The Imbalance of Astrocytic Mitochondrial Dynamics Following Blast-Induced Traumatic Brain Injury.
| Title: | The Imbalance of Astrocytic Mitochondrial Dynamics Following Blast-Induced Traumatic Brain Injury. |
|---|---|
| Authors: | Guilhaume-Correa F; Translational Biology, Medicine, and Health Graduate Program, Virginia Polytechnic Institute and State University, Roanoke, VA 24016, USA.; Pickrell AM; School of Neuroscience, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061, USA.; VandeVord PJ; Biomedical Engineering and Mechanics, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061, USA.; Salem VA Medical Center, Salem, VA 24153, USA. |
| Source: | Biomedicines [Biomedicines] 2023 Jan 24; Vol. 11 (2). Date of Electronic Publication: 2023 Jan 24. |
| Publication Type: | Journal Article |
| Language: | English |
| Journal Info: | Publisher: MDPI AG Country of Publication: Switzerland NLM ID: 101691304 Publication Model: Electronic Cited Medium: Print ISSN: 2227-9059 (Print) Linking ISSN: 22279059 NLM ISO Abbreviation: Biomedicines Subsets: PubMed not MEDLINE |
| Imprint Name(s): | Original Publication: Basel, Switzerland : MDPI AG, [2013]- |
| Abstract: | Mild blast-induced traumatic brain injury (bTBI) is a modality of injury that has been of major concern considering a large number of military personnel exposed to explosive blast waves. bTBI results from the propagation of high-pressure static blast forces and their subsequent energy transmission within brain tissue. Exposure to this overpressure energy causes a diffuse injury that leads to acute cell damage and, if chronic, leads to detrimental long-term cognitive deficits. The literature presents a neuro-centric approach to the role of mitochondria dynamics dysfunction in bTBI, and changes in astrocyte-specific mitochondrial dynamics have not been characterized. The balance between fission and fusion events is known as mitochondrial dynamics. As a result of fission and fusion, the mitochondrial structure is constantly altering its shape to respond to physiological stimuli or stress, which in turn affects mitochondrial function. Astrocytic mitochondria are recognized to play an essential role in overall brain metabolism, synaptic transmission, and neuron protection. Mitochondria are vulnerable to injury insults, leading to the increase in mitochondrial fission, a mechanism controlled by the GTPase dynamin-related protein (Drp1) and the phosphorylation of Drp1 at serine 616 (p-Drp1s616). This site is critical to mediate the Drp1 translocation to mitochondria to promote fission events and consequently leads to fragmentation. An increase in mitochondrial fragmentation could have negative consequences, such as promoting an excessive generation of reactive oxygen species or triggering cytochrome c release. The aim of the present study was to characterize the unique pattern of astrocytic mitochondrial dynamics by exploring the role of DRP1 with a combination of in vitro and in vivo bTBI models. Differential remodeling of the astrocytic mitochondrial network was observed, corresponding with increases in p-Drp1S616 four hours and seven days post-injury. Further, results showed a time-dependent reactive astrocyte phenotype transition in the rat hippocampus. This discovery can lead to innovative therapeutics targets to help prevent the secondary injury cascade after blast injury that involves mitochondria dysfunction. |
