Molecular cytogenetic interphase analysis of Phosphoinositide-specific Phospholipase C β1 gene in paraffin-embedded brain samples of major depression patients

Vasco, Vincenza Rita Lo; Polonia, Patrizia

doi:10.1016/j.jad.2011.07.023

Cited by 12 publications

(16 citation statements)

References 16 publications

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“…The diagnostic specificity of our findings aligns with studies reporting a PLCB1 gene deletion in 5 out of 15 people with Sz, 27 while only occurring in one out of 15 BD patients, 28 and in none of the 15 MDD patients examined. 29 While there are reports of other PLC isoforms being associated with BD pathogenesis and treatment response, 30, 31 our findings are consistent with PLCB1 being not highly implicated in affective disorders. 27 …”

Section: Discussionsupporting

confidence: 83%

Isoform specific differences in phospholipase C beta 1 expression in the prefrontal cortex in schizophrenia and suicide

et al. 2017

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Our previous study demonstrated that phospholipase C beta 1 mRNA was down-regulated in Brodmann’s area 46 from subjects with schizophrenia. However, phospholipase C beta 1 protein has also been shown to be lower in Brodmann’s area 8 and 9 from teenage suicide subjects, creating a potential confound in interpreting the findings in schizophrenia due to the high suicide rate associated with this disorder. To begin to reconcile and consolidate these findings, in this study, we measured mRNA and protein levels of phospholipase C beta 1 variants a and b in Brodmann’s area 46 and Brodmann’s area 9 from subjects with schizophrenia, many of whom were suicide completers, and determined the diagnostic specificity of observed findings. Consistent with our previous study, levels of phospholipase C beta 1 a and b mRNA, but not protein, were lower in Brodmann’s area 46 from subjects with schizophrenia. In Brodmann’s area 9, phospholipase C beta 1a protein levels were lower in subjects with schizophrenia, while phospholipase C beta 1b mRNA was higher and protein was lower in those that had died of suicide. Altered protein levels in Brodmann’s area 9 appeared to be diagnostically specific, as we did not detect these changes in subjects with bipolar disorder, major depressive disorder or suicide completers with no diagnosis of mental illness. We further assessed the relationship between phospholipase C beta 1 and levels of muscarinic receptors (CHRMs) that signal through this protein, in both human and Chrm knockout mouse central nervous system tissue, and found no strong relationship between the two. Understanding central nervous system differences in downstream effector pathways in schizophrenia may lead to improved treatment strategies and help to identify those at risk of suicide.

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Section: Discussionsupporting

confidence: 83%

Isoform specific differences in phospholipase C beta 1 expression in the prefrontal cortex in schizophrenia and suicide

et al. 2017

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“…PLC enzymes are described as highly tissue-specific in normal tissues (18,19,21). However, the PLC expression panels in tissues vary under abnormal conditions compared to normal counterparts (20,21,23,24,(26)(27)(28). Moreover, the subcellular distribution of PLC enzymes seems to play Avicenna J Med Biochem.…”

Section: Discussionmentioning

confidence: 99%

“…Knowledge of the expression panels of PI-PLC enzymes is a necessary and preliminary tool to address studies about their role in quiescent cells. Moreover, the expression panels of PI-PLC enzymes have been demonstrated to differ in quiescent cells with respect to the pathological or activated counterpart (18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30).…”

Section: Introductionmentioning

confidence: 99%

Comparison of Phosphoinositide-Specific Phospholipase C Expression Panels of Human Osteoblasts Versus MG-63 and Saos Osteoblast-Like Cells

Vasco¹,

Leopizzi²,

d’Abusco³

et al. 2016

Avicenna J Med Biochem

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Background: A large number of phospholipase C (PLC) enzymes, both mRNA transcripts and proteins, have been detected in osteoblasts, corroborating the importance of calcium regulation in bone tissue. MG-63 and SaOS-2 human osteosarcoma cell lines are actually considered osteoblast-like cells, and are therefore widely used as experimental models for osteoblasts. Objectives: Our aim was to verify whether MG-63 or SaOS-2 cells might also represent appropriate experimental osteoblast models for signal transduction studies, with special regard to the phosphoinositide (PI) pathway. We analyzed the expression and the subcellular distribution of enzymes related to calcium signal transduction (the PI-specific PLC family), which are known to possess high cell/tissue specificity. Materials and Methods:The expression of PLC genes was analyzed by performing RT-PCR experiments. The presence of PLC enzymes and their subcellular distribution within the cells was analyzed with immunofluorescence experiments. Results: Osteoblasts, MG-63 cells, and SaOS-2 cells have expression panels similar to those of PLC enzymes. However, slight differences were found in the expression of enzymes belonging to the PLCη subfamily. Conclusions: MG-63 and SaOS-2 osteosarcoma cell lines might not represent appropriate experimental models for studies that aim to analyze signal transduction in osteoblasts.

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“…PLC β1 is considered a molecular convergence point of several neurotransmitter pathways implicated in schizoaffective disorders and epileptic encephalopathy [97][98][99][100][101][102][103][104][105]. The human gene that codes for PLC β3 (PLCB3; OMIM *600230) maps to a genomic region associated with neurodegenerative diseases [106]. PLC γ1 was expressed by embryonic radial glia during fetal brain development [107].…”

Section: Figurementioning

confidence: 99%

Insights into Brain Signal Transduction can Provide Potential Molecular Targets to Approach and Manage Alzheimer’s Disease

Vasco¹,

Rita²

2020

OBM Neurobiology

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Mechanisms leading to neuronal cell death in human pathology are far from being fully delineated. Understanding the molecules involved in neuronal death and the timing of their recruitment might help to explain the natural history of degenerative processes, including the morphological abnormalities observed in Alzheimer's disease (AD). Moreover, it might help refine the diagnosis by defining new molecular markers as well as find effective therapies, especially for slow cognitive deficits, often associated with neurodegenerative diseases. Disturbances in signal transduction in neurons underlie human cognitive decline. Numerous studies have analyzed the different signal transduction pathways in AD, offering interesting insights into its etiology and prospective therapies. For example, studies revealed that AD is associated with abnormal neuronal Ca 2+ homeostasis, and that signal transduction pathways are involved in Ca 2+ metabolism and phosphorylative regulation of proteins. Understanding the role and timing of action of the signaling pathways recruited during the changes in brain morphology in AD progression might help elucidate the pathogenesis of the disease, paving the way for early diagnosis, prognosis refinement, and novel molecular therapeutic strategies. In this review, we discuss the different signal transduction pathways involved in AD pathogenesis.

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Molecular cytogenetic interphase analysis of Phosphoinositide-specific Phospholipase C β1 gene in paraffin-embedded brain samples of major depression patients

Cited by 12 publications

References 16 publications

Isoform specific differences in phospholipase C beta 1 expression in the prefrontal cortex in schizophrenia and suicide

Isoform specific differences in phospholipase C beta 1 expression in the prefrontal cortex in schizophrenia and suicide

Comparison of Phosphoinositide-Specific Phospholipase C Expression Panels of Human Osteoblasts Versus MG-63 and Saos Osteoblast-Like Cells

Insights into Brain Signal Transduction can Provide Potential Molecular Targets to Approach and Manage Alzheimer’s Disease

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