Induction of neuropeptide gene expression and blockade of retrograde transport in facial motor neurons following local peripheral nerve inflammation in severe combined immunodeficiency and BALB/C mice

Armstrong, Brian; Hu, Zhong‐Ting; Abad, Catalina; Yamamoto, Myrtle; Rodriguez, Williams I.; Cheng, Jerry C.; Lee, M.; Chhith, Seririthanar; Gomariz, Rosa P.; Waschek, James A.

doi:10.1016/j.neuroscience.2004.06.085

Cited by 28 publications

(24 citation statements)

References 33 publications

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“…PACAP mRNA expression has been localized to FMNs following facial nerve axotomy (Armstrong et al, 2003; Mesnard et al, 2010), and this expression requires a functional adaptive immune system (Armstrong et al, 2004a,b, 2006). Furthermore, PACAP is a neuroprotective peptide capable of inhibiting proinflammatory cytokine production, such as TNFα, in vitro (Delgado et al, 2003; Kim et al, 2000); a deficiency of PACAP in vivo results in delayed axonal regeneration of axotomized FMN (Armstrong et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Differential gene expression in the axotomized facial motor nucleus of presymptomatic SOD1 mice

Mesnard

Sanders

Jones

2011

J of Comparative Neurology

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Previously, we compared molecular profiles of one population of wild-type (WT) mouse facial motoneurons (FMNs) surviving with FMNs undergoing significant cell death after axotomy. Regardless of their ultimate fate, injured FMNs respond with a vigorous pro-survival/regenerative molecular response. In contrast, the neuropil surrounding the two different injured FMN populations contained distinct molecular differences that support a causative role for glial and/or immune-derived molecules in directing contrasting responses of the same cell types to the same injury. In the current investigation, we utilized the facial nerve axotomy model and a presymptomatic amyotrophic lateral sclerosis (ALS) mouse (SOD1) model to experimentally mimic the axonal die-back process observed in ALS pathogenesis without the confounding variable of disease onset. Pre-symptomatic SOD1 mice had a significant decrease in FMN survival compared with WT, which suggests an increased susceptibility to axotomy. Laser microdissection was used to accurately collect uninjured and axotomized facial motor nuclei of WT and presymptomatic SOD1 mice for mRNA expression pattern analyses of pro-survival/pro-regeneration genes, neuropil-specific genes, and genes involved in or responsive to the interaction of FMNs and non-neuronal cells. Axotomized pre-symptomatic SOD1 FMNs displayed a dynamic pro-survival/regenerative response to axotomy, similar to WT, despite increased cell death. However, significant differences were revealed when the axotomy-induced gene expression response of presymptomatic SOD1 neuropil was compared with WT. We propose that the increased susceptibility of presymptomatic SOD1 FMNs to axotomy-induced cell death and, by extrapolation, disease progression, is not intrinsic to the motoneuron, but rather involves a dysregulated response by non-neuronal cells in the surrounding neuropil.

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Section: Discussionmentioning

confidence: 99%

Differential gene expression in the axotomized facial motor nucleus of presymptomatic SOD1 mice

Mesnard

Sanders

Jones

2011

J of Comparative Neurology

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“…Axoplasmic transport is slowed during inflammation (Amano et al, 2001; Armstrong et al, 2004), but by unknown factors. In-vitro, CFA nerve inflammation caused a histamine-dependent reduction in axoplasmic flow.…”

Section: Discussionmentioning

confidence: 99%

Long lasting recruitment of immune cells and altered epi-perineurial thickness in focal nerve inflammation induced by complete Freund's adjuvant

Bove

Weissner²,

Barbe

2009

Journal of Neuroimmunology

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Immune-mediated nerve inflammation is involved in many painful states in humans, and causes axonal and behavioral changes in rats. While models of nerve inflammation have been characterized using electrophysiological and behavioral methods, the presence of immune cells has not been fully assessed. We inflamed rat sciatic nerves using complete Freund's adjuvant and quantified the presence of ED-1 macrophages and TCR-αβ T-cells for up to 12 weeks. We report that these immune cells are prominent extraneurally up to 12 weeks following the induction of inflammation. This observation does not easily correlate with inflammation-induced axonal mechanical sensitivity, which peaks within 1 week and is resolved after 8 weeks.

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“…The VIPR1 and VIPR2 genes encode receptors that respond equally to VIP and PACAP named VPAC1 and VPAC2 respectively (Ishihara et al, 1992; Lutz et al, 1993; Sreedharan et al, 1993; Couvineau et al, 1994), whereas the ADCYAP1R gene encodes the PACAP-preferring receptor PAC1 (Hashimoto et al, 1993; Hosoya et al, 1993; Pisegna and Wank, 1993). In mammals, both peptides are widely expressed in the central and peripheral nervous systems (Pozo and Delgado, 2004; Laburthe et al, 2007; Dickson and Finlayson, 2009; Vaudry et al, 2009), are also produced within immune cells where they play the role of a ‘cytokine-like peptide’ (Gomariz et al, 2001; Delgado et al, 2004b), and are induced in both neurons and immune cells during inflammation (Gomariz et al, 1993; Gaytan et al, 1994; Leceta et al, 1996; Zhang et al, 1998; Vassiliou et al, 2001; Abad et al, 2002; Armstrong et al, 2004; Delgado et al, 2004b; Laburthe et al, 2007; Vaudry et al, 2009). Likewise, their receptors are mainly distributed in the nervous, endocrine and immune systems (Delgado et al, 2004b; Laburthe et al, 2007; Vaudry et al, 2009).…”

Section: Vip and Pacap Backgroundmentioning

confidence: 99%

Targeting VIP and PACAP Receptor Signalling: New Therapeutic Strategies in Multiple Sclerosis

Tan

Waschek

2011

ASN Neuro

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MS (multiple sclerosis) is a chronic autoimmune and neurodegenerative pathology of the CNS (central nervous system) affecting approx. 2.5 million people worldwide. Current and emerging DMDs (disease-modifying drugs) predominantly target the immune system. These therapeutic agents slow progression and reduce severity at early stages of MS, but show little activity on the neurodegenerative component of the disease. As the latter determines permanent disability, there is a critical need to pursue alternative modalities. VIP (vasoactive intestinal peptide) and PACAP (pituitary adenylate cyclase-activating peptide) have potent anti-inflammatory and neuroprotective actions, and have shown significant activity in animal inflammatory disease models including the EAE (experimental autoimmune encephalomyelitis) MS model. Thus, their receptors have become candidate targets for inflammatory diseases. Here, we will discuss the immunomodulatory and neuroprotective actions of VIP and PACAP and their signalling pathways, and then extensively review the structure–activity relationship data and biophysical interaction studies of these peptides with their cognate receptors.

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Induction of neuropeptide gene expression and blockade of retrograde transport in facial motor neurons following local peripheral nerve inflammation in severe combined immunodeficiency and BALB/C mice

Cited by 28 publications

References 33 publications

Differential gene expression in the axotomized facial motor nucleus of presymptomatic SOD1 mice

Differential gene expression in the axotomized facial motor nucleus of presymptomatic SOD1 mice

Long lasting recruitment of immune cells and altered epi-perineurial thickness in focal nerve inflammation induced by complete Freund's adjuvant

Targeting VIP and PACAP Receptor Signalling: New Therapeutic Strategies in Multiple Sclerosis

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