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Article ; Online: Hyperbaric Oxygen Therapy after Mid-Cervical Spinal Contusion Injury.

Turner, Sara M F / Sunshine, Michael D / Chandran, Vijayendran / Smuder, Ashley J / Fuller, David D

2022 Volume 39, Issue 9-10, Page(s) 715–723

Abstract: Hyperbaric oxygen (HBO) therapy is frequently used to treat peripheral wounds or decompression sickness. Evidence suggests that HBO therapy can provide neuroprotection and has an anti-inflammatory impact after neurological injury, including spinal cord ... ...

Abstract	Hyperbaric oxygen (HBO) therapy is frequently used to treat peripheral wounds or decompression sickness. Evidence suggests that HBO therapy can provide neuroprotection and has an anti-inflammatory impact after neurological injury, including spinal cord injury (SCI). Our primary purpose was to conduct a genome-wide screening of mRNA expression changes in the injured spinal cord after HBO therapy. An mRNA gene array was used to evaluate samples taken from the contused region of the spinal cord following a lateralized mid-cervical contusion injury in adult female rats. HBO therapy consisted of daily, 1-h sessions (3.0 ATA, 100% O
MeSH term(s)	Animals ; Contusions ; Female ; Humans ; Hyperbaric Oxygenation ; Neck Injuries ; RNA, Messenger/metabolism ; Rats ; Spinal Cord/metabolism ; Spinal Cord Injuries
Chemical Substances	RNA, Messenger
Language	English
Publishing date	2022-01-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	645092-1
ISSN	1557-9042 ; 0897-7151
ISSN (online)	1557-9042
ISSN	0897-7151
DOI	10.1089/neu.2021.0412
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Article ; Online: Oxygen therapy attenuates neuroinflammation after spinal cord injury.

Sunshine, Michael D / Bindi, Victoria E / Nguyen, Branden L / Doerr, Vivian / Boeno, Franccesco P / Chandran, Vijayendran / Smuder, Ashley J / Fuller, David D

Journal of neuroinflammation

2023 Volume 20, Issue 1, Page(s) 303

Abstract: Acute hyperbaric ... ...

Abstract	Acute hyperbaric O
MeSH term(s)	Rats ; Male ; Female ; Animals ; Hyperbaric Oxygenation ; Neuroinflammatory Diseases ; Spinal Cord Injuries/complications ; Spinal Cord Injuries/therapy ; Spinal Cord Injuries/metabolism ; Spinal Cord/pathology ; Inflammation/metabolism ; Oxygen/metabolism
Chemical Substances	Oxygen (S88TT14065)
Language	English
Publishing date	2023-12-19
Publishing country	England
Document type	Journal Article
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/s12974-023-02985-6
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Article ; Online: Novel roles of phentolamine in protecting axon myelination, muscle atrophy, and functional recovery following nerve injury.

Zainul, Zarin / Ma, Bo / Koka, Mert / Wilkerson, Jenny L / Ortiz, Yuma T / Kerosuo, Laura / Chandran, Vijayendran

Scientific reports

2022 Volume 12, Issue 1, Page(s) 3344

Abstract: Incomplete functional recovery after peripheral nerve injury (PNI) often results in devastating physical disabilities in human patients. Despite improved progress in surgical and non-surgical approaches, achieving complete functional recovery following ... ...

