Gap junction protein connexin 43 and its distribution in damaged nerve cells
- Authors: Kolos E.A.1, Korzhevskii D.E.1
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Affiliations:
- Institute of Experimental Medicine
- Issue: Vol 24, No 1 (2024)
- Pages: 107-116
- Section: Original research
- Published: 11.09.2024
- URL: https://journals.eco-vector.com/MAJ/article/view/630557
- DOI: https://doi.org/10.17816/MAJ630557
- ID: 630557
Cite item
Abstract
BACKGROUND: Connexins, particularly connexin 43, form gap junctions that mediate neuron-glial communication. To date, the expression of connexin 43 in phenotypically distinct neurolemmocytes, in particular non-myelinating (Remak cells) and repair Schwann cells, has not been studied.
AIM: To determine the presence of connexin 43 in Schwann cells of the rat sciatic nerve under normal conditions and after mechanical damage by applying a ligature.
MATERIALS AND METHODS: The study was carried out on Wistar rats (n = 10). In experimental rats, the sciatic nerve was damaged by applying a ligature (40 s). 7 days after surgery, sciatic nerve segments were isolated for subsequent immunohistochemical study using antibodies to connexin 43 and glial fibrillary acidic protein (GFAP). In the control group rats, segments of intact sciatic nerves were isolated in a similar way.
RESULTS: It has been shown that in the endoneurium of the intact rat sciatic nerve there are no cells expressing connexin 43. It was found that 7 days after injury, a large number of connexin-43-immunopositive cells of irregular shape with several processes were identified in the endoneurium of the damaged nerve. There was a lack of expression of connexin 43 in GFAP-containing Schwann cells.
CONCLUSIONS: It can be stated that nerve damage leads to active synthesis of the studied protein by endoneurium cells; however, the origin of the cells expressing connexin 43 remains to be elucidated.
Keywords
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About the authors
Elena A. Kolos
Institute of Experimental Medicine
Email: koloselena1984@yandex.ru
ORCID iD: 0000-0002-9643-6831
SPIN-code: 1479-5992
Scopus Author ID: 55354374400
ResearcherId: D-1579-2012
Research Associate, Laboratory of Functional Morphology of the Central and Peripheral Nervous System, Department of General and Special Morphology
Russian Federation, 12 Academician Pavlov St., Saint Petersburg, 197022Dmitrii E. Korzhevskii
Institute of Experimental Medicine
Author for correspondence.
Email: DEK2@yandex.ru
ORCID iD: 0000-0002-2456-8165
SPIN-code: 3252-3029
Scopus Author ID: 12770589000
ResearcherId: C-2206-2012
MD, Dr. Sci. (Medicine), Professor of the Russian Academy of Sciences, Head of the Department of General and Special Morphology
Russian Federation, 12 Academician Pavlov St., Saint Petersburg, 197022References
- Chanson M, Chandross KJ, Rook MB, et al. Gating characteristics of a steeply voltage-dependent gap junction channel in rat Schwann cells. J Gen Physiol. 1993;102(5):925–946. doi: 10.1085/jgp.102.5.925
- Chandross KJ, Spray DC, Kessler JA. Gap junctions and Schwann cells. In: Kanno Y, Kataoka K, Shiba Y, et al., editors. Intercellular Communication through Gap Junctions. Vol. 4. Amsterdam: Elsevier Science B.V.; 1995. P. 273–277. doi: 10.1016/B978-0-444-81929-1.50056-3
- Balice-Gordon RJ, Bone LJ, Scherer SS. Functional gap junctions in the Schwann cell myelin sheath. J Cell Biol. 1998;142(4):1095–1104. doi: 10.1083/jcb.142.4.1095
- Bergoffen J, Scherer SS, Wang S, et al. Connexin mutations in X-linked Charcot–Marie–Tooth disease. Science. 1993;262(5142):2039–2042. doi: 10.1126/science.8266101
- Scherer SS, Deschênes SM, Xu YT, et al. Connexin32 is a myelin-related protein in the PNS and CNS. J Neurosci. 1995;15(12):8281–8294. doi: 10.1523/JNEUROSCI.15-12-08281.1995
- Scherer SS, Xu YT, Nelles E, et al. Connexin32-null mice develop demyelinating peripheral neuropathy. Glia. 1998;24(1):8–20. doi: 10.1002/(sici)1098-1136(199809)24:1<8::aid-glia2>3.0.co;2-3
- Spray DC, Dermietzel R. X-linked dominant Charcot–Marie–Tooth disease and other potential gap-junction diseases of the nervous system. Trends Neurosci. 1995;18(6):256–262.
- Spray DC, Dermietzel R. Gap junctions in the nervous system. Heidelberg: Springer-Verlag; 1996. 317 р.
