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[PMID]:28899749
[Au] Autor:Hammoud SH; Omar AG; Eid AA; El-Mas MM
[Ad] Endereço:Department of Pharmacology and Therapeutics, Faculty of Pharmacy, Beirut Arab University, Lebanon.
[Ti] Título:CYP4A/CYP2C modulation of the interaction of calcium channel blockers with cyclosporine on EDHF-mediated renal vasodilations in rats.
[So] Source:Toxicol Appl Pharmacol;334:110-119, 2017 Nov 01.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The endothelium-derived hyperpolarizing factor (EDHF) serves as a back-up mechanism that compensates for reduced nitric oxide (NO)/prostanoids bioavailability. Here we investigated whether (i) under conditions of vascular endothelium dysfunction, the immunosuppressant drug cyclosporine (CSA) upregulates EDHF-dependent renal vasodilations through altering CYP4A/CYP2C signaling, and (ii) calcium channel blockers modulate the CSA/EDHF/CYP interaction. Rats were treated with CSA, verapamil, nifedipine, or their combinations for 7days. Blood pressure (BP) was measured by tail-cuff plethysmography. Kidneys were then isolated, perfused with physiological solution containing L-NAME (NOS inhibitor) and diclofenac (cyclooxygenase inhibitor, DIC), and preconstricted with phenylephrine. CSA (25mgkg day for 7days) increased BP and augmented carbachol renal vasodilations. The co-treatment with verapamil (2mgkg day ) or nifedipine (3mgkg day ) abolished CSA hypertension and conversely affected carbachol vasodilations (increases vs. decreases). Infusion of MSPPOH (epoxyeicosatrienoic acids, EETs, inhibitor) reduced carbachol vasodilations in kidneys of all rat groups, suggesting the importance of EETs in these responses. By contrast, 20-Hydroxyeicosatetraenoic Acid (20-HETE) inhibition by HET0016 increased carbachol vasodilations in control rats, an effect that disappeared by CSA treatment, and reappeared in rats treated with CSA/verapamil or CSA/nifedipine. Renal protein expression of CYP2C and CYP4A as well as their vasoactive products (EETs/20-HETE) were increased in CSA-treated rats. Whereas the CYP2C/EETs effects of CSA were abolished by verapamil and intensified by nifedipine, the CYP4A/20-HETE effects were reduced by either CCB. Overall, nifedipine and verapamil blunts CSA hypertension but variably affected concomitantly enhanced EDHF-dependent renal vasodilations and alterations in CYP2C/CYP4A signaling.
[Mh] Termos MeSH primário: Fatores Biológicos/metabolismo
Bloqueadores dos Canais de Cálcio/farmacologia
Ciclosporina/farmacologia
Citocromo P-450 CYP4A/metabolismo
Sistema Enzimático do Citocromo P-450/metabolismo
Imunossupressores/farmacologia
[Mh] Termos MeSH secundário: Animais
Bloqueadores dos Canais de Cálcio/administração & dosagem
Ciclosporina/administração & dosagem
Citocromo P-450 CYP4A/genética
Sistema Enzimático do Citocromo P-450/genética
Interações Medicamentosas
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Imunossupressores/administração & dosagem
Rim/irrigação sanguínea
Masculino
Nifedipino/administração & dosagem
Nifedipino/farmacologia
Ratos
Ratos Sprague-Dawley
Vasodilatação/efeitos dos fármacos
Verapamil/administração & dosagem
Verapamil/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biological Factors); 0 (Calcium Channel Blockers); 0 (Immunosuppressive Agents); 0 (cytochrome P-450 CYP2C subfamily); 0 (endothelium-dependent hyperpolarization factor); 83HN0GTJ6D (Cyclosporine); 9035-51-2 (Cytochrome P-450 Enzyme System); CJ0O37KU29 (Verapamil); EC 1.14.15.3 (Cytochrome P-450 CYP4A); I9ZF7L6G2L (Nifedipine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170914
[St] Status:MEDLINE


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[PMID]:28612092
[Au] Autor:Quintanilha JCF; de Sousa VM; Visacri MB; Amaral LS; Santos RMM; Zambrano T; Salazar LA; Moriel P
[Ad] Endereço:School of Medical Sciences, University of Campinas (UNICAMP), Campinas, SP, Brazil.
