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Cells
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Cell Biology: State-of-the-Art and Perspectives in Canada
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Cell Biology: State-of-the-Art and Perspectives in Canada

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (31 May 2021) | Viewed by 18415

Special Issue Editor

Dr. Ryan Mailloux

E-Mail Website
Guest Editor
School of Human Nutrition, Faculty of Agricultural and Environmental Sciences, McGill University, Montreal, QC, Canada
Interests: mitochondria; bioenergetics; redox homeostasis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue aims to provide a comprehensive overview of state-of the-art of cell biology in Canada. We invite research papers that will consolidate our understanding in this area. The Special Issue will publish full research articles and comprehensive reviews. Potential topics include but are not limited to the following research areas:

OMICS: transcriptomics, genomics, proteomics, metabolomics, glycomics, lipidomics, interactomics, fluxomics, and biomics;

Cell structure: organelles, cytoskeleton, cell membrane, capsule,
flagella, etc.;

Cell physiology: cell growth, metabolism, protein synthesis, division, movement of proteins, active/passive transport, intra- and extracellular signaling, adhesion, DNA repair, etc.;

Redox Biology;

Reactive Oxygen Species Homeostasis and Antioxidants;

Cell movement and motility;

Autophagy;

Apoptosis;

Cell aging;

Cell techniques: cell and tissue culture, isolation and fractionation of cells, immunocytochemistry (ICC), in situ hybridization (ISH), transfection, and optogenetics;

Cell growth and differentiation;

Hematopoiesis and stem cells;

Cancer stem cells;

Genetic disorders;

CAR-T cell research

Dr. Ryan Mailloux
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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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.

Published Papers (5 papers)

