A sideways glance. Alcoholic breakdown of barriers: how ethanol can initiate a landslide towards disease

Sambuy, Yula

doi:10.1007/s12263-009-0118-5

Cited by 4 publications

(4 citation statements)

References 22 publications

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“…Malfunction of adherens junctions has been indicated in the pathologies of the immune system ( Wang et al, 2011 ; Kaymak et al, 2021 ) and the development of cancer ( Vasioukhin, 2012 ; Bischoff et al, 2020 ). Since these diseases are aggravated by alcohol consumption ( Sambuy, 2009 ; Meadows and Zhang, 2015 ), we decided to explore effects of microRNA de-regulation on the adherens junction pathway elements.…”

Section: Resultsmentioning

confidence: 99%

Non-Invasive microRNA Profiling in Saliva can Serve as a Biomarker of Alcohol Exposure and Its Effects in Humans

Mead

Boulghassoul-Pietrzykowska

Wang

et al. 2022

Front. Genet.

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Alcohol Use Disorder (AUD) is one of the most prevalent mental disorders worldwide. Considering the widespread occurrence of AUD, a reliable, cheap, non-invasive biomarker of alcohol consumption is desired by healthcare providers, clinicians, researchers, public health and criminal justice officials. microRNAs could serve as such biomarkers. They are easily detectable in saliva, which can be sampled from individuals in a non-invasive manner. Moreover, microRNAs expression is dynamically regulated by environmental factors, including alcohol. Since excessive alcohol consumption is a hallmark of alcohol abuse, we have profiled microRNA expression in the saliva of chronic, heavy alcohol abusers using microRNA microarrays. We observed significant changes in salivary microRNA expression caused by excessive alcohol consumption. These changes fell into three categories: downregulated microRNAs, upregulated microRNAs, and microRNAs upregulated de novo. Analysis of these combinatorial changes in microRNA expression suggests dysregulation of specific biological pathways leading to impairment of the immune system and development of several types of epithelial cancer. Moreover, some of the altered microRNAs are also modulators of inflammation, suggesting their contribution to pro-inflammatory mechanisms of alcohol actions. Establishment of the cellular source of microRNAs in saliva corroborated these results. We determined that most of the microRNAs in saliva come from two types of cells: leukocytes involved in immune responses and inflammation, and buccal cells, involved in development of epithelial, oral cancers. In summary, we propose that microRNA profiling in saliva can be a useful, non-invasive biomarker allowing the monitoring of alcohol abuse, as well as alcohol-related inflammation and early detection of cancer.

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Section: Resultsmentioning

confidence: 99%

Non-Invasive microRNA Profiling in Saliva can Serve as a Biomarker of Alcohol Exposure and Its Effects in Humans

Mead

Boulghassoul-Pietrzykowska

Wang

et al. 2022

Front. Genet.

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“…), that contribute to the gamut of neuronal damage observed in alcohol toxicity [ 18 , 20 , 32 ]. For example, chronic ethanol exposure in mice models resulted in decreased expression of the tight-junction proteins such as zona occludin-1 and claudin-5 [ 15 , 33 ], thereby compromising the blood-brain barrier. This impaired vascular endothelial integrity enables enhanced infiltration of leukocytes into the brain, leading to subsequent release of more cytokines and proinflammatory agents that further contribute to a pathological inflammatory phenotype in alcoholism [ 34 ].…”

Section: Alcohol Use Disorder: Focus On Pathology Associated With mentioning

confidence: 99%

Platelet Endothelial Cell Adhesion Molecule-1 and Oligodendrogenesis: Significance in Alcohol Use Disorders

et al. 2017

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Alcoholism is a chronic relapsing disorder with few therapeutic strategies that address the core pathophysiology. Brain tissue loss and oxidative damage are key components of alcoholism, such that reversal of these phenomena may help break the addictive cycle in alcohol use disorder (AUD). The current review focuses on platelet endothelial cell adhesion molecule 1 (PECAM-1), a key modulator of the cerebral endothelial integrity and neuroinflammation, and a targetable transmembrane protein whose interaction within AUD has not been well explored. The current review will elaborate on the function of PECAM-1 in physiology and pathology and infer its contribution in AUD neuropathology. Recent research reveals that oligodendrocytes, whose primary function is myelination of neurons in the brain, are a key component in new learning and adaptation to environmental challenges. The current review briefly introduces the role of oligodendrocytes in healthy physiology and neuropathology. Importantly, we will highlight the recent evidence of dysregulation of oligodendrocytes in the context of AUD and then discuss their potential interaction with PECAM-1 on the cerebral endothelium.

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“…This is due to the fact that, in the presence of ethanol, PLD converts PC into an abnormal phospholipid, phosphatidylethanol (PEth), thereby disrupting the normal PLD-mediated signalling cascade ( Fig. 2) (Alling et al, 1983;Gustavsson, 1995;Guizzetti et al, 2004;Klein, 2005;Newton and Messing, 2006;Sambuy, 2009). PEth increases membrane fluidity, although the presence of PEth in the membrane lipid bilayers may also confer some tolerance to ethanol-induced membrane disruption, inhibits ethanol activation of Na + -K + ATPase, stimulates phosphoinositide hydrolysis and activates protein kinase C and phospholipase A 2 , thus suggesting a role for PEth in ethanol modulation of signal transduction (Asaoka et al, 1988;Omodeo-Sale et al, 1991;Lundqvist et al, 1993;Aroor and Baker, 1996;Chang et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

“…PEth increases membrane fluidity, although the presence of PEth in the membrane lipid bilayers may also confer some tolerance to ethanol-induced membrane disruption, inhibits ethanol activation of Na + -K + ATPase, stimulates phosphoinositide hydrolysis and activates protein kinase C and phospholipase A 2 , thus suggesting a role for PEth in ethanol modulation of signal transduction (Asaoka et al, 1988;Omodeo-Sale et al, 1991;Lundqvist et al, 1993;Aroor and Baker, 1996;Chang et al, 2000). Thus, it has been proposed that this phospholipid is a candidate cytotoxic substance that might be responsible for some of the adverse effects exerted on several cell types by alcohol (Alling et al, 1983;Gustavsson, 1995;Aradottir et al, 2002;Sambuy, 2009). However, it is unknown whether this mechanism exists in neurons and whether ethanol is able to alter the PPIn metabolism in these cells.…”

Section: Introductionmentioning

confidence: 99%

Polyphosphoinositide Metabolism and Golgi Complex Morphology in Hippocampal Neurons in Primary Culture is Altered by Chronic Ethanol Exposure

Esteban-Pretel¹,

Marín²,

Romero³

et al. 2012

Alcohol and Alcoholism

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A sideways glance. Alcoholic breakdown of barriers: how ethanol can initiate a landslide towards disease

Cited by 4 publications

References 22 publications

Non-Invasive microRNA Profiling in Saliva can Serve as a Biomarker of Alcohol Exposure and Its Effects in Humans

Non-Invasive microRNA Profiling in Saliva can Serve as a Biomarker of Alcohol Exposure and Its Effects in Humans

Platelet Endothelial Cell Adhesion Molecule-1 and Oligodendrogenesis: Significance in Alcohol Use Disorders

Polyphosphoinositide Metabolism and Golgi Complex Morphology in Hippocampal Neurons in Primary Culture is Altered by Chronic Ethanol Exposure

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