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Lithium Enhances Remyelination of Peripheral Nerves

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Lithium Enhances Remyelination of Peripheral Nerves Lithium enhances remyelination of peripheral nerves Joelle Makoukjia,1, Martin Bellea,1, Delphine Meffrea, Ruth Stassartb, Julien Greniera, Ghjuvan’Ghjacumu Shackleforda, Robert Fledrichb, Cosima Fontec, Julien Branchua, Marie Goularda, Catherine de Waelea, Frédéric Charbonniera, Michael W. Seredab,d, Etienne-Emile Baulieuc,2, Michael Schumacherc, Sophie Bernarda, and Charbel Massaada,2 aUnité Mixte de Recherche 8194, Centre National de la Recherche Scientifique, Centre d’Etude de la Sensori Motricité, University Paris Descartes, 75270 Paris Cedex 06, France; bDepartment of Neurogenetics, Max Planck Institute of Experimental Medicine, 37075 Goettingen, Germany; cUnité Mixte de Recherche 788, Institut National de la Santé et de la Recherche Médicale, Institut Fédératif de Recherche de Bicêtre 93, University Paris-Sud 11, 94276 Le Kremlin-Bicêtre Cedex, France; and dDepartment of Clinical Neurophysiology, University of Goettingen, 37075 Goettingen, Germany Contributed by Etienne-Emile Baulieu, December 27, 2011 (sent for review November 24, 2011) Glycogen synthase kinase 3β (GSK3β) inhibitors, especially the In this study, we report several lines of evidence that the mood stabilizer lithium chloride, are also used as neuroprotective inhibitors of GSK3β (LiCl and SB216763) enhance peripheral or anti-inflammatory agents. We studied the influence of LiCl on myelin gene expression in vitro and in vivo via the binding of the remyelination of peripheral nerves. We showed that the treat- β-catenin to TCF/LEF transcription factors present in PMP22 ment of adult mice with LiCl after facial nerve crush injury stimu- and MPZ promoters. Most strikingly, LiCl administration to lated the expression of myelin genes, restored the myelin structure, mice after a crush of the facial nerve, which provokes paralysis of and accelerated the recovery of whisker movements. LiCl treat- the whiskers, elicited a rapid recovery of their movements. This ment also promoted remyelination of the sciatic nerve after crush. recovery is concomitant with the stimulation of myelin gene ex- We also demonstrated that peripheral myelin gene MPZ and PMP22 pression and the restoration of the myelin sheath structure promoter activities, transcripts, and protein levels are stimulated around the axons. LiCl also provoked the remyelination of axons by GSK3β inhibitors (LiCl and SB216763) in Schwann cells as well as after sciatic nerve crush. Consequently, our findings open per- in sciatic and facial nerves. LiCl exerts its action in Schwann cells by spectives in the treatment of demyelinating diseases by admin- increasing the amount of β-catenin and provoking its nuclear local- istering GSK3β inhibitors such as lithium. ization. We showed by ChIP experiments that LiCl treatment drives β-catenin to bind to T-cell factor/lymphoid-enhancer factor re- Results sponse elements identified in myelin genes. Taken together, our LiCl Administration Accelerates Functional Recovery and Ameliorates NEUROSCIENCE findings open perspectives in the treatment of nerve demyelin- Phenotype of Facial Nerve After Nerve Injury. Our aim is to assess ation by administering GSK3β inhibitors such as lithium. the outcome of the administration of LiCl, a widely used inhibitor of GSK3β (IC50, 10 mM), after motor nerve injury. Therefore, we Wnt/β-catenin | neuropathy developed in mice a model of facial nerve crush that provokes a local demyelination and complete subsequent palsy of the ipsi- yelin is essential for the rapid conduction of axonal lateral (crushed) whiskers, as well as absence of ipsilateral blink fl impulses. Myelination, elicited in peripheral nerves by re ex. The left facial nerve was crushed whereas the right one was M A Schwann cells, is a complex and fine-tuned process. Peripheral left intact to serve as a control (Fig. 1 ). We then analyzed by myelin gene expression [Myelin Protein Zero (MPZ) and Pe- means of WhiskerWatcher device the angular velocity of the ip- ripheral Myelin Protein 22 (PMP22)] is tightly regulated (1). silateral whisker movements before and after the crush at different Myelin gene expression is stimulated during the myelination postlesion time points [day postinjury 3 (DPI3), DPI8, and DPI14] process, which occurs in rodents between postnatal days 1 and 21 in two groups of animals: a group treated with LiCl (i.p. injection, (2). Afterward, those genes are expressed at lower levels, suffi- 50 mg/kg/d during 4 d after nerve crush) and a group treated with A cient to maintain myelin turnover. They are restimulated after PBS solution (i.e., placebo) during a similar period (Fig. 1 ). nerve injuries to initiate remyelination (3). The mean angular velocity of the whiskers was 56.44°/s in Peripheral nerve injuries are frequent, and the functional out- normal animals, and it decreased to 0.2°/s at DPI3 in nerve- comes