Nuclear phospholipase C-β1 and diacylglycerol LIPASE-α in brain cortical neurons

Caño, Gontzal Garcı́a del; Montaña, Mario; Aretxabala, Xabier; González-Burguera, Imanol; Jesús, Maider López de; Barrondo, Sergio; Sallés, Joan

doi:10.1016/j.jbior.2013.09.003

Cited by 34 publications

(14 citation statements)

References 98 publications

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“…Ca 2+ signals induced by histamine in DRG neurons were eliminated in PLCβ3 −/− mice, but responses to other agonists, such as bradykinin or UTP were intact, showing the presence and importance of other PLCβ isoforms. PLCβ isoforms may also localize to the nucleus in brain cortical neurons, where they play distinct roles from their effects at the plasma membrane (Garcia del Cano et al, 2014), but this area of research is largely unexplored in peripheral sensory neurons.…”

Section: Plc-coupled Gpcr Signaling In Sensory Neuronsmentioning

confidence: 99%

Phosphoinositide signaling in somatosensory neurons

Rohács

2016

Advances in Biological Regulation

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Somatosensory neurons of the dorsal root ganglia (DRG) and trigeminal ganglia (TG) are responsible for detecting thermal and tactile stimuli. They are also the primary neurons mediating pain and itch. A large number of cell surface receptors in these neurons couple to phospholipase C (PLC) enzymes leading to the hydrolysis of phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2] and the generation of downstream signaling molecules. These neurons also express many different ion channels, several of which are regulated by phosphoinositides. This review will summarize the knowledge on phosphoinositide signaling in these neurons, with special focus on effects on sensory and other ion channels.

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Section: Plc-coupled Gpcr Signaling In Sensory Neuronsmentioning

confidence: 99%

Phosphoinositide signaling in somatosensory neurons

Rohács

2016

Advances in Biological Regulation

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“…DAG pools in all tissues are tightly regulated since these glycerolipids serve multiple critical roles. These roles include: i) precursors for structural glycerophospholipids [7], ii) precursors for triacylglycerols (TAG) and monoacylglycerols (MAG), including the endocannabinoid 2-arachidonyl-glycerol [8–10], iii) mediators of signal transduction via activation of protein kinase C (PKC), protein kinase D (PKD), Ca(2+)/calmodulin-dependent protein kinase (PKCaMII), RasGRP1/Ras/Erk MAPK, chimaerins, and munc13 proteins that regulate neurotransmitter release [11–15], iv) regulation of immunological synapse function [16] and respiratory burst in immune cells like microglia [17]; v) required in the Golgi for transport carrier biogenesis [18]; vi) nuclear signal transduction [19], and vii) structural roles in the endoplasmic reticulum and nuclear envelope [20–21]. …”

Section: Introductionmentioning

confidence: 99%

Targeted Lipidomics of Fontal Cortex and Plasma Diacylglycerols (DAG) in Mild Cognitive Impairment and Alzheimer’s Disease: Validation of DAG Accumulation Early in the Pathophysiology of Alzheimer’s Disease

Wood

Medicherla

Sheikh

et al. 2015

JAD

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Previous studies have demonstrated augmented levels of diacylglycerols (DAG) in the frontal cortex and plasma of Alzheimer’s disease (AD) patients. We extended these findings from non-targeted liopidomics studies to design a lipidomics platform to interrogate DAGs and monoacylglycerols (MAG) in the frontal cortex and plasma of MCI subjects. Control subjects included both aged normal controls and controls with normal cognition, but AD pathology at autopsy, individuals termed non-demented AD neuropathology (NDAN). DAGs with saturated, unsaturated, and polyunsaturated fatty acid substituents were found to be elevated in MCI frontal cortex and plasma. Tandem mass spectrometry of the DAGs did not reveal any differences in the distributions of the fatty acid substitutions between MCI and control subjects. While triacylglycerols were not altered in MCI subjects there were increases in monoacylglycerol levels both in the frontal cortex and plasma. In toto, increased levels of DAGs and MAGs appear to occur early in AD pathophysiology and require both further validation in a larger patient cohort and elucidation of the lipidomics alteration(s) that lead to the accumulation of DAGs in MCI subjects.

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“…Functionally, the PI-PLC enzymes included in the b subgroup can regulate normal cell metabolism [25][26][27] and gene expression [28], but they are also implicated in the immune system [29], brain function [30,31] and hematopoiesis [32,33]. In fact, PI-PLCb1 can target cyclin D3 [23], which modulates the hematopoietic stem cell proliferation and differentiation [34,35].…”

Section: Introductionmentioning

confidence: 99%

An increased expression of PI-PLCβ1 is associated with myeloid differentiation and a longer response to azacitidine in myelodysplastic syndromes

Cocco

Finelli

Mongiorgi

et al. 2015

Journal of Leukocyte Biology

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This study tested the hypothesis that PI-PLCβ1 is associated with myeloid differentiation and that its expression could be useful for predicting the response of MDS patients to azacitidine, as the clinical effect of epigenetic treatments is often detectable only after several cycles of therapy. To this end, PI-PLCβ1 was quantified on 70 MDS patients (IPSS risk: 13 Low, 20 Int-1, 31 Int-2, 6 High) at baseline and during the first 3 cycles of azacitidine. Results were then compared with the hematologic response, as assessed after the sixth cycle of azacitidine therapy. Overall, 60 patients completed 6 cycles of azacitidine, and for them, a clinical and molecular evaluation was possible: 37 of these patients (62%) showed a specific increase of PI-PLCβ1 mRNA within the first 3 cycles, which was associated with a longer duration of response and with an increased myeloid differentiation, as evidenced by PI-PLCγ2 induction and the recruitment of specific myeloid-associated transcription factors to the PI-PLCβ1 promoter during azacitidine response. Moreover, the increase of cyclin D3 gene expression throughout all of the therapy showed that PI-PLCβ1-dependent signaling is indeed activated in azacitidine responder patients. Taken together, our results show that PI-PLCβ1 quantification in MDS predicts the response to azacitidine and is associated with an increased myeloid differentiation.

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Nuclear phospholipase C-β1 and diacylglycerol LIPASE-α in brain cortical neurons

Cited by 34 publications

References 98 publications

Phosphoinositide signaling in somatosensory neurons

Phosphoinositide signaling in somatosensory neurons

Targeted Lipidomics of Fontal Cortex and Plasma Diacylglycerols (DAG) in Mild Cognitive Impairment and Alzheimer’s Disease: Validation of DAG Accumulation Early in the Pathophysiology of Alzheimer’s Disease

An increased expression of PI-PLCβ1 is associated with myeloid differentiation and a longer response to azacitidine in myelodysplastic syndromes

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