| http://purl.uniprot.org/citations/29404485 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/29404485 | http://www.w3.org/2000/01/rdf-schema#comment | "This study investigated the role of ethanol-inducible cytochrome P450-2E1 (CYP2E1) in enhancing CYP2E1 and other P450 proteins in extracellular vesicles (EVs) from alcohol-exposed rodents and human patients with alcoholism and their effects on oxidative hepatocyte injury. Female Fischer rats and wild-type or Cyp2e1-null mice were exposed to three oral doses of binge ethanol or dextrose control at 12-hour intervals. Plasma EV and hepatic proteins from alcohol-exposed rodents, patients with alcoholism, and their respective controls were isolated and characterized. The number of EVs and the amounts of EV CYP2E1, CYP2A, CYP1A1/2, and CYP4B proteins were markedly elevated in both patients with alcoholism and alcohol-exposed rats and mice. The number of EVs and EV P450 proteins were significantly reduced in ethanol-exposed rats fed a diet containing polyunsaturated fatty acids. The increased number of EVs and EV CYP2E1 and other P450 isoforms in alcohol-exposed wild types were significantly reduced in the corresponding Cyp2e1-null mice. EV CYP2E1 amounts depended on increased oxidative and endoplasmic reticulum (ER) stress because their levels were decreased by cotreatment with the antioxidant N-acetylcysteine or the CYP2E1 inhibitor chlormethiazole but increased by ER stress-inducer thapsigargin, which was blocked by 4-phenylbutyric acid. Furthermore, cell death rates were elevated when primary hepatocytes or human hepatoma cells were exposed to EVs from alcohol-exposed rodents and patients with alcoholism, demonstrating that EVs from alcohol-exposed rats and patients with alcoholism are functional and can promote cell death by activating the apoptosis signaling pathway, including phospho-c-Jun N-terminal kinase, proapoptotic Bax, and activated caspase-3. Conclusion: CYP2E1 has an important role in elevating EV CYP2E1 and other P450 isoforms through increased oxidative and ER stress. Elevated EV-CYP2E1 detected after withdrawal from alcohol or exposure to the CYP2E1 inducer pyrazole can be a potential biomarker for liver injury. (Hepatology Communications 2017;1:675-690)."xsd:string |
| http://purl.uniprot.org/citations/29404485 | http://purl.org/dc/terms/identifier | "doi:10.1002/hep4.1066"xsd:string |
| http://purl.uniprot.org/citations/29404485 | http://purl.uniprot.org/core/author | "Clemens D.L."xsd:string |
| http://purl.uniprot.org/citations/29404485 | http://purl.uniprot.org/core/author | "Mezey E."xsd:string |
| http://purl.uniprot.org/citations/29404485 | http://purl.uniprot.org/core/author | "Cho Y.E."xsd:string |
| http://purl.uniprot.org/citations/29404485 | http://purl.uniprot.org/core/author | "Hardwick J.P."xsd:string |
| http://purl.uniprot.org/citations/29404485 | http://purl.uniprot.org/core/author | "Song B.J."xsd:string |
| http://purl.uniprot.org/citations/29404485 | http://purl.uniprot.org/core/author | "Salem N. Jr."xsd:string |
| http://purl.uniprot.org/citations/29404485 | http://purl.uniprot.org/core/date | "2017"xsd:gYear |
| http://purl.uniprot.org/citations/29404485 | http://purl.uniprot.org/core/name | "Hepatol Commun"xsd:string |
| http://purl.uniprot.org/citations/29404485 | http://purl.uniprot.org/core/pages | "675-690"xsd:string |
| http://purl.uniprot.org/citations/29404485 | http://purl.uniprot.org/core/title | "Increased ethanol-inducible cytochrome P450-2E1 and cytochrome P450 isoforms in exosomes of alcohol-exposed rodents and patients with alcoholism through oxidative and endoplasmic reticulum stress."xsd:string |
| http://purl.uniprot.org/citations/29404485 | http://purl.uniprot.org/core/volume | "1"xsd:string |
| http://purl.uniprot.org/citations/29404485 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/29404485 |
| http://purl.uniprot.org/citations/29404485 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/29404485 |
| http://purl.uniprot.org/uniprot/#_A0A0G2K5X9-mappedCitation-29404485 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29404485 |
| http://purl.uniprot.org/uniprot/#_A0A8I5ZS79-mappedCitation-29404485 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29404485 |
| http://purl.uniprot.org/uniprot/#_A0A8I5ZXI6-mappedCitation-29404485 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29404485 |
| http://purl.uniprot.org/uniprot/#_A0A8L2Q8J4-mappedCitation-29404485 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29404485 |
| http://purl.uniprot.org/uniprot/#_Q71US7-mappedCitation-29404485 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29404485 |
| http://purl.uniprot.org/uniprot/#_P05182-mappedCitation-29404485 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/29404485 |
| http://purl.uniprot.org/uniprot/A0A0G2K5X9 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/29404485 |
| http://purl.uniprot.org/uniprot/A0A8I5ZS79 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/29404485 |
| http://purl.uniprot.org/uniprot/P05182 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/29404485 |