Abstract	Incomplete functional recovery after peripheral nerve injury (PNI) often results in devastating physical disabilities in human patients. Despite improved progress in surgical and non-surgical approaches, achieving complete functional recovery following PNI remains a challenge. This study demonstrates that phentolamine may hold a significant promise in treating nerve injuries and denervation induced muscle atrophy following PNI. In a sciatic nerve crush injury mouse model, we found that phentolamine treatment enhanced motor and functional recovery, protected axon myelination, and attenuated injury-induced muscle atrophy in mice at 14 days post-injury (dpi) compared to saline treatment. In the soleus of phentolamine treated animals, we observed the downregulation of phosphorylated signal transducer and activator of transcription factor 3 (p-STAT3) as well as muscle atrophy-related genes Myogenin, muscle ring finger 1 (MuRF-1), and Forkhead box O proteins (FoxO1, FoxO3). Our results show that both nerve and muscle recovery are integral components of phentolamine treatment-induced global functional recovery in mice at 14 dpi. Moreover, phentolamine treatment improved locomotor functional recovery in the mice after spinal cord crush (SCC) injury. The fact that phentolamine is an FDA approved non-selective alpha-adrenergic blocker, clinically prescribed for oral anesthesia reversal, hypertension, and erectile dysfunction makes this drug a promising candidate for repurposing in restoring behavioral recovery following PNI and SCC injuries, axonal neuropathy, and muscle wasting disorders.
MeSH term(s)	Animals ; Axons/metabolism ; Humans ; Male ; Mice ; Muscle, Skeletal/pathology ; Muscular Atrophy/pathology ; Nerve Regeneration ; Peripheral Nerve Injuries ; Phentolamine/therapeutic use ; Recovery of Function/physiology ; Sciatic Nerve/injuries ; Sciatic Neuropathy
Chemical Substances	Phentolamine (Z468598HBV)
Language	English
Publishing date	2022-02-28
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-07253-w
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Article ; Online: Large-scale genomic study reveals robust activation of the immune system following advanced Inner Engineering meditation retreat.

Chandran, Vijayendran / Bermúdez, Mei-Ling / Koka, Mert / Chandran, Brindha / Pawale, Dhanashri / Vishnubhotla, Ramana / Alankar, Suresh / Maturi, Raj / Subramaniam, Balachundhar / Sadhasivam, Senthilkumar

Proceedings of the National Academy of Sciences of the United States of America

2021 Volume 118, Issue 51

Abstract: The positive impact of meditation on human well-being is well documented, yet its molecular mechanisms are incompletely understood. We applied a comprehensive systems biology approach starting with whole-blood gene expression profiling combined with ... ...

Abstract	The positive impact of meditation on human well-being is well documented, yet its molecular mechanisms are incompletely understood. We applied a comprehensive systems biology approach starting with whole-blood gene expression profiling combined with multilevel bioinformatic analyses to characterize the coexpression, transcriptional, and protein-protein interaction networks to identify a meditation-specific core network after an advanced 8-d Inner Engineering retreat program. We found the response to oxidative stress, detoxification, and cell cycle regulation pathways were down-regulated after meditation. Strikingly, 220 genes directly associated with immune response, including 68 genes related to interferon signaling, were up-regulated, with no significant expression changes in the inflammatory genes. This robust meditation-specific immune response network is significantly dysregulated in multiple sclerosis and severe COVID-19 patients. The work provides a foundation for understanding the effect of meditation and suggests that meditation as a behavioral intervention can voluntarily and nonpharmacologically improve the immune response for treating various conditions associated with excessive or persistent inflammation with a dampened immune system profile.
MeSH term(s)	Adult ; COVID-19/immunology ; COVID-19/metabolism ; Diet, Vegan ; Female ; Genome, Human ; Humans ; Immune System/metabolism ; Male ; Meditation ; Multiple Sclerosis/immunology ; Multiple Sclerosis/metabolism ; Protein Interaction Maps ; Transcriptome
Language	English
Publishing date	2021-12-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2110455118
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Zs.A 1148: Show issues

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Article ; Online: Chronic aryl hydrocarbon receptor activity phenocopies smoking-induced skeletal muscle impairment.

Thome, Trace / Miguez, Kayla / Willms, Alexander J / Burke, Sarah K / Chandran, Vijayendran / de Souza, Angela R / Fitzgerald, Liam F / Baglole, Carolyn / Anagnostou, Maria-Eleni / Bourbeau, Jean / Jagoe, R Thomas / Morais, Jose A / Goddard, Yana / Taivassalo, Tanja / Ryan, Terence E / Hepple, Russell T

Journal of cachexia, sarcopenia and muscle

2021 Volume 13, Issue 1, Page(s) 589–604

Abstract: Background: Chronic obstructive pulmonary disease (COPD) patients exhibit skeletal muscle atrophy, denervation, and reduced mitochondrial oxidative capacity. Whilst chronic tobacco smoke exposure is implicated in COPD muscle impairment, the mechanisms ... ...