[Ti] Título:Involvement of cytochrome P450 in cisplatin treatment: implications for toxicity.
[So] Source:Cancer Chemother Pharmacol;80(2):223-233, 2017 Aug.
[Is] ISSN:1432-0843
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: The aim of this study is to evaluate the relationship between the CYP450 enzyme family and cisplatin toxicity. METHODS: This article examined a collection of studies suggesting that CYP450 enzymes may influence cisplatin toxicity. We performed a narrative mini-review. RESULTS: The studies review showed that CYP450 enzymes have an important role in drug-induced hepatotoxicity and nephrotoxicity, mainly CYP2E1 and CYP4A11. The studies also suggested that the cisplatin and CYP2E1 interaction leads to the generation of reactive oxygen species (ROS) and other oxidants resulting in renal injury; and that ROS generated by both the use of cisplatin and by the CYP2E1 increases tissue damage, induces apoptosis, and causes liver failure. CONCLUSIONS: We observed that there is an important relationship between CYP450 and cisplatin, involving increased toxicity. However, the possible mechanisms described for the involvement of CYP450 enzymes in nephrotoxicity and hepatotoxicity induced by cisplatin need to be confirmed by further studies. Therefore, there is a need for a deeper investigation focusing on cisplatin toxicity mediated by CYP450 enzymes, which would undoubtedly contribute to a better understanding of the mechanisms that have been implicated so far.
[Mh] Termos MeSH primário: Antineoplásicos/efeitos adversos
Cisplatino/efeitos adversos
Sistema Enzimático do Citocromo P-450/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Doença Hepática Induzida por Substâncias e Drogas/enzimologia
Doença Hepática Induzida por Substâncias e Drogas/etiologia
Citocromo P-450 CYP2E1/metabolismo
Citocromo P-450 CYP4A/metabolismo
Seres Humanos
Nefropatias/induzido quimicamente
Nefropatias/enzimologia
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Reactive Oxygen Species); 9035-51-2 (Cytochrome P-450 Enzyme System); EC 1.14.13.- (Cytochrome P-450 CYP2E1); EC 1.14.15.3 (CYP4A11 protein, human); EC 1.14.15.3 (Cytochrome P-450 CYP4A); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170804
[Lr] Data última revisão:
170804
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170615
[St] Status:MEDLINE
[do] DOI:10.1007/s00280-017-3358-x


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[PMID]:28602979
[Au] Autor:Wang C; Li Y; Chen H; Zhang J; Zhang J; Qin T; Duan C; Chen X; Liu Y; Zhou X; Yang J
[Ad] Endereço:Department of Pharmacology, School of Basic Medical Sciences, Wuhan University, Wuhan, 430071, China.
[Ti] Título:Inhibition of CYP4A by a novel flavonoid FLA-16 prolongs survival and normalizes tumor vasculature in glioma.
[So] Source:Cancer Lett;402:131-141, 2017 Aug 28.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Glioblastomas rapidly become refractory to anti-VEGF therapies. We previously showed that cytochrome P450 (CYP) 4A-derived 20-hydroxyeicosatetraenoic acid (20-HETE) promotes angiogenesis. Here, we tested whether a novel flavonoid (FLA-16) prolongs survival and normalizes tumor vasculature in glioma through CYP4A inhibition. FLA-16 improved survival, reduced tumor burden, and normalized vasculature, accompanied with the decreased secretion of 20-HETE, VEGF and TGF-ß in tumor-associated macrophages (TAMs) and endothelial progenitor cells (EPCs) in C6 and U87 gliomas. FLA-16 attenuated vascular abnormalization induced by co-implantation of GL261 glioma cells with CYP4A10 macrophages or EPCs. Mechanistically, the conditional medium from TAMs and EPCs treated with FLA-16 enhanced the migration of pericyte cells, and decreased the proliferation and migration of endothelial cells, which were reversed by CYP4A overexpression or exogenous addition of 20-HETE, VEGF and TGF-ß. Furthermore, FLA-16 prevented crosstalk between TAMs and EPCs during angiogenesis. These results suggest that CYP4A inhibition by FLA-16 prolongs survival and normalizes vasculature in glioma through decreasing production of TAMs and EPCs-derived VEGF and TGF-ß. This may represent a potential therapeutic strategy to overcome resistance to anti-VEGF treatment by effects on vessels and immune cells.
