دورية أكاديمية
أعرض في EDS

Expression and Roles of Lynx1, a Modulator of Cholinergic Transmission, in Skeletal Muscles and Neuromuscular Junctions in Mice.

التفاصيل البيبلوغرافية
العنوان: Expression and Roles of Lynx1, a Modulator of Cholinergic Transmission, in Skeletal Muscles and Neuromuscular Junctions in Mice.
المؤلفون: Doss SV; Department of Molecular Biology, Cellular Biology, and Biochemistry, Brown University, Providence, RI, United States., Barbat-Artigas S; Département de Neurosciences, Université de Montréal, Montréal, QC, Canada., Lopes M; Department of Molecular Biology, Cellular Biology, and Biochemistry, Brown University, Providence, RI, United States., Pradhan BS; Laboratory of Synaptogenesis, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.; Laboratory of Synaptogenesis, Łukasiewicz Research Network-PORT Polish Center for Technology Development, Wrocław, Poland., Prószyński TJ; Laboratory of Synaptogenesis, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.; Laboratory of Synaptogenesis, Łukasiewicz Research Network-PORT Polish Center for Technology Development, Wrocław, Poland., Robitaille R; Département de Neurosciences, Université de Montréal, Montréal, QC, Canada.; Centre de Recherche Interdisciplinaire sur le Cerveau et L'Apprentissage (CIRCA), Montreal, QC, Canada., Valdez G; Department of Molecular Biology, Cellular Biology, and Biochemistry, Brown University, Providence, RI, United States.; Center for Translational Neuroscience, Robert J. and Nancy D. Carney Institute for Brain Science and Brown Institute for Translational Science, Brown University, Providence, RI, United States.; Department of Neurology, Warren Alpert Medical School of Brown University, Providence, RI, United States.
المصدر: Frontiers in cell and developmental biology [Front Cell Dev Biol] 2022 Mar 16; Vol. 10, pp. 838612. Date of Electronic Publication: 2022 Mar 16 (Print Publication: 2022).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Frontiers Media S.A Country of Publication: Switzerland NLM ID: 101630250 Publication Model: eCollection Cited Medium: Print ISSN: 2296-634X (Print) Linking ISSN: 2296634X NLM ISO Abbreviation: Front Cell Dev Biol Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: Lausanne : Frontiers Media S.A., [2013]-
مستخلص: Lynx1 is a glycosylphosphatidylinositol (GPI)-linked protein shown to affect synaptic plasticity through modulation of nicotinic acetylcholine receptor (nAChR) subtypes in the brain. Because of this function and structural similarity to α-bungarotoxin, which binds muscle-specific nAChRs with high affinity, Lynx1 is a promising candidate for modulating nAChRs in skeletal muscles. However, little is known about the expression and roles of Lynx1 in skeletal muscles and neuromuscular junctions (NMJs). Here, we show that Lynx1 is expressed in skeletal muscles, increases during development, and concentrates at NMJs. We also demonstrate that Lynx1 interacts with muscle-specific nAChR subunits. Additionally, we present data indicating that Lynx1 deletion alters the response of skeletal muscles to cholinergic transmission and their contractile properties. Based on these findings, we asked if Lynx1 deletion affects developing and adult NMJs. Loss of Lynx1 had no effect on NMJs at postnatal day 9 (P9) and moderately increased their size at P21. Thus, Lynx1 plays a minor role in the structural development of NMJs. In 7- and 12-month-old mice lacking Lynx1, there is a marked increase in the incidence of NMJs with age- and disease-associated morphological alterations. The loss of Lynx1 also reduced the size of adult muscle fibers. Despite these effects, Lynx1 deletion did not alter the rate of NMJ reinnervation and stability following motor axon injury. These findings suggest that Lynx1 is not required during fast remodeling of the NMJ, as is the case during reformation following crushing of motor axons and development. Instead, these data indicate that the primary role of Lynx1 may be to maintain the structure and function of adult and aging NMJs.
Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
(Copyright © 2022 Doss, Barbat-Artigas, Lopes, Pradhan, Prószyński, Robitaille and Valdez.)