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Research

Jump to: Review

21 pages, 3418 KiB  
Article
Regulation of Transplanted Cell Homing by FGF1 and PDGFB after Doxorubicin Myocardial Injury
by Mark Baguma-Nibasheka, Tiam Feridooni, Feixiong Zhang and Kishore B.S. Pasumarthi
Cells 2021, 10(11), 2998; https://doi.org/10.3390/cells10112998 - 03 Nov 2021
Cited by 5 | Viewed by 2103
Abstract
There is no effective treatment for the total recovery of myocardial injury caused by an anticancer drug, doxorubicin (Dox). In this study, using a Dox-induced cardiac injury model, we compared the cardioprotective effects of ventricular cells harvested from 11.5-day old embryonic mice (E11.5) [...] Read more.
There is no effective treatment for the total recovery of myocardial injury caused by an anticancer drug, doxorubicin (Dox). In this study, using a Dox-induced cardiac injury model, we compared the cardioprotective effects of ventricular cells harvested from 11.5-day old embryonic mice (E11.5) with those from E14.5 embryos. Our results indicate that tail-vein-infused E11.5 ventricular cells are more efficient at homing into the injured adult myocardium, and are more angiogenic, than E14.5 ventricular cells. In addition, E11.5 cells were shown to mitigate the cardiomyopathic effects of Dox. In vitro, E11.5 ventricular cells were more migratory than E14.5 cells, and RT-qPCR analysis revealed that they express significantly higher levels of cytokine receptors Fgfr1, Fgfr2, Pdgfra, Pdgfrb and Kit. Remarkably, mRNA levels for Fgf1, Fgf2, Pdgfa and Pdgfb were also found to be elevated in the Dox-injured adult heart, as were the FGF1 and PDGFB protein levels. Addition of exogenous FGF1 or PDGFB was able to enhance E11.5 ventricular cell migration in vitro, and, whereas their neutralizing antibodies decreased cell migration. These results indicate that therapies raising the levels of FGF1 and PDGFB receptors in donor cells and or corresponding ligands in an injured heart could improve the efficacy of cell-based interventions for myocardial repair. Full article
(This article belongs to the Special Issue Cell Biology: State-of-the-Art and Perspectives in Canada)
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16 pages, 3222 KiB  
Article
Immobilization of Jagged1 Enhances Vascular Smooth Muscle Cells Maturation by Activating the Notch Pathway
by Kathleen Zohorsky, Shigang Lin and Kibret Mequanint
Cells 2021, 10(8), 2089; https://doi.org/10.3390/cells10082089 - 14 Aug 2021
Cited by 4 | Viewed by 3611
Abstract
In Notch signaling, the Jagged1-Notch3 ligand-receptor pairing is implicated for regulating the phenotype maturity of vascular smooth muscle cells. However, less is known about the role of Jagged1 presentation strategy in this regulation. In this study, we used bead-immobilized Jagged1 to direct phenotype [...] Read more.
In Notch signaling, the Jagged1-Notch3 ligand-receptor pairing is implicated for regulating the phenotype maturity of vascular smooth muscle cells. However, less is known about the role of Jagged1 presentation strategy in this regulation. In this study, we used bead-immobilized Jagged1 to direct phenotype control of primary human coronary artery smooth muscle cells (HCASMC), and to differentiate embryonic multipotent mesenchymal progenitor (10T1/2) cell towards a vascular lineage. This Jagged1 presentation strategy was sufficient to activate the Notch transcription factor HES1 and induce early-stage contractile markers, including smooth muscle α-actin and calponin in HCASMCs. Bead-bound Jagged1 was unable to regulate the late-stage markers myosin heavy chain and smoothelin; however, serum starvation and TGFβ1 were used to achieve a fully contractile smooth muscle cell. When progenitor 10T1/2 cells were used for Notch3 signaling, pre-differentiation with TGFβ1 was required for a robust Jagged1 specific response, suggesting a SMC lineage commitment was necessary to direct SMC differentiation and maturity. The presence of a magnetic tension force to the ligand-receptor complex was evaluated for signaling efficacy. Magnetic pulling forces downregulated HES1 and smooth muscle α-actin in both HCASMCs and progenitor 10T1/2 cells. Taken together, this study demonstrated that (i) bead-bound Jagged1 was sufficient to activate Notch3 and promote SMC differentiation/maturation and (ii) magnetic pulling forces did not activate Notch3, suggesting the bead alone was able to provide necessary clustering or traction forces for Notch activation. Notch is highly context-dependent; therefore, these findings provide insights to improve biomaterial-driven Jagged1 control of SMC behavior. Full article
(This article belongs to the Special Issue Cell Biology: State-of-the-Art and Perspectives in Canada)
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16 pages, 3779 KiB  
Article
HDAC8 Activates AKT through Upregulating PLCB1 and Suppressing DESC1 Expression in MEK1/2 Inhibition-Resistant Cells
by Soon-Duck Ha, Naomi Lewin, Shawn S. C. Li and Sung-Ouk Kim
Cells 2021, 10(5), 1101; https://doi.org/10.3390/cells10051101 - 04 May 2021
Cited by 9 | Viewed by 3899
Abstract
Inhibition of the RAF-MEK1/2-ERK signaling pathway is an ideal strategy for treating cancers with NRAS or BRAF mutations. However, the development of resistance due to incomplete inhibition of the pathway and activation of compensatory cell proliferation pathways is a major impediment of the [...] Read more.
Inhibition of the RAF-MEK1/2-ERK signaling pathway is an ideal strategy for treating cancers with NRAS or BRAF mutations. However, the development of resistance due to incomplete inhibition of the pathway and activation of compensatory cell proliferation pathways is a major impediment of the targeted therapy. The anthrax lethal toxin (LT), which cleaves and inactivates MEKs, is a modifiable biomolecule that can be delivered selectively to tumor cells and potently kills various tumor cells. However, resistance to LT and the mechanism involved are yet to be explored. Here, we show that LT, through inhibiting MEK1/2-ERK activation, inhibits the proliferation of cancer cells with NRAS/BRAF mutations. Among them, the human colorectal tumor HT-29 and murine melanoma B16-BL6 cells developed resistance to LT in 2 to 3 days of treatment. These resistant cells activated AKT through a histone deacetylase (HDAC) 8-dependent pathway. Using an Affymetrix microarray, followed by qPCR validation, we identified that the differential expression of the phospholipase C-β1 (PLCB1) and squamous cell carcinoma-1 (DESC1) played an important role in HDAC8-mediated AKT activation and resistance to MEK1/2-ERK inhibition. By using inhibitors, small interference RNAs and/or expression vectors, we found that the inhibition of HDAC8 suppressed PLCB1 expression and induced DESC1 expression in the resistant cells, which led to the inhibition of AKT and re-sensitization to LT and MEK1/2 inhibition. These results suggest that targeting PLCB1 and DESC1 is a novel strategy for inhibiting the resistance to MEK1/2 inhibition. Full article
(This article belongs to the Special Issue Cell Biology: State-of-the-Art and Perspectives in Canada)
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Review

