Vβ germline transcript expression that precedes V(D)J recombination. These data show that modifications of H3K27me3 at the TCRβ locus likely contribute to an explanation of why the TCR repertoire is affected by gravity changes and imply, for the first time, EZH2 in the regulation of the TCRβ locus chromatin structure. Full article
(This article belongs to the Special Issue Cellular and Molecular Signaling Meet the Space Environment)
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15 pages, 3351 KiB  
Article
Activation of Focal Adhesion Kinase Restores Simulated Microgravity-Induced Inhibition of Osteoblast Differentiation via Wnt/Β-Catenin Pathway
by Cuihong Fan, Zhaojia Wu, David M. L. Cooper, Adam Magnus, Kim Harrison, B. Frank Eames, Rajni Chibbar, Gary Groot, Junqiong Huang, Harald Genth, Jun Zhang, Xing Tan, Yulin Deng and Jim Xiang
Int. J. Mol. Sci. 2022, 23(10), 5593; https://doi.org/10.3390/ijms23105593 - 17 May 2022
Cited by 16 | Viewed by 2787
Abstract
Simulated microgravity (SMG) inhibits osteoblast differentiation (OBD) and induces bone loss via the inhibition of the Wnt/β-catenin pathway. However, the mechanism by which SMG alters the Wnt/β-catenin pathway is unknown. We previously demonstrated that SMG altered the focal adhesion kinase (FAK)-regulated mTORC1, AMPK [...] Read more.
Simulated microgravity (SMG) inhibits osteoblast differentiation (OBD) and induces bone loss via the inhibition of the Wnt/β-catenin pathway. However, the mechanism by which SMG alters the Wnt/β-catenin pathway is unknown. We previously demonstrated that SMG altered the focal adhesion kinase (FAK)-regulated mTORC1, AMPK and ERK1/2 pathways, leading to the inhibition of tumor cell proliferation/metastasis and promoting cell apoptosis. To examine whether FAK similarly mediates SMG-dependent changes to Wnt/β-catenin in osteoblasts, we characterized mouse MC3T3-E1 cells cultured under clinostat-modeled SMG (µg) conditions. Compared to cells cultured under ground (1 g) conditions, SMG reduces focal adhesions, alters cytoskeleton structures, and down-regulates FAK, Wnt/β-catenin and Wnt/β-catenin-regulated molecules. Consequently, protein-2 (BMP2), type-1 collagen (COL1), alkaline-phosphatase activity and matrix mineralization are all inhibited. In the mouse hindlimb unloading (HU) model, SMG-affected tibial trabecular bone loss is significantly reduced, according to histological and micro-computed tomography analyses. Interestingly, the FAK activator, cytotoxic necrotizing factor-1 (CNF1), significantly suppresses all of the SMG-induced alterations in MC3T3-E1 cells and the HU model. Therefore, our data demonstrate the critical role of FAK in the SMG-induced inhibition of OBD and bone loss via the Wnt/β-catenin pathway, offering FAK signaling as a new therapeutic target not only for astronauts at risk of OBD inhibition and bone loss, but also osteoporotic patients. Full article
(This article belongs to the Special Issue Cellular and Molecular Signaling Meet the Space Environment)
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18 pages, 4820 KiB  
Article
Severe Muscle Deconditioning Triggers Early Extracellular Matrix Remodeling and Resident Stem Cell Differentiation into Adipocytes in Healthy Men
by Corentin Guilhot, Théo Fovet, Pierre Delobel, Manon Dargegen, Bernard J. Jasmin, Thomas Brioche, Angèle Chopard and Guillaume Py
Int. J. Mol. Sci. 2022, 23(10), 5489; https://doi.org/10.3390/ijms23105489 - 14 May 2022
Cited by 10 | Viewed by 3289
Abstract
Besides the loss of muscle mass and strength, increased intermuscular adipose tissue (IMAT) is now a well-recognized consequence of muscle deconditioning as experienced in prolonged microgravity. IMAT content may alter the muscle stem cell microenvironment. We hypothesized that extracellular matrix structure alterations and [...] Read more.