- Meier C, Dermietzel R, Davidson KG, et al. Connexin32-containing gap junctions in Schwann cells at the internodal zone of partial myelin compaction and in Schmidt–Lanterman incisures. J Neurosci. 2004;24(13):3186–3198. doi: 10.1523/JNEUROSCI.5146-03.2004
- Li J, Habbes HW, Eiberger J, et al. Analysis of connexin expression during mouse Schwann cell development identifies connexin29 as a novel marker for the transition of neural crest to precursor cells. Glia. 2007;55(1):93–103. doi: 10.1002/glia.20427
- Bortolozzi M. What’s the function of connexin 32 in the peripheral nervous system? Front Mol Neurosci. 2018;11:227. doi: 10.3389/fnmol.2018.00227
- Yoshimura T, Satake M, Kobayashi T. Connexin43 is another gap junction protein in the peripheral nervous system. J Neurochem. 1996;67(3):1252–1258. doi: 10.1046/j.1471-4159.1996.67031252.x
- Mambetisaeva ET, Gire V, Evans WH. Multiple connexin expression in peripheral nerve, Schwann cells, and Schwannoma cells. J Neurosci Res. 1999;57(2):166–175. doi: 10.1002/(SICI)1097-4547(19990715)57:2<166::AID-JNR2>3.0.CO;2-Y
- Zhao S, Spray DC. Localization of Cx26, Cx32 and Cx43 in myelinating Schwann cells of mouse sciatic nerve during postnatal development. In: Werner R, editor. Gap Junctions. Amsterdam: IOS Press; 1998. P. 198–202.
- Nagaoka T, Oyamada M, Okajima S, Takamatsu T. Differential expression of gap junction proteins connexin26, 32, and 43 in normal and crush-injured rat sciatic nerves. Close relationship between connexin43 and occludin in the perineurium. J Histochem Cytochem. 1999;47(7):937–948. doi: 10.1177/002215549904700711
- Jessen KR, Morgan L, Stewart HJ, Mirsky R. Three markers of adult non-myelin-forming Schwann cells, 217c(Ran-1), A5E3 and GFAP: development and regulation by neuron-Schwann cell interactions. Development. 1990;109(1):91–103. doi: 10.1242/dev.109.1.91
- Triolo D, Dina G, Lorenzetti I, et al. Loss of glial fibrillary acidic protein (GFAP) impairs Schwann cell proliferation and delays nerve regeneration after damage. J Cell Sci. 2006;119(Pt 19):3981–3993. doi: 10.1242/jcs.03168
- Jessen KR, Mirsky R. Negative regulation of myelination: relevance for development, injury, and demyelinating disease. Glia. 2008;56(14):1552–1565. doi: 10.1002/glia.20761
- Jessen KR, Mirsky R. The repair Schwann cell and its function in regenerating nerves. J Physiol. 2016;594(13):3521–3531. doi: 10.1113/JP270874
- Jessen KR, Mirsky R. The success and failure of the Schwann cell response to nerve injury. Front Cell Neurosci. 2019;13:33. doi: 10.3389/fncel.2019.00033
- Zochodne DW. Neurobiology of peripheral nerve regeneration. New York: Cambridge University Press; 2008. 276 p.
- Fornaro M, Marcus D, Rattin J, Goral J. Dynamic environmental physical cues activate mechanosensitive responses in the repair Schwann cell phenotype. Cells. 2021;10(2):425. doi: 10.3390/cells10020425
- Taveggia C, Feltri ML. Beyond wrapping: canonical and noncanonical functions of Schwann cells. Annu Rev Neurosci. 2022;45:561–580. doi: 10.1146/annurev-neuro-110920-030610
- Cisterna BA, Arroyo P, Puebla C. Role of connexin-based gap junction channels in communication of myelin sheath in Schwann cells. Front Cell Neurosci. 2019;13:69. doi: 10.3389/fncel.2019.00069
- Sandri C, Van Buren JM, Akert K. Membrane morphology of the vertebrate nervous system. Prog Brain Res. 1977:46:1–384.
- Tetzlaff W. Tight junction contact events and temporary gap junctions in the sciatic nerve fibres of the chicken during Wallerian degeneration and subsequent regeneration. J Neurocytol. 1982;11:839–858. doi: 10.1007/BF01153522
- Chandross KJ, Kessler JA, Cohen RI, et al. Altered connexin expression after peripheral nerve injury. Mol Cell Neurosci. 1996;7(6):501–518. doi: 10.1006/mcne.1996.0036
- Chen ZL, Yu WM, Strickland S. Peripheral regeneration. Annu Rev Neurosci. 2007;30:209–233. doi: 10.1146/annurev.neuro.30.051606.094337
- Mirsky R, Woodhoo A, Parkinson DB, et al. Novel signals controlling embryonic Schwann cell development, myelination and dedifferentiation. J Peripher Nerv Syst. 2008;13(2):122–135. doi: 10.1111/j.1529-8027.2008.00168.x
- Balakrishnan A, Belfiore L, Chu TH, et al. Insights into the role and potential of Schwann cells for peripheral nerve repair from studies of development and injury. Front Mol Neurosci. 2021;13:608442. doi: 10.3389/fnmol.2020.608442
- Jessen KR, Mirsky R, Lloyd AC. Schwann cells: development and role in nerve repair. Cold Spring Harb Perspect Biol. 2015;7(7):a020487. doi: 10.1101/cshperspect.a020487
- Jessen KR, Arthur-Farraj P. Repair Schwann cell update: Adaptive reprogramming, EMT, and stemness in regenerating nerves. Glia. 2019;67(3):421–437. doi: 10.1002/glia.23532
- Boerboom A, Dion V, Chariot A, Franzen R. Molecular mechanisms involved in Schwann cell plasticity. Front Mol Neurosci. 2017;10:38. doi: 10.3389/fnmol.2017.00038