Abstract	Background: Chronic obstructive pulmonary disease (COPD) patients exhibit skeletal muscle atrophy, denervation, and reduced mitochondrial oxidative capacity. Whilst chronic tobacco smoke exposure is implicated in COPD muscle impairment, the mechanisms involved are ambiguous. The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that activates detoxifying pathways with numerous exogenous ligands, including tobacco smoke. Whereas transient AHR activation is adaptive, chronic activation can be toxic. On this basis, we tested the hypothesis that chronic smoke-induced AHR activation causes adverse muscle impact. Methods: We used clinical patient muscle samples, and in vitro (C2C12 myotubes) and in vivo models (mouse), to perform gene expression, mitochondrial function, muscle and neuromuscular junction morphology, and genetic manipulations (adeno-associated virus-mediated gene transfer). Results: Sixteen weeks of tobacco smoke exposure in mice caused muscle atrophy, neuromuscular junction degeneration, and reduced oxidative capacity. Similarly, smoke exposure reprogrammed the muscle transcriptome, with down-regulation of mitochondrial and neuromuscular junction genes. In mouse and human patient specimens, smoke exposure increased muscle AHR signalling. Mechanistically, experiments in cultured myotubes demonstrated that smoke condensate activated the AHR, caused mitochondrial impairments, and induced an AHR-dependent myotube atrophy. Finally, to isolate the role of AHR activity, expression of a constitutively active AHR mutant without smoke exposure caused atrophy and mitochondrial impairments in cultured myotubes, and muscle atrophy and neuromuscular junction degeneration in mice. Conclusions: These results establish that chronic AHR activity, as occurs in smokers, phenocopies the atrophy, mitochondrial impairment, and neuromuscular junction degeneration caused by chronic tobacco smoke exposure.
MeSH term(s)	Animals ; Humans ; Mice ; Muscle, Skeletal/metabolism ; Pulmonary Disease, Chronic Obstructive/genetics ; Receptors, Aryl Hydrocarbon/genetics ; Receptors, Aryl Hydrocarbon/metabolism ; Smoke/adverse effects ; Smoking/adverse effects
Chemical Substances	Receptors, Aryl Hydrocarbon ; Smoke
Language	English
Publishing date	2021-11-01
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2586864-0
ISSN	2190-6009 ; 2190-5991
ISSN (online)	2190-6009
ISSN	2190-5991
DOI	10.1002/jcsm.12826
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Article ; Online: Inducible and reversible phenotypes in a novel mouse model of Friedreich's Ataxia.

Chandran, Vijayendran / Gao, Kun / Swarup, Vivek / Versano, Revital / Dong, Hongmei / Jordan, Maria C / Geschwind, Daniel H

eLife

2017 Volume 6

Abstract: Friedreich's ataxia (FRDA), the most common inherited ataxia, is caused by recessive mutations that reduce the levels of frataxin (FXN), a mitochondrial iron binding protein. We developed an inducible mouse model ... ...

Abstract	Friedreich's ataxia (FRDA), the most common inherited ataxia, is caused by recessive mutations that reduce the levels of frataxin (FXN), a mitochondrial iron binding protein. We developed an inducible mouse model of
MeSH term(s)	Animals ; Disease Models, Animal ; Friedreich Ataxia/pathology ; Gene Expression Regulation ; Gene Knockdown Techniques ; Humans ; Iron-Binding Proteins/biosynthesis ; Iron-Binding Proteins/genetics ; Mice ; Phenotype ; Frataxin
Chemical Substances	Iron-Binding Proteins
Language	English
Publishing date	2017-12-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.30054
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Article ; Online: Transcriptomic Approaches to Neural Repair.

Dulin, Jennifer N / Antunes-Martins, Ana / Chandran, Vijayendran / Costigan, Michael / Lerch, Jessica K / Willis, Dianna E / Tuszynski, Mark H

The Journal of neuroscience : the official journal of the Society for Neuroscience

2015 Volume 35, Issue 41, Page(s) 13860–13867

Abstract: Understanding why adult CNS neurons fail to regenerate their axons following injury remains a central challenge of neuroscience research. A more complete appreciation of the biological mechanisms shaping the injured nervous system is a crucial ... ...

