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Article ; Online: Translating Translation to Mechanisms of Cardiac Hypertrophy.

Zeitz, Michael J / Smyth, James W

Journal of cardiovascular development and disease

2020 Volume 7, Issue 1

Abstract: Cardiac hypertrophy in response to chronic pathological stress is a common feature occurring with many forms of heart disease. This pathological hypertrophic growth increases the risk for arrhythmias and subsequent heart failure. While several factors ... ...

Abstract	Cardiac hypertrophy in response to chronic pathological stress is a common feature occurring with many forms of heart disease. This pathological hypertrophic growth increases the risk for arrhythmias and subsequent heart failure. While several factors promoting cardiac hypertrophy are known, the molecular mechanisms governing the progression to heart failure are incompletely understood. Recent studies on altered translational regulation during pathological cardiac hypertrophy are contributing to our understanding of disease progression. In this brief review, we describe how the translational machinery is modulated for enhanced global and transcript selective protein synthesis, and how alternative modes of translation contribute to the disease state. Attempts at controlling translational output through targeting of mTOR and its regulatory components are detailed, as well as recently emerging targets for pre-clinical investigation.
Language	English
Publishing date	2020-03-10
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2777082-5
ISSN	2308-3425 ; 2308-3425
ISSN (online)	2308-3425
ISSN	2308-3425
DOI	10.3390/jcdd7010009
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Alternative mechanisms of translation initiation: An emerging dynamic regulator of the proteome in health and disease.

James, Carissa C / Smyth, James W

Life sciences

2018 Volume 212, Page(s) 138–144

Abstract: Eukaryotic mRNAs were historically thought to rely exclusively on recognition and binding of their 5' cap by initiation factors to effect protein translation. While internal ribosome entry sites (IRESs) are well accepted as necessary for the cap- ... ...

Abstract	Eukaryotic mRNAs were historically thought to rely exclusively on recognition and binding of their 5' cap by initiation factors to effect protein translation. While internal ribosome entry sites (IRESs) are well accepted as necessary for the cap-independent translation of many viral genomes, there is now recognition that eukaryotic mRNAs also undergo non-canonical modes of translation initiation. Recently, high-throughput assays have identified thousands of mammalian transcripts with translation initiation occurring at non-canonical start codons, upstream of and within protein coding regions. In addition to IRES-mediated events, regulatory mechanisms of translation initiation have been described involving alternate 5' cap recognition, mRNA sequence elements, and ribosome selection. These mechanisms ensure translation of specific mRNAs under conditions where cap-dependent translation is shut down and contribute to pathological states including cardiac hypertrophy and cancer. Such global and gene-specific dynamic regulation of translation presents us with an increasing number of novel therapeutic targets. While these newly discovered modes of translation initiation have been largely studied in isolation, it is likely that several act on the same mRNA and exquisite coordination is necessary to maintain 'normal' translation. In this short review, we summarize the current state of knowledge of these alternative mechanisms of eukaryotic protein translation, their contribution to normal and pathological cell biology, and the potential of targeting translation initiation therapeutically in human disease.
MeSH term(s)	Disease ; Gene Expression Regulation ; Health Status ; Humans ; Protein Biosynthesis ; Proteome/metabolism
Chemical Substances	Proteome
Language	English
Publishing date	2018-10-02
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2018.09.054
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Article: Increased interaction between connexin43 and microtubules is critical for glioblastoma stem-like cell maintenance and tumorigenicity.

Smyth, James W / Guo, Sujuan / O'Rourke, Lorie / Deaver, Stacie / Dahlka, Jacob / Nurmemmedov, Elmar / Sheng, Zhi / Gourdie, Robert G / Lamouille, Samy

bioRxiv : the preprint server for biology

2024

Abstract: Glioblastoma (GBM) is the most common primary tumor of the central nervous system. One major challenge in GBM treatment is the resistance to chemotherapy and radiotherapy observed in subpopulations of cancer cells, including GBM stem-like cells (GSCs). ... ...

