دورية أكاديمية

Altered Spinal Homeostasis and Maladaptive Plasticity in GFAP Null Mice Following Peripheral Nerve Injury.

التفاصيل البيبلوغرافية
العنوان: Altered Spinal Homeostasis and Maladaptive Plasticity in GFAP Null Mice Following Peripheral Nerve Injury.
المؤلفون: De Luca C; Neural Network Morphology & Systems Biology Lab, Division of Human Anatomy, Department of Mental and Physical Health and Preventive Medicine, University of Campania 'Luigi Vanvitelli', 80138 Naples, Italy., Virtuoso A; Neural Network Morphology & Systems Biology Lab, Division of Human Anatomy, Department of Mental and Physical Health and Preventive Medicine, University of Campania 'Luigi Vanvitelli', 80138 Naples, Italy., Korai SA; Neural Network Morphology & Systems Biology Lab, Division of Human Anatomy, Department of Mental and Physical Health and Preventive Medicine, University of Campania 'Luigi Vanvitelli', 80138 Naples, Italy., Cirillo R; Neural Network Morphology & Systems Biology Lab, Division of Human Anatomy, Department of Mental and Physical Health and Preventive Medicine, University of Campania 'Luigi Vanvitelli', 80138 Naples, Italy., Gargano F; Unit of Anesthesia, Intensive Care and Pain Management, Department of Medicine, Campus Bio-Medico University of Rome, 00128 Rome, Italy., Papa M; Neural Network Morphology & Systems Biology Lab, Division of Human Anatomy, Department of Mental and Physical Health and Preventive Medicine, University of Campania 'Luigi Vanvitelli', 80138 Naples, Italy.; SYSBIO Centre of Systems Biology ISBE.ITALY, University of Milano-Bicocca, 20126 Milano, Italy., Cirillo G; Neural Network Morphology & Systems Biology Lab, Division of Human Anatomy, Department of Mental and Physical Health and Preventive Medicine, University of Campania 'Luigi Vanvitelli', 80138 Naples, Italy.
المصدر: Cells [Cells] 2022 Apr 05; Vol. 11 (7). Date of Electronic Publication: 2022 Apr 05.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: MDPI Country of Publication: Switzerland NLM ID: 101600052 Publication Model: Electronic Cited Medium: Internet ISSN: 2073-4409 (Electronic) Linking ISSN: 20734409 NLM ISO Abbreviation: Cells Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Basel, Switzerland : MDPI
مواضيع طبية MeSH: Peripheral Nerve Injuries*, Animals ; Gliosis/metabolism ; Glutamic Acid/metabolism ; Homeostasis ; Hyperalgesia ; Mice ; Mice, Knockout ; Neuroglia/metabolism ; Vimentin
مستخلص: The maladaptive response of the central nervous system (CNS) following nerve injury is primarily linked to the activation of glial cells (reactive gliosis) that produce an inflammatory reaction and a wide cellular morpho-structural and functional/metabolic remodeling. Glial acidic fibrillary protein (GFAP), a major protein constituent of astrocyte intermediate filaments (IFs), is the hallmark of the reactive astrocytes, has pleiotropic functions and is significantly upregulated in the spinal cord after nerve injury. Here, we investigated the specific role of GFAP in glial reaction and maladaptive spinal cord plasticity following sciatic nerve spared nerve injury (SNI) in GFAP KO and wild-type (WT) animals. We evaluated the neuropathic behavior (thermal hyperalgesia, allodynia) and the expression of glial (vimentin, Iba1) and glutamate/GABA system markers (GLAST, GLT1, EAAC1, vGLUT, vGAT, GAD) in lumbar spinal cord sections of KO/WT animals. SNI induced neuropathic behavior in both GFAP KO and WT mice, paralleled by intense microglial reaction (Iba1 expression more pronounced in KO mice), reactive astrocytosis (vimentin increase) and expression remodeling of glial/neuronal glutamate/GABA transporters. In conclusion, it is conceivable that the lack of GFAP could be detrimental to the CNS as it lacks a critical sensor for neuroinflammation and morpho-functional-metabolic rewiring after nerve injury. Understanding the maladaptive morpho-functional changes of glial cells could represent the first step for a new glial-based targeted approach for mechanisms of disease in the CNS.
