Chromogranin A and Vesicular Monoamine Transporter 2 Immunolocalization in Protein Bodies of Human Locus Coeruleus Neurons

Kloukina-Pantazidou, Ismini; Chrysanthou‐Piterou, Margarita; Havaki, Sophia; Issidorides, Marietta R.

doi:10.3109/01913123.2012.750410

Cited by 3 publications

(3 citation statements)

References 24 publications

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“…These neurosecretory granules can be found in multiple cell types, including NE cells, endocrine, exocrine, and hematopoietic cells. They can also be found in neurons . Our study confirms the presence of neurosecretory granules in SCC of the prostate, but presents additional new findings indicating that the transdifferenratiaion goes beyond neuroendocrine into neuronal.…”

Section: Discussionsupporting

confidence: 84%

Neuronal Trans‐Differentiation in Prostate Cancer Cells

et al. 2016

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Neuroendocrine (NE) differentiation in prostate cancer (PCa) is an aggressive phenotype associated with therapy resistance. The complete phenotype of these cells is poorly understood. Clinical classification is based predominantly on the expression of standard NE markers. We analyzed the phenotype of NE carcinoma of the prostate utilizing in vitro methods, in silico, and immunohistochemical analyses of human disease. Results LNCaP cells, subjected to a variety of stressors (0.1% (v/v) fetal bovine serum, cyclic AMP) induced a reproducible phenotype consistent with neuronal trans-differentiation. Cells developed long cytoplasmic processes resembling neurons. As expected, serum deprived cells had decreased expression in androgen receptor and prostate specific antigen. A significant increase in neuronal markers also was observed. Gene array analysis demonstrated that LNCaP cells subjected to low serum or cAMP showed statistically significant manifestation of a human brain gene expression signature. In an in silico experiment using human data, we identified that only hormone resistant metastatic prostate cancer showed enrichment of the “brain profile”. Gene ontology analysis demonstrated categories involved in neuronal differentiation. Three neuronal markers were validated in a large human tissue cohort. This study proposes that the later stages of PCa evolution involves neuronal trans-differentiation, which would enable PCa cells to acquire independence from the neural axis, critical in primary tumors.

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Section: Discussionsupporting

confidence: 84%

Neuronal Trans‐Differentiation in Prostate Cancer Cells

et al. 2016

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“…In MeCP2-deficient mice, the expression of Nr2f2 is up-regulated, which may down-regulate Chgb and cause excess monoamine accumulation in the extracellular fluid and impair neurons. This finding suggests that influence of MeCP2 deficiency can be aggravated through a downstream target gene cascade in astrocytes ( Kloukina-Pantazidou et al, 2013 ; Delepine et al, 2015 ). Interestingly, in response to LPS stimulation, MeCP2-deficient astrocytes released fewer cytokines such as IL-1β and IL-6 ( Maezawa et al, 2009 ).…”

Section: Mecp2 In Astrocytesmentioning

confidence: 87%

MeCP2 Deficiency in Neuroglia: New Progress in the Pathogenesis of Rett Syndrome

Jin

Chen

Xiao

2017

Front. Mol. Neurosci.

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Rett syndrome (RTT) is an X-linked neurodevelopmental disease predominantly caused by mutations of the methyl-CpG-binding protein 2 (MeCP2) gene. Generally, RTT has been attributed to neuron-centric dysfunction. However, increasing evidence has shown that glial abnormalities are also involved in the pathogenesis of RTT. Mice that are MeCP2-null specifically in glial cells showed similar behavioral and/or neuronal abnormalities as those found in MeCP2-null mice, a mouse model of RTT. MeCP2 deficiency in astrocytes impacts the expression of glial intermediate filament proteins such as fibrillary acidic protein (GFAP) and S100 and induces neuron toxicity by disturbing glutamate metabolism or enhancing microtubule instability. MeCP2 deficiency in oligodendrocytes (OLs) results in down-regulation of myelin gene expression and impacts myelination. While MeCP2-deficient microglia cells fail in response to environmental stimuli, release excessive glutamate, and aggravate impairment of the neuronal circuit. In this review, we mainly focus on the progress in determining the role of MeCP2 in glial cells involved in RTT, which may provide further insight into a therapeutic intervention for RTT.

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“…Similarly, the procedures using confocal laser microscopy have been performed, but these approaches also do not enable the evaluation of subcellular degeneration using submicrometer resolution of both degenerated neurons and activated microglial cells [13,14]. However, another study aimed to detect degeneration and/or intracellular changes of neurons using electron microscopy has been reported [15][16][17][18][19]. This method is advantageous, in enabling the detection of the subcellular degeneration of neurons because of its resolution.…”

Section: Introductionmentioning

confidence: 97%

Three-Dimensional Electron Microscopy Reconstruction of Degenerative Dopaminergic Neurons Surrounded by Activated Microglia in Substantia Nigra

Nakadate

Tanaka-Nakadate

2015

Ultrastructural Pathology

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There is an urgent need to investigate the reason for the pathogenic mechanism of intractable central neurological diseases such as Parkinson's disease. It has been reported that the activation of microglial cells is involved in the pathology of these diseases. However, due to technical difficulties, the relationship between degenerative neurons and activated microglial cells remains unclear. Therefore, we tried the improved analysis technique to clarify the spatial relationship between these cell types. We were able to establish an analysis technique that consists of a three-dimensional reconstruction method using serial immunoelectron micrographs after having identified both degenerative neurons and activated microglial cells under optical microscope. Using this technique, we have relatively easily been able to clarify the spatial relationship between degenerative neurons and activated microglial cells. Furthermore, using this technique it is possible to determine the neuronal degeneration process in detail, because it is able to identify structures implicated in degeneration, such as accumulation of lipofuscin in degenerated neuronal somata and phagocytotic structures of microglial cells. In future, this technical approach may be applied to elucidate the relationship between degenerative neurons and activated glial cells in human diseases.

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Chromogranin A and Vesicular Monoamine Transporter 2 Immunolocalization in Protein Bodies of Human Locus Coeruleus Neurons

Cited by 3 publications

References 24 publications

Neuronal Trans‐Differentiation in Prostate Cancer Cells

Neuronal Trans‐Differentiation in Prostate Cancer Cells

MeCP2 Deficiency in Neuroglia: New Progress in the Pathogenesis of Rett Syndrome

Three-Dimensional Electron Microscopy Reconstruction of Degenerative Dopaminergic Neurons Surrounded by Activated Microglia in Substantia Nigra

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