Components of the NGF signaling complex are altered in mdx mouse superior cervical ganglion and its target organs

Lombardi, Loredana; Stefano, Maria Egle De; Paggi, Paola

doi:10.1016/j.nbd.2008.07.021

Cited by 11 publications

(25 citation statements)

References 51 publications

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“…Consistent with these data is the observation that, in adult mdx mice, Wnt5a , Mknk2 and Atf4 transcripts revert from downregulation to upregulation. In particular, late upregulation of Wnt5a is in accord with the previously observed recovery at this age of TrkA‐p75 NTR levels (Lombardi et al. , 2008).…”

Section: Discussionsupporting

confidence: 88%

“…A characteristic component of the astrocyte cytoskeleton, VIM is also expressed by sensory and autonomic neurons following axon damage, where it promotes retrograde injury signaling to the cell body (Hanz & Fainzilber, 2006). The increase in Vim expression is possibly consequent on a reduction in NGF signaling, a phenomenon that is, in certain respects, comparable to physical interruption of an axon, which in the mdx mouse SCG is suggested by previous (Lombardi et al. , 2008) and present data, such as downregulation of the NGF receptor gene p75 NTR .…”

Section: Discussionsupporting

confidence: 83%

“…Large‐scale expression of gene transcripts was determined in the SCGs of wild‐type and mdx mice at three postnatal dates, which are characterized by different aspects of neuron and neural circuit differentiation and that were previously investigated for structural, molecular and functional differences between the two genotypes (De Stefano et al. , 2005; Lombardi et al. , 2008; Di Angelantonio et al.…”

Section: Resultsmentioning

confidence: 99%

“…These alterations were detected as early as P0, when neuronal loss had not yet occurred, suggesting that, in mdx mice, the absence of Dp427 impaired axonal growth and differentiation (De Stefano et al. , 2005; Lombardi et al. , 2008).…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, sympathetic neuron innervation of the muscular targets was always affected with respect to the wild-type, and all SCG neurons, independently of their target, showed reductions in axon defasciculation and terminal sprouting. These alterations were detected as early as P0, when neuronal loss had not yet occurred, suggesting that, in mdx mice, the absence of Dp427 impaired axonal growth and differentiation (De Stefano et al, 2005;Lombardi et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

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Lack of dystrophin in mdx mice modulates the expression of genes involved in neuron survival and differentiation

Licursi

Caiello

Lombardi

et al. 2012

Eur J of Neuroscience

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Duchenne muscular dystrophy is an X-linked disease characterized by progressive and lethal muscular wasting. Dystrophic patients, however, are also afflicted by several neurological disorders, the importance of which is generally underestimated. As promising therapies for muscles are currently in clinical trial stages, with the potential to provide an increase in the lifespan of young patients, determination of the genetic and molecular aspects characterizing this complex disease is crucial in order to allow the development of therapeutic approaches specifically designed for the nervous system. In this study, differences in gene expression in the superior cervical ganglion of postnatal day (P)5, P10 and 6-7-week-old wild-type and genetically dystrophic mdx mice were evaluated by DNA microarray analysis. The main aim was to verify whether the lack of dystrophin affected the transcript levels of genes related to different aspects of neuron development and differentiation. Ontological analysis of more than 500 modulated genes showed significant differences in genetic class enrichment at each postnatal date. Upregulated genes mainly fell in the categories of vesicular trafficking, and cytoskeletal and synaptic organization, whereas downregulated genes were associated with axon development, growth factors, intracellular signal transduction, metabolic processes, gene expression regulation, synapse morphogenesis, and nicotinic receptor clustering. These data strongly suggest that the structural and functional alterations previously described in both the autonomic and central nervous systems of mdx mice with respect to wild-type mice and related to crucial aspects of neuron life (i.e. postnatal development, differentiation, and plasticity) result not only from protein post-translational modifications, but also from direct and/or indirect modulation of gene expression.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionsupporting

confidence: 83%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Lack of dystrophin in mdx mice modulates the expression of genes involved in neuron survival and differentiation

Licursi

Caiello

Lombardi

et al. 2012

Eur J of Neuroscience

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Macrophages producing chondroitin sulfate proteoglycan‐4 induce neuro‐cardiac junction impairment in Duchenne muscular dystrophy

Milan,

Maiullari,

Chirivì

et al. 2024

The Journal of Pathology

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Duchenne muscular dystrophy (DMD) is caused by the absence of the full form of the dystrophin protein, which is essential for maintaining the structural integrity of muscle cells, including those in the heart and respiratory system. Despite progress in understanding the molecular mechanisms associated with DMD, myocardial insufficiency persists as the primary cause of mortality, and existing therapeutic strategies remain limited. This study investigates the hypothesis that a dysregulation of the biological communication between infiltrating macrophages (MPs) and neurocardiac junctions exists in dystrophic cardiac tissue. In a mouse model of DMD (mdx), this phenomenon is influenced by the over‐release of chondroitin sulfate proteoglycan‐4 (CSPG4), a key inhibitor of nerve sprouting and a modulator of the neural function, by MPs infiltrating the cardiac tissue and associated with dilated cardiomyopathy, a hallmark of DMD. Givinostat, the histone deacetylase inhibitor under current development as a clinical treatment for DMD, is effective at both restoring a physiological microenvironment at the neuro‐cardiac junction and cardiac function in mdx mice in addition to a reduction in cardiac fibrosis, MP‐mediated inflammation, and tissue CSPG4 content. This study provides novel insight into the pathophysiology of DMD in the heart, identifying potential new biological targets. © 2024 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.

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The Heart-Brain Connection in Patients with Duchenne Muscular Dystrophy

Bearzi

Rizzi

2020

Brain and Heart Dynamics

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Components of the NGF signaling complex are altered in mdx mouse superior cervical ganglion and its target organs

Cited by 11 publications

References 51 publications

Lack of dystrophin in mdx mice modulates the expression of genes involved in neuron survival and differentiation

Lack of dystrophin in mdx mice modulates the expression of genes involved in neuron survival and differentiation

Macrophages producing chondroitin sulfate proteoglycan‐4 induce neuro‐cardiac junction impairment in Duchenne muscular dystrophy

The Heart-Brain Connection in Patients with Duchenne Muscular Dystrophy

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