References: Glia. 2015 Jun;63(6):1036-56. (PMID: 25731615)
Biotechnol Adv. 2012 Jan-Feb;30(1):223-32. (PMID: 21620945)
Nat Rev Neurosci. 2005 Aug;6(8):626-40. (PMID: 16025096)
Neurosci Lett. 2014 Apr 17;565:7-13. (PMID: 24508671)
J Neuropathol Exp Neurol. 2019 Feb 1;78(2):123-129. (PMID: 30605553)
Curr Opin Cell Biol. 2015 Feb;32:121-30. (PMID: 25726916)
Cell Mol Neurobiol. 2016 Jan;36(1):37-46. (PMID: 26084599)
Int J Mol Sci. 2021 Mar 24;22(7):. (PMID: 33804873)
Acta Neurochir Suppl. 2003;86:267-9. (PMID: 14753450)
Free Radic Biol Med. 2018 May 20;120:380-394. (PMID: 29635011)
Proc Natl Acad Sci U S A. 1996 Jun 25;93(13):6361-6. (PMID: 8692820)
J Lipid Res. 2020 May;61(5):655-666. (PMID: 31862695)
Prog Neurobiol. 2011 Mar;93(3):421-43. (PMID: 21219963)
J Physiol. 2004 Aug 15;559(Pt 1):3-15. (PMID: 15218071)
Acta Neurochir Suppl. 2004;89:87-92. (PMID: 15335106)
Neurosci Lett. 2012 Nov 14;530(1):85-90. (PMID: 22981978)
Neural Regen Res. 2020 May;15(5):838-842. (PMID: 31719244)
Mol Neurobiol. 2015 Dec;52(3):1440-1457. (PMID: 25352445)
J Neurotrauma. 2020 Dec 1;37(23):2460-2467. (PMID: 32854584)
Eur J Pain. 2013 Jul;17(6):799-810. (PMID: 23193101)
Cells. 2020 Jul 02;9(7):. (PMID: 32630739)
Neuron. 2013 Jan 9;77(1):10-8. (PMID: 23312512)
Neuron Glia Biol. 2007 May;3(2):141-53. (PMID: 18634571)
J Neurosci Methods. 1994 Jul;53(1):55-63. (PMID: 7990513)
Adv Neurobiol. 2021;26:55-73. (PMID: 34888830)
Pain. 2000 Aug;87(2):149-158. (PMID: 10924808)
Hum Mutat. 2020 Jun;41(6):1131-1137. (PMID: 32126152)
Cell Rep. 2018 May 29;23(9):2667-2677. (PMID: 29847797)
Trends Neurosci. 2003 Oct;26(10):523-30. (PMID: 14522144)
J Neurosci Res. 2011 Aug;89(8):1302-15. (PMID: 21557293)
J Cell Biol. 1999 May 3;145(3):503-14. (PMID: 10225952)
Neurosci Biobehav Rev. 2014 May;42:35-54. (PMID: 24509064)
Pain. 1988 Jan;32(1):77-88. (PMID: 3340425)
J Neurodev Disord. 2019 Dec 16;11(1):27. (PMID: 31838996)
Int J Mol Sci. 2021 Oct 20;22(21):. (PMID: 34768733)
Proc Natl Acad Sci U S A. 2021 Mar 30;118(13):. (PMID: 33753498)
Nat Rev Immunol. 2018 Apr;18(4):225-242. (PMID: 29151590)
Nat Neurosci. 2021 Mar;24(3):312-325. (PMID: 33589835)
Int J Mol Sci. 2020 Feb 24;21(4):. (PMID: 32102370)
Neural Regen Res. 2016 Sep;11(9):1422-1423. (PMID: 27857743)
Nat Rev Neurosci. 2001 Mar;2(3):185-93. (PMID: 11256079)
J Comp Neurol. 2003 Nov 3;466(1):119-35. (PMID: 14515244)
Neuroscience. 2016 Feb 9;314:189-99. (PMID: 26642807)
Neural Plast. 2012;2012:425818. (PMID: 23091738)
Brain Res. 2000 May 12;864(2):220-9. (PMID: 10802029)
Brain Res Bull. 2001 Oct-Nov 1;56(3-4):173-82. (PMID: 11719248)
Neurobiol Dis. 2011 Mar;41(3):630-9. (PMID: 21111819)
Neuron Glia Biol. 2007 Nov;3(4):335-51. (PMID: 18634565)
J Cereb Blood Flow Metab. 2000 Jul;20(7):1040-4. (PMID: 10908037)
Neurochem Res. 2005 Sep;30(9):1093-100. (PMID: 16292501)
Biochem Soc Trans. 2006 Feb;34(Pt 1):51-4. (PMID: 16417481)
Neuroreport. 1998 Jun 1;9(8):1691-6. (PMID: 9665584)
PLoS One. 2016 Mar 30;11(3):e0152750. (PMID: 27028103)
فهرسة مساهمة: Keywords: GFAP; neuropathic behavior; peripheral nerve injury; reactive astrogliosis; spinal cord
المشرفين على المادة: 0 (Vimentin)
3KX376GY7L (Glutamic Acid)
تواريخ الأحداث: Date Created: 20220412 Date Completed: 20220413 Latest Revision: 20220516
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC8997460
DOI: 10.3390/cells11071224
PMID: 35406788
قاعدة البيانات: MEDLINE
الوصف
تدمد:2073-4409
DOI:10.3390/cells11071224