References: Neuron. 1999 May;23(1):105-14. (PMID: 10402197)
Int J Dev Neurosci. 1990;8(6):629-42. (PMID: 2288241)
Biochem Soc Trans. 2020 Jun 30;48(3):1129-1138. (PMID: 32573677)
Nat Neurosci. 2018 Feb;21(2):218-227. (PMID: 29358666)
Proc Natl Acad Sci U S A. 2005 Aug 2;102(31):11088-93. (PMID: 16043708)
Neuron. 2006 Sep 7;51(5):587-600. (PMID: 16950157)
J Neurosci. 1990 Mar;10(3):894-908. (PMID: 2156964)
J Neurosci. 2016 Sep 7;36(36):9472-8. (PMID: 27605620)
Development. 2015 Dec 1;142(23):4038-48. (PMID: 26483211)
Pharmacol Ther. 2005 Jan;105(1):69-84. (PMID: 15626456)
J Biol Chem. 2011 Mar 25;286(12):10618-27. (PMID: 21252236)
Development. 2007 Dec;134(23):4167-76. (PMID: 17959719)
Neuron. 2000 Oct;28(1):41-51. (PMID: 11086982)
Nat Rev Neurosci. 2014 Nov;15(11):703-18. (PMID: 25493308)
J Immunol. 1993 Jun 15;150(12):5379-90. (PMID: 8515066)
Cell. 1993 Jan;72 Suppl:99-121. (PMID: 8428377)
J Cell Biol. 2004 Mar 29;164(7):1077-87. (PMID: 15037598)
Auton Neurosci. 2002 Mar 18;96(2):113-8. (PMID: 11958476)
Front Psychiatry. 2013 Nov 11;4:146. (PMID: 24273519)
Science. 2010 Nov 26;330(6008):1238-40. (PMID: 21071629)
J Biol Chem. 2014 Nov 7;289(45):31423-32. (PMID: 25193667)
Annu Rev Neurosci. 1999;22:389-442. (PMID: 10202544)
PLoS One. 2012;7(11):e43302. (PMID: 23139735)
Front Physiol. 2013 Dec 12;4:363. (PMID: 24376424)
Neuron. 2002 Nov 14;36(4):635-48. (PMID: 12441053)
J Cell Biol. 1995 Feb;128(4):563-76. (PMID: 7532173)
J Neurochem. 2020 Oct;155(1):45-61. (PMID: 32222974)
Elife. 2016 Sep 19;5:. (PMID: 27644106)
J Neurosci. 2017 Jan 4;37(1):70-82. (PMID: 28053031)
J Cell Sci. 2016 Mar 1;129(5):898-911. (PMID: 26769899)
Neuron. 2002 Mar 14;33(6):893-903. (PMID: 11906696)
Brain Res. 1985 Feb 25;328(1):170-5. (PMID: 3871653)
PLoS One. 2017 Dec 5;12(12):e0188715. (PMID: 29206881)
Biochem J. 2013 Mar 1;450(2):265-74. (PMID: 23410039)
Br J Pharmacol. 1996 Apr;117(8):1785-91. (PMID: 8732292)
Exp Neurol. 2010 Sep;225(1):183-95. (PMID: 20599977)
PLoS One. 2018 Jul 3;13(7):e0199643. (PMID: 29969495)
J Biol Chem. 2013 May 31;288(22):15888-99. (PMID: 23585571)
J Physiol. 1968 Dec;199(3):729-41. (PMID: 4303919)
J Vis Exp. 2016 Aug 11;(114):. (PMID: 27585036)
J Biol Chem. 2015 Sep 11;290(37):22370-84. (PMID: 26198629)
J Mol Neurosci. 2014 Jul;53(3):525-36. (PMID: 25027556)
Nat Neurosci. 2007 Aug;10(8):953-62. (PMID: 17643119)
Neuron. 2006 Sep 7;51(5):601-12. (PMID: 16950158)
Proc Natl Acad Sci U S A. 2010 Aug 17;107(33):14863-8. (PMID: 20679195)
FASEB J. 2017 Apr;31(4):1398-1420. (PMID: 28100642)
Neurobiol Aging. 2016 Oct;46:13-21. (PMID: 27460145)
فهرسة مساهمة: Keywords: Lynx1; acetylcholine receptor; aging; cholinergic transmission; neuromuscular junction; skeletal muscle; synaptic plasticity
تواريخ الأحداث: Date Created: 20220404 Latest Revision: 20220405
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC8967655
DOI: 10.3389/fcell.2022.838612
PMID: 35372356
قاعدة البيانات: MEDLINE
الوصف
تدمد:2296-634X
DOI:10.3389/fcell.2022.838612