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13 pages, 2220 KiB  
Review
Transcriptionally Active Chromatin—Lessons Learned from the Chicken Erythrocyte Chromatin Fractionation
by Tasnim H. Beacon and James R. Davie
Cells 2021, 10(6), 1354; https://doi.org/10.3390/cells10061354 - 30 May 2021
Cited by 6 | Viewed by 3528
Abstract
The chicken erythrocyte model system has been valuable to the study of chromatin structure and function, specifically for genes involved in oxygen transport and the innate immune response. Several seminal features of transcriptionally active chromatin were discovered in this system. Davie and colleagues [...] Read more.
The chicken erythrocyte model system has been valuable to the study of chromatin structure and function, specifically for genes involved in oxygen transport and the innate immune response. Several seminal features of transcriptionally active chromatin were discovered in this system. Davie and colleagues capitalized on the unique features of the chicken erythrocyte to separate and isolate transcriptionally active chromatin and silenced chromatin, using a powerful native fractionation procedure. Histone modifications, histone variants, atypical nucleosomes (U-shaped nucleosomes) and other chromatin structural features (open chromatin) were identified in these studies. More recently, the transcriptionally active chromosomal domains in the chicken erythrocyte genome were mapped by combining this chromatin fractionation method with next-generation DNA and RNA sequencing. The landscape of histone modifications relative to chromatin structural features in the chicken erythrocyte genome was reported in detail, including the first ever mapping of histone H4 asymmetrically dimethylated at Arg 3 (H4R3me2a) and histone H3 symmetrically dimethylated at Arg 2 (H3R2me2s), which are products of protein arginine methyltransferases (PRMTs) 1 and 5, respectively. PRMT1 is important in the establishment and maintenance of chicken erythrocyte transcriptionally active chromatin. Full article
(This article belongs to the Special Issue Cell Biology: State-of-the-Art and Perspectives in Canada)
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28 pages, 380 KiB  
Review
Role of the Endocannabinoid System in the Adipose Tissue with Focus on Energy Metabolism
by Volatiana Rakotoarivelo, Jyoti Sihag and Nicolas Flamand
Cells 2021, 10(6), 1279; https://doi.org/10.3390/cells10061279 - 21 May 2021
Cited by 25 | Viewed by 4482
Abstract
The endocannabinoid system is involved in a wide range of processes including the control of energy acquisition and expenditure. Endocannabinoids and their receptors are present in the central nervous system but also in peripheral tissues, notably the adipose tissues. The endocannabinoid system interacts [...] Read more.
The endocannabinoid system is involved in a wide range of processes including the control of energy acquisition and expenditure. Endocannabinoids and their receptors are present in the central nervous system but also in peripheral tissues, notably the adipose tissues. The endocannabinoid system interacts with two main hormones regulating appetite, namely leptin and ghrelin. The inhibitory effect of the cannabinoid receptor 1 (CB1) antagonist rimonabant on fat mass suggested that the endocannabinoid system can also have a peripheral action in addition to its effect on appetite reduction. Thus, several investigations have focused on the peripheral role of the endocannabinoid system in the regulation of metabolism. The white adipose tissue stores energy as triglycerides while the brown adipose tissue helps to dissipate energy as heat. The endocannabinoid system regulates several functions of the adipose tissues to favor energy accumulation. In this review we will describe the presence of the endocannabinoid system in the adipose tissue. We will survey the role of the endocannabinoid system in the regulation of white and brown adipose tissue metabolism and how the eCB system participates in obesity and metabolic diseases. Full article
(This article belongs to the Special Issue Cell Biology: State-of-the-Art and Perspectives in Canada)
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