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  1. Article ; Online: Cellular Sources and Neuroprotective Roles of Interleukin-10 in the Facial Motor Nucleus after Axotomy.

    Runge, Elizabeth M / Setter, Deborah O / Iyer, Abhirami K / Regele, Eric J / Kennedy, Felicia M / Sanders, Virginia M / Jones, Kathryn J

    Cells

    2022  Volume 11, Issue 19

    Abstract: Facial motoneuron (FMN) survival is mediated by CD4+ T cells in an interleukin-10 (IL-10)-dependent manner after facial nerve axotomy (FNA), but CD4+ T cells themselves are not the source of this neuroprotective IL-10. The aims of this study were to (1) ... ...

    Abstract Facial motoneuron (FMN) survival is mediated by CD4+ T cells in an interleukin-10 (IL-10)-dependent manner after facial nerve axotomy (FNA), but CD4+ T cells themselves are not the source of this neuroprotective IL-10. The aims of this study were to (1) identify the temporal and cell-specific induction of IL-10 expression in the facial motor nucleus and (2) elucidate the neuroprotective capacity of this expression after axotomy. Immunohistochemistry revealed that FMN constitutively produced IL-10, whereas astrocytes were induced to make IL-10 after FNA.
    MeSH term(s) Animals ; Axotomy ; Facial Nerve Injuries/genetics ; Facial Nerve Injuries/metabolism ; Facial Nucleus/metabolism ; Flavin Mononucleotide/metabolism ; Interleukin-10/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Motor Neurons/metabolism ; Neuroprotection ; RNA, Messenger/metabolism
    Chemical Substances RNA, Messenger ; Interleukin-10 (130068-27-8) ; Flavin Mononucleotide (7N464URE7E)
    Language English
    Publishing date 2022-10-09
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells11193167
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: CD4+ T cell expression of the IL-10 receptor is necessary for facial motoneuron survival after axotomy.

    Runge, Elizabeth M / Iyer, Abhirami K / Setter, Deborah O / Kennedy, Felicia M / Sanders, Virginia M / Jones, Kathryn J

    Journal of neuroinflammation

    2020  Volume 17, Issue 1, Page(s) 121

    Abstract: Background: After peripheral nerve transection, facial motoneuron (FMN) survival depends on an intact CD4+ T cell population and a central source of interleukin-10 (IL-10). However, it has not been determined previously whether CD4+ T cells participate ... ...

    Abstract Background: After peripheral nerve transection, facial motoneuron (FMN) survival depends on an intact CD4+ T cell population and a central source of interleukin-10 (IL-10). However, it has not been determined previously whether CD4+ T cells participate in the central neuroprotective IL-10 cascade after facial nerve axotomy (FNA).
    Methods: Immunohistochemical labeling of CD4+ T cells, pontine vasculature, and central microglia was used to determine whether CD4+ T cells cross the blood-brain barrier and enter the facial motor nucleus (FMNuc) after FNA. The importance of IL-10 signaling in CD4+ T cells was assessed by performing adoptive transfer of IL-10 receptor beta (IL-10RB)-deficient CD4+ T cells into immunodeficient mice prior to injury. Histology and qPCR were utilized to determine the impact of IL-10RB-deficient T cells on FMN survival and central gene expression after FNA. Flow cytometry was used to determine whether IL-10 signaling in T cells was necessary for their differentiation into neuroprotective subsets.
    Results: CD4+ T cells were capable of crossing the blood-brain barrier and associating with reactive microglial nodules in the axotomized FMNuc. Full induction of central IL-10R gene expression after FNA was dependent on CD4+ T cells, regardless of their own IL-10R signaling capability. Surprisingly, CD4+ T cells lacking IL-10RB were incapable of mediating neuroprotection after axotomy and promoted increased central expression of genes associated with microglial activation, antigen presentation, T cell co-stimulation, and complement deposition. There was reduced differentiation of IL-10RB-deficient CD4+ T cells into regulatory CD4+ T cells in vitro.
    Conclusions: These findings support the interdependence of IL-10- and CD4+ T cell-mediated mechanisms of neuroprotection after axotomy. CD4+ T cells may potentiate central responsiveness to IL-10, while IL-10 signaling within CD4+ T cells is necessary for their ability to rescue axotomized motoneuron survival. We propose that loss of IL-10 signaling in CD4+ T cells promotes non-neuroprotective autoimmunity after FNA.
    MeSH term(s) Animals ; Axotomy/methods ; CD4-Positive T-Lymphocytes/metabolism ; Cell Survival/physiology ; Cells, Cultured ; Facial Nerve/metabolism ; Facial Nerve Injuries/genetics ; Facial Nerve Injuries/metabolism ; Female ; Gene Expression ; Mice ; Mice, 129 Strain ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Motor Neurons/metabolism ; Receptors, Interleukin-10/biosynthesis ; Receptors, Interleukin-10/genetics
    Chemical Substances Receptors, Interleukin-10
    Language English
    Publishing date 2020-04-17
    Publishing country England
    Document type Journal Article
    ISSN 1742-2094
    ISSN (online) 1742-2094
    DOI 10.1186/s12974-020-01772-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Facial nerve repair utilizing intraoperative repair strategies.