[Mh] Termos MeSH primário: Inibidores da Angiogênese/farmacologia
Neoplasias Encefálicas/tratamento farmacológico
Chalconas/farmacologia
Citocromo P-450 CYP4A/antagonistas & inibidores
Inibidores das Enzimas do Citocromo P-450/farmacologia
Células Progenitoras Endoteliais/efeitos dos fármacos
Flavonoides/farmacologia
Glioma/tratamento farmacológico
Macrófagos/efeitos dos fármacos
Neovascularização Patológica
[Mh] Termos MeSH secundário: Animais
Neoplasias Encefálicas/irrigação sanguínea
Neoplasias Encefálicas/enzimologia
Neoplasias Encefálicas/patologia
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Meios de Cultivo Condicionados/metabolismo
Citocromo P-450 CYP4A/metabolismo
Relação Dose-Resposta a Droga
Resistência a Medicamentos Antineoplásicos
Células Progenitoras Endoteliais/enzimologia
Células Progenitoras Endoteliais/patologia
Glioma/irrigação sanguínea
Glioma/enzimologia
Glioma/patologia
Seres Humanos
Ácidos Hidroxieicosatetraenoicos/metabolismo
Macrófagos/enzimologia
Macrófagos/patologia
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Camundongos Nus
Comunicação Parácrina/efeitos dos fármacos
Pericitos/efeitos dos fármacos
Pericitos/metabolismo
Pericitos/patologia
Ratos Wistar
Fatores de Tempo
Fator de Crescimento Transformador beta/metabolismo
Carga Tumoral/efeitos dos fármacos
Microambiente Tumoral
Fator A de Crescimento do Endotélio Vascular/metabolismo
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenesis Inhibitors); 0 (Chalcones); 0 (Culture Media, Conditioned); 0 (Cytochrome P-450 Enzyme Inhibitors); 0 (FLA-16 compound); 0 (Flavonoids); 0 (Hydroxyeicosatetraenoic Acids); 0 (Transforming Growth Factor beta); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A); 79551-86-3 (20-hydroxy-5,8,11,14-eicosatetraenoic acid); EC 1.14.15.3 (Cytochrome P-450 CYP4A)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170613
[St] Status:MEDLINE


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[PMID]:28557975
[Au] Autor:Alnabulsi A; Swan R; Cash B; Alnabulsi A; Murray GI
[Ad] Endereço:Department of Pathology, School of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Foresterhill, Aberdeen AB25, 2ZD, UK.
[Ti] Título:The differential expression of omega-3 and omega-6 fatty acid metabolising enzymes in colorectal cancer and its prognostic significance.
[So] Source:Br J Cancer;116(12):1612-1620, 2017 Jun 06.
[Is] ISSN:1532-1827
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Colorectal cancer is a common malignancy and one of the leading causes of cancer-related deaths. The metabolism of omega fatty acids has been implicated in tumour growth and metastasis. METHODS: This study has characterised the expression of omega fatty acid metabolising enzymes CYP4A11, CYP4F11, CYP4V2 and CYP4Z1 using monoclonal antibodies we have developed. Immunohistochemistry was performed on a tissue microarray containing 650 primary colorectal cancers, 285 lymph node metastasis and 50 normal colonic mucosa. RESULTS: The differential expression of CYP4A11 and CYP4F11 showed a strong association with survival in both the whole patient cohort (hazard ratio (HR)=1.203, 95% CI=1.092-1.324, χ =14.968, P=0.001) and in mismatch repair-proficient tumours (HR=1.276, 95% CI=1.095-1.488, χ =9.988, P=0.007). Multivariate analysis revealed that the differential expression of CYP4A11 and CYP4F11 was independently prognostic in both the whole patient cohort (P=0.019) and in mismatch repair proficient tumours (P=0.046). CONCLUSIONS: A significant and independent association has been identified between overall survival and the differential expression of CYP4A11 and CYP4F11 in the whole patient cohort and in mismatch repair-proficient tumours.