are often not satisfactory. Demyelination can occur as a crushed animals, indicating a dramatic alteration of whisker B result of neuronal or Schwann cell injury and is usually accom- movements after facial nerve injury (Fig. 1 ). The placebo-trea- panied or followed by axonal degeneration. Acquired neuropa- ted animals recovered slowly: at DPI8, the velocity was 7.96°/s, thies may be caused by aberrant immune responses, local injury, and at 14 d, the whisker movements were still below normal levels ischemia, metabolic disorders, toxic agents, or viral infections. To (44.99°/s vs. 56.44°/s for normal animals). Interestingly, the i.p. date, few therapeutic treatments are available. They are mostly LiCl administration after the facial nerve crush accelerated the fl functional recovery during the first 8 d after lesion creation. The based on anti-in ammatory agents. fi Few cellular signals are known to directly regulate the expres- angular velocity was signi cantly improved after 3 d of treatment sion of myelin genes. For instance, we have shown that the Wnt/ with LiCl: 3.48°/s with LiCl vs. 0.2°/s with placebo. At 8 d, we also β-catenin signaling pathway is a direct driver of myelin gene ex- observed an improvement in the movements of the whiskers, pression (4). Wnt activation inhibits glycogen synthase kinase 3β which became almost normal (43.08°/s with LiCl vs. 7.96°/s with (GSK3β) enzyme and prevents β-catenin degradation. The stabi- placebo). At 14 d, we can consider that the animal recovered lized β-catenin is translocated into the nucleus, where it regulates gene transcription by interacting with transcription factors called T-cell factor/lymphoid-enhancer factors (TCF/LEF or TCFs). Author contributions: R.S., C.d.W., F.C., M.W.S., S.B., and C.M. designed research; J.M., β M.B., D.M., R.S., J.G., G.S., R.F., C.F., J.B., M.G., C.d.W., and S.B. performed research; J.M., Lithium is an enzymatic inhibitor of GSK3 ,andmimicstheWnt/ C.d.W., F.C., M.W.S., M.S., S.B., and C.M. analyzed data; and E.-E.B., M.S., and C.M. wrote β-catenin signaling pathway. This drug is widely used as a long-term the paper. mood stabilizer in the treatment of bipolar and depressive disorders The authors declare no conflict of interest. (5). Growing evidence demonstrates that lithium has neuropro- 1J.M. and M.B. contributed equally to this work. tective (6) and antiapoptotic (7) properties, and can therefore be 2To whom correspondence may be addressed. E-mail: [email protected] or charbel. used as a treatment in several neurodegenerative diseases [e.g., [email protected]. ’ Huntington disease (8), Alzheimer s disease (9), Parkinson disease This article contains supporting information online at www.pnas.org/lookup/suppl/doi:10. (10)] and in experimental autoimmune encephalomyelitis (11). 1073/pnas.1121367109/-/DCSupplemental. www.pnas.org/cgi/doi/10.1073/pnas.1121367109 PNAS | March 6, 2012 | vol. 109 | no. 10 | 3973–3978 Downloaded by guest on September 26, 2021 Fig. 1. Effect of LiCl administration on functional recovery of whiskers and phenotype of the facial nerve after nerve crush. (A) Nerve crush of the left facial nerve was performed in 8-wk-old mice. One group received four i.p. injections of LiCl (50 mg/kg/d) directly after the nerve crush during 4 d. The other group received PBS solution injection as a placebo (Pl). Normal animals (control) did not undergo nerve crush. (B) The mean angular velocity of the whisker movements of all animals was analyzed by means of WhiskerWatcher software at DPI3, DPI8, and DPI14. Results are expressed in degrees per second and represent the mean of six animals per group; the angular velocity of the whiskers of each animal was analyzed three times (***P < 0.005, Kruskal–Wallis test). (C) Eight days after the facial nerve crush (DPI8), the facial nerve was isolated. Ultrathin cross-sections were prepared from epon-embedded adult facial nerves and stained for myelin. 1 and 2, Low-magnification EM images of a section of facial nerve. (Scale bar: 2 μM.) 3 and 4, High-magnification EM images of a representative axon. (Scale bar: 1 μM.) 5 and 6, High-magnification EM images of myelin layers. (Scale bar: 100 nm.) (D) Myelin thickness was estimated by g- ratio determination by using EM images obtained from facial nerves (12 images per animal, three animals per condition). Data are means ± SEM. (E)The percentage of myelinated axons per square micrometer was calculated by using EM images. Three animals per condition were used. Data are means ± SEM. (F) Facial nerves were dissected at DPI3. Quantitative RT-PCR experiments were performed by using primers recognizing PMP22 and MPZ genes. 26S and GAPDH RNA were used to normalize quantitative RT-PCR (*P < 0.05 and **P < 0.01 by Mann–Whitney test vs. control). completely because we did not have any significant mean angular mRNA expression of MPZ (threefold) and PMP22 (sixfold; Fig. velocity difference between the normal animals (56.44°/s) and 2B) compared with placebo-treated mice.
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