| References: | J Neurosci. 2015 Dec 2;35(48):15996-6011. (PMID: 26631479); Neurosci Lett. 2020 Nov 20;739:135405. (PMID: 32979460); J Cereb Blood Flow Metab. 2003 Feb;23(2):219-31. (PMID: 12571453); J Cell Biol. 2020 May 4;219(5):. (PMID: 32236517); Psychoneuroendocrinology. 2016 May;67:113-23. (PMID: 26881837); Nat Neurosci. 2019 Oct;22(10):1635-1648. (PMID: 31551592); Biomed Sci Instrum. 2015;51:439-45. (PMID: 25996750); Biochem Soc Trans. 2014 Oct;42(5):1302-10. (PMID: 25233407); Nat Neurosci. 2015 Jul;18(7):942-52. (PMID: 26108722); J Neurosci. 2013 Jul 31;33(31):12870-86. (PMID: 23904622); Neuron. 2017 Feb 8;93(3):587-605.e7. (PMID: 28132831); Rejuvenation Res. 2005 Spring;8(1):3-5. (PMID: 15798367); Neurosci Lett. 2014 Apr 17;565:23-9. (PMID: 24361547); EMBO Rep. 2011 Jun;12(6):565-73. (PMID: 21508961); Nat Rev Mol Cell Biol. 2020 Apr;21(4):204-224. (PMID: 32071438); Front Mol Neurosci. 2016 Aug 08;9:64. (PMID: 27551260); Annu Rev Genet. 2012;46:265-87. (PMID: 22934639); J Biomech. 2005 May;38(5):1093-105. (PMID: 15797591); Stem Cell Res. 2021 Oct 12;57:102572. (PMID: 34662843); PLoS One. 2012;7(6):e39421. (PMID: 22768078); Ann N Y Acad Sci. 2010 Jul;1201:34-9. (PMID: 20649536); Science. 2012 Aug 31;337(6098):1062-5. (PMID: 22936770); Cell Commun Signal. 2020 Apr 15;18(1):62. (PMID: 32293472); Neuroscience. 2013 Dec 3;253:9-20. (PMID: 23999126); J Neurotrauma. 2011 Jan;28(1):85-94. (PMID: 21091267); Brain Res. 2007 Jul 16;1158:103-15. (PMID: 17555726); Aging Cell. 2017 Feb;16(1):39-51. (PMID: 27623715); Biochem Pharmacol. 2010 Jan 15;79(2):77-89. (PMID: 19765548); Int J Mol Sci. 2021 Jun 10;22(12):. (PMID: 34200828); J Neurosci Res. 2016 Sep;94(9):827-36. (PMID: 27317559); Mol Biol Cell. 2001 Aug;12(8):2245-56. (PMID: 11514614); Shock. 2015 Aug;44 Suppl 1:71-8. (PMID: 25521536); Curr Protoc Neurosci. 2019 Jun;88(1):e71. (PMID: 31216394); Sci Rep. 2016 May 10;6:25713. (PMID: 27162174); Toxicology. 2017 Nov 1;391:109-115. (PMID: 28655545); J Neurotrauma. 2017 Jan 15;34(2):517-528. (PMID: 27163293); J Neurotrauma. 2017 Sep;34(S1):S44-S52. (PMID: 28937952); Oxid Med Cell Longev. 2018 Apr 1;2018:6501031. (PMID: 29805731); Neurotoxicology. 2018 Jan;64:204-218. (PMID: 28539244); Best Pract Res Clin Endocrinol Metab. 2012 Dec;26(6):711-23. (PMID: 23168274); Cell Rep. 2021 Apr 13;35(2):108952. (PMID: 33852851); Physiol Rev. 2014 Oct;94(4):1077-98. (PMID: 25287860); J Cell Biol. 1998 Oct 19;143(2):351-8. (PMID: 9786947); Front Aging Neurosci. 2020 Dec 10;12:614410. (PMID: 33362533); Acta Neuropathol. 2016 Mar;131(3):323-45. (PMID: 26671410); Exp Neurol. 2016 Jan;275 Pt 3:305-315. (PMID: 25828533); Neurosci Lett. 2008 Apr 4;434(3):247-52. (PMID: 18342445); Physiology (Bethesda). 