Abstract	Glioblastoma (GBM) is the most common primary tumor of the central nervous system. One major challenge in GBM treatment is the resistance to chemotherapy and radiotherapy observed in subpopulations of cancer cells, including GBM stem-like cells (GSCs). These cells hold the ability to self-renew or differentiate following treatment, participating in tumor recurrence. The gap junction protein connexin43 (Cx43) has complex roles in oncogenesis and we have previously demonstrated an association between Cx43 and GBM chemotherapy resistance. Here, we report, for the first time, increased direct interaction between non-junctional Cx43 with microtubules in the cytoplasm of GSCs. We hypothesize that non-junctional Cx43/microtubule complexing is critical for GSC maintenance and survival and sought to specifically disrupt this interaction while maintaining other Cx43 functions, such as gap junction formation. Using a Cx43 mimetic peptide of the carboxyl terminal tubulin-binding domain of Cx43 (JM2), we successfully ablated Cx43 interaction with microtubules in GSCs. Importantly, administration of JM2 significantly decreased GSC survival
Language	English
Publishing date	2024-01-27
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.01.26.576347
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Article: Connexin 43 Regulates Intercellular Mitochondrial Transfer from Human Mesenchymal Stromal Cells to Chondrocytes.

Irwin, Rebecca M / Thomas, Matthew A / Fahey, Megan J / Mayán, María D / Smyth, James W / Delco, Michelle L

bioRxiv : the preprint server for biology

2024

Abstract: Background: The phenomenon of intercellular mitochondrial transfer from mesenchymal stromal cells (MSCs) has shown promise for improving tissue healing after injury and has potential for treating degenerative diseases like osteoarthritis (OA). Recently ... ...

Abstract	Background: The phenomenon of intercellular mitochondrial transfer from mesenchymal stromal cells (MSCs) has shown promise for improving tissue healing after injury and has potential for treating degenerative diseases like osteoarthritis (OA). Recently MSC to chondrocyte mitochondrial transfer has been documented, but the mechanism of transfer is unknown. Full-length connexin43 (Cx43, encoded by Methods: Oxidative stress was induced in immortalized human chondrocytes using tert-Butyl hydroperoxide (t-BHP) and cells were evaluated for mitochondrial membrane depolarization and reactive oxygen species (ROS) production. Human bone-marrow derived MSCs were transduced for mitochondrial fluorescence using lentiviral vectors. MSC Cx43 expression was knocked down using siRNA or overexpressed (GJA1+ and GJA1-20k+) using lentiviral transduction. Chondrocytes and MSCs were co-cultured for 24 hrs in direct contact or separated using transwells. Mitochondrial transfer was quantified using flow cytometry. Co-cultures were fixed and stained for actin and Cx43 to visualize cell-cell interactions during transfer. Results: Mitochondrial transfer was significantly higher in t-BHP-stressed chondrocytes. Contact co-cultures had significantly higher mitochondrial transfer compared to transwell co-cultures. Confocal images showed direct cell contacts between MSCs and chondrocytes where Cx43 staining was enriched at the terminal ends of actin cellular extensions containing mitochondria in MSCs. MSC Cx43 expression was associated with the magnitude of mitochondrial transfer to chondrocytes; knocking down Cx43 significantly decreased transfer while Cx43 overexpression significantly increased transfer. Interestingly, GJA1-20k expression was highly correlated with incidence of mitochondrial transfer from MSCs to chondrocytes. Conclusions: Overexpression of GJA1-20k in MSCs increases mitochondrial transfer to chondrocytes, highlighting GJA1-20k as a potential target for promoting mitochondrial transfer from MSCs as a regenerative therapy for cartilage tissue repair in OA.
Language	English
Publishing date	2024-03-20
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.03.18.585552
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Article ; Online: Complex I protein NDUFS2 is vital for growth, ROS generation, membrane integrity, apoptosis, and mitochondrial energetics.

Bandara, Aloka B / Drake, Joshua C / James, Carissa C / Smyth, James W / Brown, David A

Mitochondrion

2021 Volume 58, Page(s) 160–168

Abstract: Complex I is the largest and most intricate of the protein complexes of mitochondrial electron transport chain (ETC). This L-shaped enzyme consists of a peripheral hydrophilic matrix domain and a membrane-bound orthogonal hydrophobic domain. The ... ...