Besides the loss of muscle mass and strength, increased intermuscular adipose tissue (IMAT) is now a well-recognized consequence of muscle deconditioning as experienced in prolonged microgravity. IMAT content may alter the muscle stem cell microenvironment. We hypothesized that extracellular matrix structure alterations and microenvironment remodeling induced by fast and severe muscle disuse could modulate fibro-adipogenic progenitor fate and behavior. We used the dry immersion (DI) model that rapidly leads to severe muscle deconditioning due to drastic hypoactivity. We randomly assigned healthy volunteers (n = 18 men) to the control group (only DI, n = 9; age = 33.8 ± 4) or to the DI + thigh cuff group (n = 9; age = 33.4 ± 7). Participants remained immersed in the supine position in a thermo-neutral water bath for 5 days. We collected vastus lateralis biopsies before (baseline) and after DI. 5 days of DI are sufficient to reduce muscle mass significantly, as indicated by the decreased myofiber cross-sectional area in vastus lateralis samples (−18% vs. baseline, p < 0.05). Early and late adipogenic differentiation transcription factors protein levels were upregulated. Platelet-derived growth Factors alpha (PDGFR⍺) protein level and PDGFR⍺-positive cells were increased after 5 days of DI. Extracellular matrix structure was prone to remodeling with an altered ECM composition with 4 major collagens, fibronectin, and Connective Tissue Growth Factor mRNA decreases (p < 0.001 vs. baseline). Wearing thigh cuffs did not have any preventive effect on the measured variable. Our results show that altered extracellular matrix structure and signaling pathways occur early during DI, a severe muscle wasting model, favoring fibro-adipogenic progenitor differentiation into adipocytes. Full article
(This article belongs to the Special Issue Cellular and Molecular Signaling Meet the Space Environment)
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20 pages, 2588 KiB  
Article
Reciprocal Homer1a and Homer2 Isoform Expression Is a Key Mechanism for Muscle Soleus Atrophy in Spaceflown Mice
by Dieter Blottner, Gabor Trautmann, Sandra Furlan, Guido Gambara, Katharina Block, Martina Gutsmann, Lian-Wen Sun, Paul F. Worley, Luisa Gorza, Martina Scano, Paola Lorenzon, Imre Vida, Pompeo Volpe and Michele Salanova
Int. J. Mol. Sci. 2022, 23(1), 75; https://doi.org/10.3390/ijms23010075 - 22 Dec 2021
Cited by 5 | Viewed by 3484
Abstract
The molecular mechanisms of skeletal muscle atrophy under extended periods of either disuse or microgravity are not yet fully understood. The transition of Homer isoforms may play a key role during neuromuscular junction (NMJ) imbalance/plasticity in space. Here, we investigated the expression pattern [...] Read more.
The molecular mechanisms of skeletal muscle atrophy under extended periods of either disuse or microgravity are not yet fully understood. The transition of Homer isoforms may play a key role during neuromuscular junction (NMJ) imbalance/plasticity in space. Here, we investigated the expression pattern of Homer short and long isoforms by gene array, qPCR, biochemistry, and laser confocal microscopy in skeletal muscles from male C57Bl/N6 mice (n = 5) housed for 30 days in space (Bion-flight = BF) compared to muscles from Bion biosatellite on the ground-housed animals (Bion ground = BG) and from standard cage housed animals (Flight control = FC). A comparison study was carried out with muscles of rats subjected to hindlimb unloading (HU). Gene array and qPCR results showed an increase in Homer1a transcripts, the short dominant negative isoform, in soleus (SOL) muscle after 30 days in microgravity, whereas it was only transiently increased after four days of HU. Conversely, Homer2 long-form was downregulated in SOL muscle in both models. Homer immunofluorescence intensity analysis at the NMJ of BF and HU animals showed comparable outcomes in SOL but not in the extensor digitorum longus (EDL) muscle. Reduced Homer crosslinking at the NMJ consequent to increased Homer1a and/or reduced Homer2 may contribute to muscle-type specific atrophy resulting from microgravity and HU disuse suggesting mutual mechanisms. Full article
(This article belongs to the Special Issue Cellular and Molecular Signaling Meet the Space Environment)
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Review

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31 pages, 771 KiB  
Review
Extraterrestrial Gynecology: Could Spaceflight Increase the Risk of Developing Cancer in Female Astronauts? An Updated Review
by Rosa Drago-Ferrante, Riccardo Di Fiore, Fathi Karouia, Yashwanth Subbannayya, Saswati Das, Begum Aydogan Mathyk, Shehbeel Arif, Ana Paula Guevara-Cerdán, Allen Seylani, Aman Singh Galsinh, Weronika Kukulska, Joseph Borg, Sherif Suleiman, David Marshall Porterfield, Andrea Camera, Lane K. Christenson, April Elizabeth Ronca, Jonathan G. Steller, Afshin Beheshti and Jean Calleja-Agius
Int. J. Mol. Sci. 2022, 23(13), 7465; https://doi.org/10.3390/ijms23137465 - 5 Jul 2022
Cited by 9 | Viewed by 7138
Abstract
Outer space is an extremely hostile environment for human life, with ionizing radiation from galactic cosmic rays and microgravity posing the most significant hazards to the health of astronauts. Spaceflight has also been shown to have an impact on established cancer hallmarks, possibly [...] Read more.
Outer space is an extremely hostile environment for human life, with ionizing radiation from galactic cosmic rays and microgravity posing the most significant hazards to the health of astronauts. Spaceflight has also been shown to have an impact on established cancer hallmarks, possibly increasing carcinogenic risk. Terrestrially, women have a higher incidence of radiation-induced cancers, largely driven by lung, thyroid, breast, and ovarian cancers, and therefore, historically, they have been permitted to spend significantly less time in space than men. In the present review, we focus on the effects of microgravity and radiation on the female reproductive system, particularly gynecological cancer. The aim is to provide a summary of the research that has been carried out related to the risk of gynecological cancer, highlighting what further studies are needed to pave the way for safer exploration class missions, as well as postflight screening and management of women astronauts following long-duration spaceflight. Full article
(This article belongs to the Special Issue Cellular and Molecular Signaling Meet the Space Environment)
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