2018 Mar 1;33(2):99-112. (PMID: 29412059); EMBO Rep. 2007 Oct;8(10):939-44. (PMID: 17721437); BMC Psychiatry. 2020 Feb 17;20(1):71. (PMID: 32066415); Nat Rev Neurosci. 2004 Feb;5(2):146-56. (PMID: 14735117); Bioessays. 2015 Jun;37(6):687-700. (PMID: 25847815); Biomed Sci Instrum. 2013;49:312-9. (PMID: 23686215); Trends Neurosci. 2009 Dec;32(12):638-47. (PMID: 19782411); J Cell Biol. 2010 Dec 13;191(6):1141-58. (PMID: 21149567); J Neurotrauma. 2010 Feb;27(2):383-9. (PMID: 19852583); Ageing Res Rev. 2020 May;59:101039. (PMID: 32105849); Mol Cell Biochem. 2004 Jan-Feb;256-257(1-2):209-18. (PMID: 14977182); Alzheimers Dement. 2014 Jun;10(3 Suppl):S97-104. (PMID: 24924680); J Biol Chem. 2007 Jul 27;282(30):21583-7. (PMID: 17553808); Nature. 1999 Feb 4;397(6718):441-6. (PMID: 9989411); Cell Metab. 2011 Dec 7;14(6):724-38. (PMID: 22152301); Front Integr Neurosci. 2016 Feb 29;10:7. (PMID: 26973475); Front Cell Dev Biol. 2021 Jan 07;8:608026. (PMID: 33537300); Trends Immunol. 2020 Sep;41(9):758-770. (PMID: 32819810); Cell. 2003 Feb 21;112(4):481-90. (PMID: 12600312); Cell Metab. 2013 Dec 3;18(6):844-59. (PMID: 24315370); Headache. 2012 May;52(5):732-8. (PMID: 22404747); NMR Biomed. 2012 Dec;25(12):1331-9. (PMID: 22549883); J Neuropathol Exp Neurol. 2021 Jan 20;80(2):112-128. (PMID: 33421075); Restor Neurol Neurosci. 2010;28(3):311-21. (PMID: 20479526); Nat Cell Biol. 2009 Aug;11(8):958-66. (PMID: 19578372); Proc Natl Acad Sci U S A. 2008 Mar 4;105(9):3581-6. (PMID: 18299565); Acta Histochem. 2017 Apr;119(3):315-326. (PMID: 28314612); Front Neurosci. 2020 Nov 05;14:536682. (PMID: 33224019); Nat Neurosci. 2021 Mar;24(3):312-325. (PMID: 33589835); Glia. 2005 Jun;50(4):427-434. (PMID: 15846805); Behav Res Ther. 2006 Apr;44(4):561-83. (PMID: 15972206); Pain Med. 2014 May;15(5):782-90. (PMID: 24548466); J Neurosci. 2007 Nov 7;27(45):12255-66. (PMID: 17989291); Mol Biol Cell. 2008 Jun;19(6):2402-12. (PMID: 18353969); Curr Biol. 2018 Feb 19;28(4):R170-R185. (PMID: 29462587); J Physiol. 2000 Nov 15;529 Pt 1:57-68. (PMID: 11080251); PLoS One. 2017 Sep 8;12(9):e0184265. (PMID: 28886114); J Biol Chem. 2007 Apr 13;282(15):11521-9. (PMID: 17301055); Neurosci Lett. 2014 Jun 6;570:33-7. (PMID: 24726403); Front Endocrinol (Lausanne). 2020 Jun 11;11:374. (PMID: 32595603); J Neurosci. 2019 Mar 6;39(10):1930-1943. (PMID: 30626699); Int J Mol Sci. 2021 Jun 15;22(12):. (PMID: 34203960); Mol Brain. 2018 Nov 9;11(1):64. (PMID: 30409147); Mol Cell. 1999 Nov;4(5):815-26. (PMID: 10619028); Neurochem Res. 2000 Oct;25(9-10):1439-51. (PMID: 11059815) |
| Grant Information: | No number Virginia Tech |
| Contributed Indexing: | Keywords: acute; astrocytes; blast-induced traumatic brain injury; fission and dynamin-related protein; mild; mitochondrial dynamics; sub-acute |
| Entry Date(s): | Date Created: 20230225 Latest Revision: 20230228 |
| Update Code: | 20260130 |
| PubMed Central ID: | PMC9953570 |
| DOI: | 10.3390/biomedicines11020329 |
| PMID: | 36830865 |
| Database: | MEDLINE |
Journal Article