Abstract	Complex I is the largest and most intricate of the protein complexes of mitochondrial electron transport chain (ETC). This L-shaped enzyme consists of a peripheral hydrophilic matrix domain and a membrane-bound orthogonal hydrophobic domain. The interfacial region between these two arms is known to be critical for binding of ubiquinone moieties and has also been shown to be the binding site of Complex I inhibitors. Knowledge on specific roles of the ETC interfacial region proteins is scarce due to lack of knockout cell lines and animal models. Here we mutated nuclear encoded NADH dehydrogenase [ubiquinone] iron-sulfur protein 2 (NDUFS2), one of three protein subunits of the interfacial region, in a human embryonic kidney cell line 293 using a CRISPR/Cas9 procedure. Disruption of NDUFS2 significantly decreased cell growth in medium, Complex I specific respiration, glycolytic capacity, ATP pool and cell-membrane integrity, but significantly increased Complex II respiration, ROS generation, apoptosis, and necrosis. Treatment with idebenone, a clinical benzoquinone currently being investigated in other indications, partially restored growth, ATP pool, and oxygen consumption of the mutant. Overall, our results suggest that NDUFS2 is vital for growth and metabolism of mammalian cells, and respiratory defects of NDUFS2 dysfunction can be partially corrected with treatment of an established mitochondrial therapeutic candidate. This is the first report to use CRISPR/Cas9 approach to construct a knockout NDUFS2 cell line and use the constructed mutant to evaluate the efficacy of a known mitochondrial therapeutic to enhance bioenergetic capacity.
MeSH term(s)	Adenosine Triphosphate/biosynthesis ; Apoptosis/physiology ; CRISPR-Cas Systems ; Energy Metabolism/physiology ; Glycolysis ; HEK293 Cells ; Humans ; Mitochondria/metabolism ; NADH Dehydrogenase/physiology ; Oxygen Consumption ; Reactive Oxygen Species/metabolism
Chemical Substances	Reactive Oxygen Species ; Adenosine Triphosphate (8L70Q75FXE) ; NADH Dehydrogenase (EC 1.6.99.3) ; NDUFS2 protein, human (EC 7.1.1.2)
Language	English
Publishing date	2021-03-18
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2056923-3
ISSN	1872-8278 ; 1567-7249
ISSN (online)	1872-8278
ISSN	1567-7249
DOI	10.1016/j.mito.2021.03.003
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Article ; Online: Visualizing cardiac ion channel trafficking pathways.

Smyth, James W / Shaw, Robin M

Methods in enzymology

2018 Volume 505, Page(s) 187–202

Abstract: Understanding cardiac electrical and mechanical function requires knowledge of cardiac muscle at the subcellular level. Traditional biochemical and electrophysiological techniques have provided invaluable information in the description of ion channels ... ...

Abstract	Understanding cardiac electrical and mechanical function requires knowledge of cardiac muscle at the subcellular level. Traditional biochemical and electrophysiological techniques have provided invaluable information in the description of ion channels and their occurrence in various tissues. This knowledge is the basis for our current ability to understand how subcellular ion channel localization occurs and is regulated. We are now in an era whereby individual ion channels can be followed from the moment of their synthesis to placement on the plasma membrane, movements within the membrane, internalization back into the cytoplasm, and degradation. Such insight opens many possibilities for the dissection of regulatory elements governing ion channel expression and function, which will in turn be translated to future therapies for cardiac disease. In this chapter, we discuss the structure of cardiomyocytes and their submembrane domains, the ion channels that we study, and the techniques that can be employed to visualize cardiac ion channel trafficking in real time.
MeSH term(s)	Animals ; Cell Membrane/metabolism ; Cell Tracking/methods ; Connexin 43/genetics ; Connexin 43/metabolism ; Fluorescent Dyes ; Gap Junctions/metabolism ; HeLa Cells ; Humans ; Ion Channels/genetics ; Ion Channels/metabolism ; Mice ; Microscopy, Confocal/methods ; Myocardium/cytology ; Myocardium/metabolism ; Myocytes, Cardiac/cytology ; Myocytes, Cardiac/metabolism ; Protein Transport ; Recombinant Fusion Proteins/genetics ; Recombinant Fusion Proteins/metabolism
Chemical Substances	Connexin 43 ; Fluorescent Dyes ; Ion Channels ; Recombinant Fusion Proteins
Language	English
Publishing date	2018-10-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1557-7988
ISSN (online)	1557-7988
DOI	10.1016/B978-0-12-388448-0.00018-8
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Folate regulates RNA m

Xu, Xiguang / Johnson, Zachary / Wang, Amanda / Padget, Rachel L / Smyth, James W / Xie, Hehuang

BMC biology

2022 Volume 20, Issue 1, Page(s) 261

Abstract: Background: Folate is an essential B-group vitamin and a key methyl donor with important biological functions including DNA methylation regulation. Normal neurodevelopment and physiology are sensitive to the cellular folate levels. Either deficiency or ... ...