[Mh] Termos MeSH primário: Neoplasias Colorretais/química
Neoplasias Colorretais/enzimologia
Citocromo P-450 CYP4A/análise
Família 4 do Citocromo P450/análise
[Mh] Termos MeSH secundário: Idoso
Colo/química
Neoplasias Colorretais/patologia
Reparo de Erro de Pareamento de DNA
Ácidos Graxos Ômega-3/metabolismo
Ácidos Graxos Ômega-6/metabolismo
Feminino
Seres Humanos
Mucosa Intestinal/química
Metástase Linfática
Masculino
Prognóstico
Taxa de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fatty Acids, Omega-3); 0 (Fatty Acids, Omega-6); EC 1.14.13.- (CYP4V2 protein, human); EC 1.14.13.194 (CYP4F11 protein, human); EC 1.14.14.1 (CYP4Z1 protein, human); EC 1.14.14.1 (Cytochrome P450 Family 4); EC 1.14.15.3 (CYP4A11 protein, human); EC 1.14.15.3 (Cytochrome P-450 CYP4A)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170531
[St] Status:MEDLINE
[do] DOI:10.1038/bjc.2017.135


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[PMID]:28533430
[Au] Autor:Albertolle ME; Kim D; Nagy LD; Yun CH; Pozzi A; Savas Ü; Johnson EF; Guengerich FP
[Ad] Endereço:From the Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-0146.
[Ti] Título:Heme-thiolate sulfenylation of human cytochrome P450 4A11 functions as a redox switch for catalytic inhibition.
[So] Source:J Biol Chem;292(27):11230-11242, 2017 Jul 07.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cytochrome P450 (P450, CYP) 4A11 is a human fatty acid ω-hydroxylase that catalyzes the oxidation of arachidonic acid to the eicosanoid 20-hydroxyeicosatetraenoic acid (20-HETE), which plays important roles in regulating blood pressure regulation. Variants of P450 4A11 have been associated with high blood pressure and resistance to anti-hypertensive drugs, and 20-HETE has both pro- and antihypertensive properties relating to increased vasoconstriction and natriuresis, respectively. These physiological activities are likely influenced by the redox environment, but the mechanisms are unclear. Here, we found that reducing agents ( dithiothreitol and tris(2-carboxyethyl)phosphine) strongly enhanced the catalytic activity of P450 4A11, but not of 10 other human P450s tested. Conversely, added H O attenuated P450 4A11 catalytic activity. Catalytic roles of five of the potentially eight implicated Cys residues of P450 4A11 were eliminated by site-directed mutagenesis. Using an isotope-coded dimedone/iododimedone-labeling strategy and mass spectrometry of peptides, we demonstrated that the heme-thiolate cysteine (Cys-457) is selectively sulfenylated in an H O concentration-dependent manner. This sulfenylation could be reversed by reducing agents, including dithiothreitol and dithionite. Of note, we observed heme ligand cysteine sulfenylation of P450 4A11 e in kidneys and livers derived from transgenic mice. We also detected sulfenylation of murine P450 4a12 and 4b1 heme peptides in kidneys. To our knowledge, reversible oxidation of the heme thiolate has not previously been observed in P450s and may have relevance for 20-HETE-mediated functions.