    Brown, Brandon L / Sandelski, Morgan M / Drejet, Sarah M / Runge, Elizabeth M / Shipchandler, Taha Z / Jones, Kathryn J / Walker, Chandler L

    Laryngoscope investigative otolaryngology

    2020  Volume 5, Issue 3, Page(s) 552–559

    Abstract: Objectives: To determine whether functional and anatomical outcomes following suture neurorrhaphy are improved by the addition of electrical stimulation with or without the addition of polyethylene glycol (PEG).: Methods: In a rat model of facial ... ...

    Abstract Objectives: To determine whether functional and anatomical outcomes following suture neurorrhaphy are improved by the addition of electrical stimulation with or without the addition of polyethylene glycol (PEG).
    Methods: In a rat model of facial nerve injury, complete facial nerve transection and repair was performed via (a) suture neurorrhaphy alone, (b) neurorrhaphy with the addition of brief (30 minutes) intraoperative electrical stimulation, or (c) neurorrhaphy with the addition electrical stimulation and PEG. Functional recovery was assessed weekly for 16 weeks. At 16 weeks postoperatively, motoneuron survival, amount of regrowth, and specificity of regrowth were assessed by branch labeling and tissue analysis.
    Results: The addition of brief intraoperative electrical stimulation improved all functional outcomes compared to suturing alone. The addition of PEG to electrical stimulation impaired this benefit. Motoneuron survival, amount of regrowth, and specificity of regrowth were unaltered at 16 weeks postoperative in all treatment groups.
    Conclusion: The addition of brief intraoperative electrical stimulation to neurorrhaphy in this rodent model shows promising neurological benefit in the surgical repair of facial nerve injury.
    Level of evidence: Animal study.
    Language English
    Publishing date 2020-05-28
    Publishing country United States
    Document type Journal Article
    ISSN 2378-8038
    ISSN 2378-8038
    DOI 10.1002/lio2.411
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Functional and Anatomical Outcomes of Facial Nerve Injury With Application of Polyethylene Glycol in a Rat Model.

    Brown, Brandon L / Asante, Tony / Welch, Haley R / Sandelski, Morgan M / Drejet, Sarah M / Shah, Kishan / Runge, Elizabeth M / Shipchandler, Taha Z / Jones, Kathryn J / Walker, Chandler L

    JAMA facial plastic surgery

    2018  Volume 21, Issue 1, Page(s) 61–68

    Abstract: Importance: Functional and anatomical outcomes after surgical repair of facial nerve injury may be improved with the addition of polyethylene glycol (PEG) to direct suture neurorrhaphy. The application of PEG has shown promise in treating spinal nerve ... ...