Abstract	Background: Folate is an essential B-group vitamin and a key methyl donor with important biological functions including DNA methylation regulation. Normal neurodevelopment and physiology are sensitive to the cellular folate levels. Either deficiency or excess of folate may lead to neurological disorders. Recently, folate has been linked to tRNA cytosine-5 methylation (m Results: NSCs cultured in three different concentrations of folate showed distinct mRNA methylation profiles. Despite uncovering only a few differentially expressed genes, hundreds of differentially translated genes were identified in NSCs with folate deficiency or supplementation. The differentially translated genes induced by low folate are associated with cytoplasmic translation and mitochondrial function, while the differentially translated genes induced by high folate are associated with increased neural stem cell proliferation. Interestingly, compared to total mRNAs, polysome mRNAs contained high levels of m Conclusions: Altogether, our study reports a transcriptome-wide influence of folate on mRNA m
MeSH term(s)	Mice ; Animals ; Folic Acid ; RNA ; Neural Stem Cells/metabolism ; DNA Methylation ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Mammals/genetics
Chemical Substances	Folic Acid (935E97BOY8) ; RNA (63231-63-0) ; RNA, Messenger
Language	English
Publishing date	2022-11-23
Publishing country	England
Document type	Journal Article
ZDB-ID	2133020-7
ISSN	1741-7007 ; 1741-7007
ISSN (online)	1741-7007
ISSN	1741-7007
DOI	10.1186/s12915-022-01467-0
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Article ; Online: Folate regulates RNA m5C modification and translation in neural stem cells

Xiguang Xu / Zachary Johnson / Amanda Wang / Rachel L. Padget / James W. Smyth / Hehuang Xie

BMC Biology, Vol 20, Iss 1, Pp 1-

2022 Volume 16

Abstract: Abstract Background Folate is an essential B-group vitamin and a key methyl donor with important biological functions including DNA methylation regulation. Normal neurodevelopment and physiology are sensitive to the cellular folate levels. Either ... ...

Abstract	Abstract Background Folate is an essential B-group vitamin and a key methyl donor with important biological functions including DNA methylation regulation. Normal neurodevelopment and physiology are sensitive to the cellular folate levels. Either deficiency or excess of folate may lead to neurological disorders. Recently, folate has been linked to tRNA cytosine-5 methylation (m5C) and translation in mammalian mitochondria. However, the influence of folate intake on neuronal mRNA m5C modification and translation remains largely unknown. Here, we provide transcriptome-wide landscapes of m5C modification in poly(A)-enriched RNAs together with mRNA transcription and translation profiles for mouse neural stem cells (NSCs) cultured in three different concentrations of folate. Results NSCs cultured in three different concentrations of folate showed distinct mRNA methylation profiles. Despite uncovering only a few differentially expressed genes, hundreds of differentially translated genes were identified in NSCs with folate deficiency or supplementation. The differentially translated genes induced by low folate are associated with cytoplasmic translation and mitochondrial function, while the differentially translated genes induced by high folate are associated with increased neural stem cell proliferation. Interestingly, compared to total mRNAs, polysome mRNAs contained high levels of m5C. Furthermore, an integrative analysis indicated a transcript-specific relationship between RNA m5C methylation and mRNA translation efficiency. Conclusions Altogether, our study reports a transcriptome-wide influence of folate on mRNA m5C methylation and translation in NSCs and reveals a potential link between mRNA m5C methylation and mRNA translation.
Keywords	RNA cytosine-5 methylation ; Mouse neural stem cell ; Folic acid ; Polysome profiling ; RNA bisulfite sequencing ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2022-11-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Acute Adenoviral Infection Elicits an Arrhythmogenic Substrate Prior to Myocarditis.

