Journal of neurodegeneration & regeneration最新文献

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Delayed functional recovery in presymptomatic mSOD1^G93A mice following facial nerve crush axotomy. 面神经压迫性轴切术后症状前mSOD1G93A小鼠功能恢复延迟。

Journal of neurodegeneration & regeneration Pub Date : 2013-01-01

Nichole A Mesnard, Melissa M Haulcomb, Lisa Tanzer, Virginia M Sanders, Kathryn J Jones

{"title":"Delayed functional recovery in presymptomatic mSOD1G93A mice following facial nerve crush axotomy.","authors":"Nichole A Mesnard, Melissa M Haulcomb, Lisa Tanzer, Virginia M Sanders, Kathryn J Jones","doi":"","DOIUrl":"","url":null,"abstract":"Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease involving progressive loss of motoneurons (MN). Axonal pathology and presynaptic deaf-ferentation precede MN degeneration during disease progression in patients and the ALS mouse model (mSOD1). Previously, we determined that a functional adaptive immune response is required for complete functional recovery following a facial nerve crush axotomy in wild-type (WT) mice. In this study, we investigated the effects of facial nerve crush axotomy on functional recovery and facial MN survival in presymptomatic mSOD1 mice, relative to WT mice. The results indicate that functional recovery and facial MN survival levels are significantly reduced in presymptomatic mSOD1, relative to WT, and similar to what has previously been observed in immunodeficient mice. It is concluded that a potential immune system defect exists in the mSOD1 mouse that negatively impacts neuronal survival and regeneration following target disconnection associated with peripheral nerve axotomy.","PeriodicalId":88918,"journal":{"name":"Journal of neurodegeneration & regeneration","volume":"4 1","pages":"21-25"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3963697/pdf/nihms561617.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32211883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Effects of facial nerve axotomy on Th2-associated and Th1-associated chemokine mRNA expression in the facial motor nucleus of wild-type and presymptomatic SOD1 mice. 面神经切断术对野生型和症状前SOD1小鼠面肌运动核中th2相关和th1相关趋化因子mRNA表达的影响

Journal of neurodegeneration & regeneration Pub Date : 2009-09-01

Derek A Wainwright, Nichole A Mesnard, Junping Xin, Virginia M Sanders, Kathryn J Jones

{"title":"Effects of facial nerve axotomy on Th2-associated and Th1-associated chemokine mRNA expression in the facial motor nucleus of wild-type and presymptomatic SOD1 mice.","authors":"Derek A Wainwright, Nichole A Mesnard, Junping Xin, Virginia M Sanders, Kathryn J Jones","doi":"","DOIUrl":"","url":null,"abstract":"The authors have previously demonstrated a neuroprotective mechanism of facial motoneuron (FMN) survival after facial nerve transection that is dependent on CD4(+)T helper 2 (Th2) cell interactions with peripheral antigen presenting cells, as well as central nervous system (CNS) resident microglia. Pituitary adenylyl cyclase activating polypeptide is expressed by injured FMN and increases Th2-associated chemokine expression in cultured murine microglia. Collectively, these data suggest a model involving CD4(+) Th2 cell migration to the facial motor nucleus after injury via microglial expression of Th2-associated chemokines. In this study, the authors tested the hypothesis that Th2-associated chemokine expression occurs in the facial motor nucleus after facial nerve axotomy at the stylomastoid foramen. Initial microarray analysis of Th2-associated and Th1-associated chemokine mRNA levels was accomplished after facial nerve axotomy in wild type (WT) and presymptomatic mutant superoxide dismutase 1 (mSOD1) [model of familial amyotrophic lateral sclerosis (ALS)] mice. Based on that initial microarray analysis, the Th2-associated chemokine, CCL11, and Th1-associated chemokine, CXCL11, were further analyzed by RT-PCR. The results indicate that facial nerve injury predominantly increases Th2-associated chemokine, but not Th1-associated chemokine mRNA levels in the mouse facial motor nucleus. Interestingly, no differences were detected between WT and mSOD1 mice for CCL11 and CXCL11 after injury. These data provide a basis for further investigation into Th2-associated chemokine expression in the facial motor nucleus after FMN injury, which may lead to more specifically targeted therapeutics in motoneuron diseases, such as ALS.","PeriodicalId":88918,"journal":{"name":"Journal of neurodegeneration & regeneration","volume":"2 1","pages":"39-44"},"PeriodicalIF":0.0,"publicationDate":"2009-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2861580/pdf/nihms-164649.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28961045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Differential actions of pituitary adenylyl cyclase-activating polypeptide and interferon gamma on Th2- and Th1-associated chemokine expression in cultured murine microglia. 垂体腺苷酸环化酶激活多肽和干扰素γ对培养小鼠小胶质细胞中Th2-和th1相关趋化因子表达的差异作用。

Journal of neurodegeneration & regeneration Pub Date : 2008-10-01

Derek A Wainwright, Junping Xin, Virginia M Sanders, Kathryn J Jones

{"title":"Differential actions of pituitary adenylyl cyclase-activating polypeptide and interferon gamma on Th2- and Th1-associated chemokine expression in cultured murine microglia.","authors":"Derek A Wainwright, Junping Xin, Virginia M Sanders, Kathryn J Jones","doi":"","DOIUrl":"","url":null,"abstract":"Microglia are the immune cells that reside in the central nervous system (CNS). Following the facial nerve injury in the mouse, microglia are activated in the facial motor nucleus, coincident with an increase in the proinflammatory cytokine interferon-gamma (IFN-γ). The authors have previously shown that maximal facial motoneuron (FMN) survival after injury depends on the CD4(+)T-cell interaction with microglia. Furthermore, it appears that the anti-inflammatory T helper (Th) 2 CD4(+) T-cell subset is required in the facial nucleus, although the mechanism of CNS recruitment is not known. Pituitary adenylyl cyclase-activating polypeptide (PACAP) is a neuropeptide that has previously been demonstrated to be expressed by injured FMN. Interestingly, PACAP has been shown to act on peripheral macrophages by inducing chemokine expression capable of recruiting Th2 cells. Whether CNS-resident microglia, a related lineage to peripheral macrophages, respond to PACAP by expressing Th2-associated chemokines is not known. In this study, fluorescence-activated cell sorting was utilized to measure the frequency of microglia positive for different chemokines after exposure to various treatments. The results indicate that PACAP increases the frequency of microglia expressing Th2-associated chemokine, CCL11, and decreases the frequency of microglia expressing Th1-associated chemokine, CXCL11. In contrast, IFN-γ decreases the frequency of microglia expressing Th2-associated chemokine, CCL11, and increases the frequency of microglia expressing Th1-associated chemokine, CXCL11. Treatment with both PACAP and IFN-γ reversed the proinflammatory effect of IFN-γ. Given the recent focus on the therapeutic value of Th2 cells in the CNS during neurode-generative disease, PACAP may be a future therapeutic target for improving neuroregeneration after injury.","PeriodicalId":88918,"journal":{"name":"Journal of neurodegeneration & regeneration","volume":"1 1","pages":"31-34"},"PeriodicalIF":0.0,"publicationDate":"2008-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2864491/pdf/nihms157973.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28970889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0