Abstract	Understanding why adult CNS neurons fail to regenerate their axons following injury remains a central challenge of neuroscience research. A more complete appreciation of the biological mechanisms shaping the injured nervous system is a crucial prerequisite for the development of robust therapies to promote neural repair. Historically, the identification of regeneration associated signaling pathways has been impeded by the limitations of available genetic and molecular tools. As we progress into an era in which the high-throughput interrogation of gene expression is commonplace and our knowledge base of interactome data is rapidly expanding, we can now begin to assemble a more comprehensive view of the complex biology governing axon regeneration. Here, we highlight current and ongoing work featuring transcriptomic approaches toward the discovery of novel molecular mechanisms that can be manipulated to promote neural repair. Significance statement: Transcriptional profiling is a powerful technique with broad applications in the field of neuroscience. Recent advances such as single-cell transcriptomics, CNS cell type-specific and developmental stage-specific expression libraries are rapidly enhancing the power of transcriptomics for neuroscience applications. However, extracting biologically meaningful information from large transcriptomic datasets remains a formidable challenge. This mini-symposium will highlight current work using transcriptomic approaches to identify regulatory networks in the injured nervous system. We will discuss analytical strategies for transcriptomics data, the significance of noncoding RNA networks, and the utility of multiomic data integration. Though the studies featured here specifically focus on neural repair, the approaches highlighted in this mini-symposium will be of broad interest and utility to neuroscientists working in diverse areas of the field.
MeSH term(s)	Animals ; Central Nervous System Diseases/genetics ; Central Nervous System Diseases/metabolism ; Gene Expression Profiling/methods ; Humans ; Nerve Regeneration/physiology ; Transcriptome/physiology
Language	English
Publishing date	2015-08-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.2599-15.2015
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Zs.A 1668: Show issues

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Article: Alteration in basal and depolarization induced transcriptional network in iPSC derived neurons from Timothy syndrome.

Tian, Yuan / Voineagu, Irina / Paşca, Sergiu P / Won, Hyejung / Chandran, Vijayendran / Horvath, Steve / Dolmetsch, Ricardo E / Geschwind, Daniel H

Genome medicine

2014 Volume 6, Issue 10, Page(s) 75

Abstract: Background: Common genetic variation and rare mutations in genes encoding calcium channel subunits have pleiotropic effects on risk for multiple neuropsychiatric disorders, including autism spectrum disorder (ASD) and schizophrenia. To gain further ... ...

Abstract	Background: Common genetic variation and rare mutations in genes encoding calcium channel subunits have pleiotropic effects on risk for multiple neuropsychiatric disorders, including autism spectrum disorder (ASD) and schizophrenia. To gain further mechanistic insights by extending previous gene expression data, we constructed co-expression networks in Timothy syndrome (TS), a monogenic condition with high penetrance for ASD, caused by mutations in the L-type calcium channel, Cav1.2. Methods: To identify patient-specific alterations in transcriptome organization, we conducted a genome-wide weighted co-expression network analysis (WGCNA) on neural progenitors and neurons from multiple lines of induced pluripotent stem cells (iPSC) derived from normal and TS (G406R in CACNA1C) individuals. We employed transcription factor binding site enrichment analysis to assess whether TS associated co-expression changes reflect calcium-dependent co-regulation. Results: We identified reproducible developmental and activity-dependent gene co-expression modules conserved in patient and control cell lines. By comparing cell lines from case and control subjects, we also identified co-expression modules reflecting distinct aspects of TS, including intellectual disability and ASD-related phenotypes. Moreover, by integrating co-expression with transcription factor binding analysis, we showed the TS-associated transcriptional changes were predicted to be co-regulated by calcium-dependent transcriptional regulators, including NFAT, MEF2, CREB, and FOXO, thus providing a mechanism by which altered Ca(2+) signaling in TS patients leads to the observed molecular dysregulation. Conclusions: We applied WGCNA to construct co-expression networks related to neural development and depolarization in iPSC-derived neural cells from TS and control individuals for the first time. These analyses illustrate how a systems biology approach based on gene networks can yield insights into the molecular mechanisms of neural development and function, and provide clues as to the functional impact of the downstream effects of Ca(2+) signaling dysregulation on transcription.
Language	English
Publishing date	2014-10-10
Publishing country	England
Document type	Journal Article
ZDB-ID	2484394-5
ISSN	1756-994X
ISSN	1756-994X
DOI	10.1186/s13073-014-0075-5
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Article ; Online: Integrative functional genomic analyses implicate specific molecular pathways and circuits in autism.