Padget, Rachel L / Zeitz, Michael J / Blair, Grace A / Wu, Xiaobo / North, Michael D / Tanenbaum, Mira T / Stanley, Kari E / Phillips, Chelsea M / King, D Ryan / Lamouille, Samy / Gourdie, Robert G / Hoeker, Gregory S / Swanger, Sharon A / Poelzing, Steven / Smyth, James W

Circulation research

2024 Volume 134, Issue 7, Page(s) 892–912

Abstract: Background: Viral cardiac infection represents a significant clinical challenge encompassing several etiological agents, disease stages, complex presentation, and a resulting lack of mechanistic understanding. Myocarditis is a major cause of sudden ... ...

Abstract	Background: Viral cardiac infection represents a significant clinical challenge encompassing several etiological agents, disease stages, complex presentation, and a resulting lack of mechanistic understanding. Myocarditis is a major cause of sudden cardiac death in young adults, where current knowledge in the field is dominated by later disease phases and pathological immune responses. However, little is known regarding how infection can acutely induce an arrhythmogenic substrate before significant immune responses. Adenovirus is a leading cause of myocarditis, but due to species specificity, models of infection are lacking, and it is not understood how adenoviral infection may underlie sudden cardiac arrest. Mouse adenovirus type-3 was previously reported as cardiotropic, yet it has not been utilized to understand the mechanisms of cardiac infection and pathology. Methods: We have developed mouse adenovirus type-3 infection as a model to investigate acute cardiac infection and molecular alterations to the infected heart before an appreciable immune response or gross cardiomyopathy. Results: Optical mapping of infected hearts exposes decreases in conduction velocity concomitant with increased Cx43 Conclusions: Together, these findings demonstrate that adenoviral infection creates an arrhythmogenic substrate through direct targeting of gap junction and ion channel function in the heart. Such alterations are known to precipitate arrhythmias and likely contribute to sudden cardiac death in acutely infected patients.
MeSH term(s)	Humans ; Mice ; Animals ; Connexin 43/genetics ; Myocarditis ; Induced Pluripotent Stem Cells ; Arrhythmias, Cardiac/genetics ; Arrhythmias, Cardiac/pathology ; Myocytes, Cardiac/physiology ; Gap Junctions ; Adenoviridae/genetics ; Death, Sudden, Cardiac
Chemical Substances	Connexin 43
Language	English
Publishing date	2024-02-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.122.322437
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Article: Alternative mechanisms of translation initiation: An emerging dynamic regulator of the proteome in health and disease

James, Carissa C / Smyth, James W

Life sciences. 2018 Nov. 01, v. 212

2018

Abstract: Eukaryotic mRNAs were historically thought to rely exclusively on recognition and binding of their 5′ cap by initiation factors to effect protein translation. While internal ribosome entry sites (IRESs) are well accepted as necessary for the cap- ... ...

Abstract	Eukaryotic mRNAs were historically thought to rely exclusively on recognition and binding of their 5′ cap by initiation factors to effect protein translation. While internal ribosome entry sites (IRESs) are well accepted as necessary for the cap-independent translation of many viral genomes, there is now recognition that eukaryotic mRNAs also undergo non-canonical modes of translation initiation. Recently, high-throughput assays have identified thousands of mammalian transcripts with translation initiation occurring at non-canonical start codons, upstream of and within protein coding regions. In addition to IRES-mediated events, regulatory mechanisms of translation initiation have been described involving alternate 5′ cap recognition, mRNA sequence elements, and ribosome selection. These mechanisms ensure translation of specific mRNAs under conditions where cap-dependent translation is shut down and contribute to pathological states including cardiac hypertrophy and cancer. Such global and gene-specific dynamic regulation of translation presents us with an increasing number of novel therapeutic targets. While these newly discovered modes of translation initiation have been largely studied in isolation, it is likely that several act on the same mRNA and exquisite coordination is necessary to maintain ‘normal’ translation. In this short review, we summarize the current state of knowledge of these alternative mechanisms of eukaryotic protein translation, their contribution to normal and pathological cell biology, and the potential of targeting translation initiation therapeutically in human disease.
Keywords	human diseases ; hypertrophy ; internal ribosome entry sites ; mammals ; messenger RNA ; neoplasms ; open reading frames ; proteome ; ribosomes ; start codon ; therapeutics ; translation (genetics)
Language	English
Dates of publication	2018-1101
Size	p. 138-144.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2018.09.054
Database	NAL-Catalogue (AGRICOLA)

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