The DOI matches its Crossref record; 54 of the 54 references it cites were found in a registry or an index.
Mitochondria and microRNA crosstalk in traumatic brain injury
Abstract
Traumatic brain injury (TBI) is a leading cause of long-term impairments in higher cognitive functioning, including deficits in attention and memory. It is well known that some of these persistent deficits are related, in part, to ongoing secondary injury events characterized by pervasive biochemical and pathophysiological stressors, including a rapid and sustained phase of mitochondrial dysfunction. A loss of mitochondrial function impacts a number of important cellular events and we have begun to investigate the novel hypothesis that mitochondria play a critical role in regulating the cellular activity of specific microRNAs in response to cellular demands and stressors. In this special issue report, we summarize briefly the rationale for investigating the crosstalk between mitochondria and microRNA, and provide recent preliminary data suggesting that mitochondria-microRNA interactions are modified in response to TBI-related cellular stressors. We postulate that this interaction is critical for regulating appropriate cellular microRNA responses, which opens up opportunities for therapeutic interventions targeting both mitochondrial function and microRNA activity.
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In the citing paper
“We reported previously that several inflammatory-responsive miRNAs (e.g., miR-146a, miR-142-3p, and miR-142-5p) are preferentially associated with mitochondria isolated from rat hippocampus”
From The Mitochondria-Associated ER Membranes Are Novel Subcellular Locations Enriched for Inflammatory-Responsive MicroRNAs (2020) · cites this paper as [30]
In the citing paper
“and that these miRNAs display a mitochondria-to-cytoplasm compartmental shift following a severe TBI [30, 31].”
From The Mitochondria-Associated ER Membranes Are Novel Subcellular Locations Enriched for Inflammatory-Responsive MicroRNAs (2020) · cites this paper as [30]
In the citing paper
“These include three miRNAs, miR-146a, miR-142-3p, and miR-142-5p, that were previously identified to be highly enriched in rat hippocampal mitochondria [30, 31], as well as several other miRNAs including miR-223 and two neuronal-enriched miRNAs, miR-124 and miR-107 [62].”
From The Mitochondria-Associated ER Membranes Are Novel Subcellular Locations Enriched for Inflammatory-Responsive MicroRNAs (2020) · cites this paper as [30]
Citations
Cites
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MicroRNAs Modulate Hematopoietic Lineage Differentiation
Chen, C.-Z., Li, L., Lodish, H. F., & Bartel, D. P. (2004) · Science · doi:10.1126/science.1091903 · Cited by 3,257
miR-146a is a significant brake on autoimmunity, myeloproliferation, and cancer in mice
Boldin, M. P., Taganov, K. D., Rao, D. S., Yang, L., Zhao, J. L., Kalwani, M., Garcia-Flores, Y., Luong, M., Devrekanli, A., Xu, J., et al. (2011) · Journal of Experimental Medicine · doi:10.1084/jem.20101823 · Cited by 861
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Apoptosis After Traumatic Brain Injury
RAGHUPATHI, R., GRAHAM, D. I., & McINTOSH, T. K. (2000) · Journal of Neurotrauma · doi:10.1089/neu.2000.17.927 · Cited by 412
Caspase‐3 Mediated Neuronal Death After Traumatic Brain Injury in Rats
Clark, R. S. B., Kochanek, P. M., Watkins, S. C., Chen, M., Dixon, C. E., Seidberg, N. A., Melick, J., Loeffert, J. E., Nathaniel, P. D., Jin, K. L., et al. (2000) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2000.740740.x · Cited by 405
Mitochondrial permeability transition in CNS trauma: Cause or effect of neuronal cell death?
Sullivan, P. G., Rabchevsky, A. G., Waldmeier, P. C., & Springer, J. E. (2005) · Journal of Neuroscience Research · doi:10.1002/jnr.20292 · Cited by 383
Self-citationSingh, I. N., Sullivan, P. G., Deng, Y., Mbye, L. H., & Hall, E. D. (2006) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1038/sj.jcbfm.9600297 · Cited by 367
Self-citationNuclear miRNA Regulates the Mitochondrial Genome in the Heart
Das, S., Ferlito, M., Kent, O. A., Fox-Talbot, K., Wang, R., Liu, D., Raghavachari, N., Yang, Y., Wheelan, S. J., Murphy, E., et al. (2012) · Circulation Research · doi:10.1161/circresaha.112.267732 · Cited by 364
Cyclosporin A Attenuates Acute Mitochondrial Dysfunction Following Traumatic Brain Injury
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Self-citation
Cited by
Wang, W.-X., Prajapati, P., Nelson, P. T., & Springer, J. E. (2020) · Molecular Neurobiology · doi:10.1007/s12035-020-01937-y · Cited by 49
Self-citation
Metadata
- Authors
- Wang, W.-X., Sullivan, P. G., & Springer, J. E.
- ORCID
- Springer, Joe E.
- Venue
- Progress in Neuro-Psychopharmacology and Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2017-02
- Volume
- 73
- Pages
- 104-108
- ISSN
- 0278-5846
- Cited by
- 22
- References
- 54
- Language
- en
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- Funders
- Kentucky Spinal Cord and Head Injury Research Trust. (15-12A)
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- Wang, W.-X., Sullivan, P. G., & Springer, J. E. (2017). Mitochondria and microRNA crosstalk in traumatic brain injury. Progress in Neuro-Psychopharmacology and Biological Psychiatry. https://doi.org/10.1016/j.pnpbp.2016.02.011
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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