Parikshak, Neelroop N / Luo, Rui / Zhang, Alice / Won, Hyejung / Lowe, Jennifer K / Chandran, Vijayendran / Horvath, Steve / Geschwind, Daniel H

Cell

2013 Volume 155, Issue 5, Page(s) 1008–1021

Abstract: Genetic studies have identified dozens of autism spectrum disorder (ASD) susceptibility genes, raising two critical questions: (1) do these genetic loci converge on specific biological processes, and (2) where does the phenotypic specificity of ASD arise, ...

Abstract	Genetic studies have identified dozens of autism spectrum disorder (ASD) susceptibility genes, raising two critical questions: (1) do these genetic loci converge on specific biological processes, and (2) where does the phenotypic specificity of ASD arise, given its genetic overlap with intellectual disability (ID)? To address this, we mapped ASD and ID risk genes onto coexpression networks representing developmental trajectories and transcriptional profiles representing fetal and adult cortical laminae. ASD genes tightly coalesce in modules that implicate distinct biological functions during human cortical development, including early transcriptional regulation and synaptic development. Bioinformatic analyses suggest that translational regulation by FMRP and transcriptional coregulation by common transcription factors connect these processes. At a circuit level, ASD genes are enriched in superficial cortical layers and glutamatergic projection neurons. Furthermore, we show that the patterns of ASD and ID risk genes are distinct, providing a biological framework for further investigating the pathophysiology of ASD.
MeSH term(s)	Brain/embryology ; Brain/physiopathology ; Cerebral Cortex/physiopathology ; Child Development Disorders, Pervasive/genetics ; Child Development Disorders, Pervasive/metabolism ; Gene Expression Regulation ; Gene Regulatory Networks ; Genome-Wide Association Study ; Humans ; Neurons/metabolism ; Transcription, Genetic
Language	English
Publishing date	2013-11-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2013.10.031
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Zs.A 1167: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 58: Show issues

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Article ; Online: Mechanistic Differences in Neuropathic Pain Modalities Revealed by Correlating Behavior with Global Expression Profiling.

Cell reports

2018 Volume 22, Issue 5, Page(s) 1301–1312

Abstract: Chronic neuropathic pain is a major morbidity of neural injury, yet its mechanisms are incompletely understood. Hypersensitivity to previously non-noxious stimuli (allodynia) is a common symptom. Here, we demonstrate that the onset of cold ... ...

Abstract	Chronic neuropathic pain is a major morbidity of neural injury, yet its mechanisms are incompletely understood. Hypersensitivity to previously non-noxious stimuli (allodynia) is a common symptom. Here, we demonstrate that the onset of cold hypersensitivity precedes tactile allodynia in a model of partial nerve injury, and this temporal divergence was associated with major differences in global gene expression in innervating dorsal root ganglia. Transcripts whose expression change correlates with the onset of cold allodynia were nociceptor related, whereas those correlating with tactile hypersensitivity were immune cell centric. Ablation of TrpV1 lineage nociceptors resulted in mice that did not acquire cold allodynia but developed normal tactile hypersensitivity, whereas depletion of macrophages or T cells reduced neuropathic tactile allodynia but not cold hypersensitivity. We conclude that neuropathic pain incorporates reactive processes of sensory neurons and immune cells, each leading to distinct forms of hypersensitivity, potentially allowing drug development targeted to each pain type.
MeSH term(s)	Animals ; Behavior, Animal ; Cold Temperature ; Hyperalgesia/etiology ; Hyperalgesia/immunology ; Hyperalgesia/physiopathology ; Macrophages/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neuralgia/complications ; Neuralgia/immunology ; Neuralgia/physiopathology ; Sensory Receptor Cells/metabolism ; T-Lymphocytes/immunology ; TRPV Cation Channels/deficiency ; Touch ; Transcriptome
Chemical Substances	TRPV Cation Channels ; TRPV1 protein, mouse
Language	English
Publishing date	2018-01-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2018.01.006
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