    Abstract Importance: Functional and anatomical outcomes after surgical repair of facial nerve injury may be improved with the addition of polyethylene glycol (PEG) to direct suture neurorrhaphy. The application of PEG has shown promise in treating spinal nerve injuries, but its efficacy has not been evaluated in treatment of cranial nerve injuries.
    Objective: To determine whether PEG in addition to neurorrhaphy can improve functional outcomes and synkinesis after facial nerve injury.
    Design, setting, and subjects: In this animal experiment, 36 rats underwent right facial nerve transection and neurorrhaphy with addition of PEG. Weekly behavioral scoring was done for 10 rats for 6 weeks and 14 rats for 16 weeks after the operations. In the 16-week study, the buccal branches were labeled and tissue analysis was performed. In the 6-week study, the mandibular and buccal branches were labeled and tissue analysis was performed. Histologic analysis was performed for 10 rats in a 1-week study to assess the association of PEG with axonal continuity and Wallerian degeneration. Six rats served as the uninjured control group. Data were collected from February 8, 2016, through July 10, 2017.
    Intervention: Polyethylene glycol applied to the facial nerve after neurorrhaphy.
    Main outcomes and measures: Functional recovery was assessed weekly for the 16- and 6-week studies, as well as motoneuron survival, amount of regrowth, specificity of regrowth, and aberrant branching. Short-term effects of PEG were assessed in the 1-week study.
    Results: Among the 40 male rats included in the study, PEG addition to neurorrhaphy showed no functional benefit in eye blink reflex (mean [SEM], 3.57 [0.88] weeks; 95% CI, -2.8 to 1.9 weeks; P = .70) or whisking function (mean [SEM], 4.00 [0.72] weeks; 95% CI, -3.6 to 2.4 weeks; P = .69) compared with suturing alone at 16 weeks. Motoneuron survival was not changed by PEG in the 16-week (mean, 132.1 motoneurons per tissue section; 95% CI, -21.0 to 8.4; P = .13) or 6-week (mean, 131.1 motoneurons per tissue section; 95% CI, -11.0 to 10.0; P = .06) studies. Compared with controls, neither surgical group showed differences in buccal branch regrowth at 16 (36.9 motoneurons per tissue section; 95% CI, -14.5 to 22.0; P = .28) or 6 (36.7 motoneurons per tissue section; 95% CI, -7.8 to 18.5; P = .48) weeks or in the mandibular branch at 6 weeks (25.2 motoneurons per tissue section; 95% CI, -14.5 to 15.5; P = .99). Addition of PEG had no advantage in regrowth specificity compared with suturing alone at 16 weeks (15.3% buccal branch motoneurons with misguided projections; 95% CI, -7.2% to 11.0%; P = .84). After 6 weeks, the number of motoneurons with misguided projections to the mandibular branch showed no advantage of PEG treatment compared with suturing alone (12.1% buccal branch motoneurons with misguided projections; 95% CI, -8.2% to 9.2%; P = .98). In the 1-week study, improved axonal continuity and muscular innervation were not observed in PEG-treated rats.
    Conclusions and relevance: Although PEG has shown efficacy in treating other nervous system injuries, PEG in addition to neurorraphy was not beneficial in a rat model of facial nerve injury. The addition of PEG to suturing may not be warranted in the surgical repair of facial nerve injury.
    Level of evidence: NA.
    MeSH term(s) Animals ; Disease Models, Animal ; Facial Nerve Injuries/drug therapy ; Facial Nerve Injuries/surgery ; Male ; Neurosurgical Procedures ; Polyethylene Glycols/administration & dosage ; Rats ; Rats, Wistar ; Recovery of Function ; Suture Techniques
    Chemical Substances Polyethylene Glycols (3WJQ0SDW1A)
    Language English
    Publishing date 2018-05-23
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2702062-9
    ISSN 2168-6092 ; 2168-6076
    ISSN (online) 2168-6092
    ISSN 2168-6076
    DOI 10.1001/jamafacial.2018.0308
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    Zs.A 5869: Show issues Location:
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  5. Article ; Online: Neurotrophin-4 is more potent than brain-derived neurotrophic factor in promoting, attracting and suppressing geniculate ganglion neurite outgrowth.

    Runge, Elizabeth M / Hoshino, Natalia / Biehl, Matthew J / Ton, Son / Rochlin, M William

    Developmental neuroscience

    2012  Volume 34, Issue 5, Page(s) 389–401

    Abstract: The geniculate ganglion, which provides innervation to taste buds in the anterior tongue and palate, is unique among sensory ganglia in that its neurons depend on both neurotrophin-4 (NT4) and brain-derived neurotrophic factor (BDNF) for survival. ... ...

    Abstract The geniculate ganglion, which provides innervation to taste buds in the anterior tongue and palate, is unique among sensory ganglia in that its neurons depend on both neurotrophin-4 (NT4) and brain-derived neurotrophic factor (BDNF) for survival. Whereas BDNF is additionally implicated in taste axon guidance at targeting stages, much less is known about the guidance role of NT4 during targeting, or about either neurotrophin during initial pathfinding. NT4 and BDNF have distinct expression patterns in vivo, raising the possibility of distinct roles. We characterized the influence of NT4 and BDNF on geniculate neurites in collagen I gels at early embryonic through postnatal stages. During early pathfinding to the tongue (embryonic days 12-13; E12-13), NT4 and BDNF promote significantly longer outgrowth than during intralingual targeting (E15-18). NT4 is more potent than BDNF at stimulating neurite outgrowth and both factors exhibit concentration optima, i.e. intermediate concentrations (0.25 ng/ml NT4 or 25 ng/ml BDNF) promote maximal neurite extension and high concentrations (10 ng/ml NT4 or 200 ng/ml BDNF) suppress it. Only partial suppression was seen at E12 (when axons first emerge from the ganglion in vivo) and postnatally, but nearly complete suppression occurred from E13 to E18. We show that cell death is not responsible for suppression. Although blocking the p75 receptor reduces outgrowth at the optimum concentrations of NT4 and BDNF, it did not reduce suppression of outgrowth. We also report that NT4, like BDNF, can act as a chemoattractant for geniculate neurites, and that the tropic influence is strongest during intralingual targeting (E15-18). NT4 does not appear to act as an attractant in vivo, but it may prevent premature invasion of the epithelium by suppressing axon growth.
    MeSH term(s) Animals ; Axons/metabolism ; Brain-Derived Neurotrophic Factor/pharmacology ; Dose-Response Relationship, Drug ; Female ; Geniculate Ganglion/cytology ; Geniculate Ganglion/drug effects ; Geniculate Ganglion/growth & development ; Nerve Growth Factors/pharmacology ; Neurites/drug effects ; Pregnancy ; Rats ; Receptor, Nerve Growth Factor/biosynthesis ; Receptor, Nerve Growth Factor/genetics ; Tongue/embryology ; Tongue/metabolism
    Chemical Substances Brain-Derived Neurotrophic Factor ; Nerve Growth Factors ; Receptor, Nerve Growth Factor ; neurotrophin 4 (P658DCA9XD)
    Language English
    Publishing date 2012-11-09
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 556887-0
    ISSN 1421-9859 ; 0378-5866
    ISSN (online) 1421-9859
    ISSN 0378-5866
    DOI 10.1159/000342996
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Neurotrophin-4 Is More Potent than Brain-Derived Neurotrophic Factor in Promoting, Attracting and Suppressing Geniculate Ganglion Neurite Outgrowth

    Runge, Elizabeth M. / Hoshino, Natalia / Biehl, Matthew J. / Ton, Son / Rochlin, M. William

    Developmental Neuroscience

    2012  Volume 34, Issue 5, Page(s) 389–401

    Abstract: The geniculate ganglion, which provides innervation to taste buds in the anterior tongue and palate, is unique among sensory ganglia in that its neurons depend on both neurotrophin-4 (NT4) and brain-derived neurotrophic factor (BDNF) for survival. ... ...

    Institution Biology Department, Loyola University Chicago, Chicago, Ill., USA
    Abstract The geniculate ganglion, which provides innervation to taste buds in the anterior tongue and palate, is unique among sensory ganglia in that its neurons depend on both neurotrophin-4 (NT4) and brain-derived neurotrophic factor (BDNF) for survival. Whereas BDNF is additionally implicated in taste axon guidance at targeting stages, much less is known about the guidance role of NT4 during targeting, or about either neurotrophin during initial pathfinding. NT4 and BDNF have distinct expression patterns in vivo, raising the possibility of distinct roles. We characterized the influence of NT4 and BDNF on geniculate neurites in collagen I gels at early embryonic through postnatal stages. During early pathfinding to the tongue (embryonic days 12–13; E12–13), NT4 and BDNF promote significantly longer outgrowth than during intralingual targeting (E15–18). NT4 is more potent than BDNF at stimulating neurite outgrowth and both factors exhibit concentration optima, i.e. intermediate concentrations (0.25 ng/ml NT4 or 25 ng/ml BDNF) promote maximal neurite extension and high concentrations (10 ng/ml NT4 or 200 ng/ml BDNF) suppress it. Only partial suppression was seen at E12 (when axons first emerge from the ganglion in vivo) and postnatally, but nearly complete suppression occurred from E13 to E18. We show that cell death is not responsible for suppression. Although blocking the p75 receptor reduces outgrowth at the optimum concentrations of NT4 and BDNF, it did not reduce suppression of outgrowth. We also report that NT4, like BDNF, can act as a chemoattractant for geniculate neurites, and that the tropic influence is strongest during intralingual targeting (E15–18). NT4 does not appear to act as an attractant in vivo, but it may prevent premature invasion of the epithelium by suppressing axon growth.
    Keywords Axon ; Guidance ; Neurotrophin ; Epithelium ; Taste ; Development ; p75
    Language English
    Publishing date 2012-11-09
    Publisher S. Karger AG
    Publishing place Basel, Switzerland
    Document type Article
    Note Original Paper
    ZDB-ID 556887-0
    ISSN 1421-9859 ; 0378-5866
    ISSN (online) 1421-9859
    ISSN 0378-5866
    DOI 10.1159/000342996
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