[Mh] Termos MeSH primário: Citocromo P-450 CYP4A/química
Ditiotreitol/química
Heme/química
Peróxido de Hidrogênio/química
[Mh] Termos MeSH secundário: Animais
Catálise
Citocromo P-450 CYP4A/genética
Citocromo P-450 CYP4A/metabolismo
Ditiotreitol/metabolismo
Heme/genética
Heme/metabolismo
Seres Humanos
Peróxido de Hidrogênio/metabolismo
Ácidos Hidroxieicosatetraenoicos/biossíntese
Ácidos Hidroxieicosatetraenoicos/química
Ácidos Hidroxieicosatetraenoicos/genética
Rim/enzimologia
Fígado/enzimologia
Camundongos
Camundongos Transgênicos
Oxirredução
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hydroxyeicosatetraenoic Acids); 42VZT0U6YR (Heme); 79551-86-3 (20-hydroxy-5,8,11,14-eicosatetraenoic acid); BBX060AN9V (Hydrogen Peroxide); EC 1.14.15.3 (CYP4A11 protein, human); EC 1.14.15.3 (Cytochrome P-450 CYP4A); T8ID5YZU6Y (Dithiothreitol)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170524
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.792200


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[PMID]:28481877
[Au] Autor:Chen XW; Yu TJ; Zhang J; Li Y; Chen HL; Yang GF; Yu W; Liu YZ; Liu XX; Duan CF; Tang HL; Qiu M; Wang CL; Zheng H; Yue J; Guo AM; Yang J
[Ad] Endereço:Department of Pharmacology, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
[Ti] Título:CYP4A in tumor-associated macrophages promotes pre-metastatic niche formation and metastasis.
[So] Source:Oncogene;36(35):5045-5057, 2017 Aug 31.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Tumor-associated macrophages (TAMs) play an essential role in metastasis. However, what enables TAMs to have a superior capacity to establish pre-metastatic microenvironment in distant organs is unclear. Here we have begun to uncover the effects of cytochrome P450 (CYP) 4A in TAMs on lung pre-metastatic niche formation and metastasis. CYP4A TAM infiltration was positively associated with metastasis, pre-metastatic niche formation and poor prognosis in breast cancer patients. The pharmacological inhibition of CYP4A reduced lung pre-metastatic niche formation (evidenced by a decrease in vascular endothelial growth factor receptor 1 positive (VEGFR1 ) myeloid cell recruitment and pro-metastatic protein expression) and metastatic burden, accompanied with TAM polarization away from the M2 phenotype in spontaneous metastasis models of 4T1 breast cancer and B16F10 melanoma. Co-implantation of 4T1 cells with CYP4A10 macrophages promoted lung pre-metastatic niche formation and metastasis. Depletion of TAMs disrupted lung pre-metastatic niches and thereby prevented metastasis. Treatment with the CM from CYP4A10 M2 macrophages (M2) increased pre-metastatic niche formation and metastatic burden in the lungs, whereas CYP4A inhibition attenuated these effects. In vitro TAM polarization away from the M2 phenotype induced by CYP4A inhibition decreased VEGFR1 myeloid cell migration and fibronectin expression, accompanied with downregulation of STAT3 signaling. Conversely, overexpression of CYP4A or exogenous addition of 20-hydroxyeicosatetraenoic acid promoted M2 polarization and cytokine production of macrophages and thereby enhanced migration of VEGFR1 myeloid cells, which were reversed by siRNA or pharmacological inhibition of STAT3. Importantly, a combined blocking M2 macrophage-derived factors TGF-ß, VEGF and SDF-1 abolished VEGFR1 myeloid cell migration and fibroblast activation induced by CYP4A. In summary, CYP4A in TAMs is crucial for lung pre-metastatic niche formation and metastasis, and may serve as a potential therapeutic target in human cancer.
[Mh] Termos MeSH primário: Neoplasias da Mama/enzimologia
Citocromo P-450 CYP4A/metabolismo
Macrófagos/enzimologia
Melanoma Experimental/enzimologia
[Mh] Termos MeSH secundário: Animais
Neoplasias da Mama/genética
Neoplasias da Mama/patologia
Linhagem Celular Tumoral
Citocromo P-450 CYP4A/genética
Feminino
Xenoenxertos
Seres Humanos
Macrófagos/patologia
Melanoma Experimental/genética
Melanoma Experimental/patologia
Camundongos
Camundongos Endogâmicos C57BL
Metástase Neoplásica
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 1.14.15.3 (Cytochrome P-450 CYP4A)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170509
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2017.118


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[PMID]:28328948
[Au] Autor:Hanif A; Edin ML; Zeldin DC; Morisseau C; Falck JR; Nayeem MA
[Ad] Endereço:Basic Pharmaceutical Sciences, School of Pharmacy, Center for Basic and Translational Stroke Research. West Virginia University, Morgantown, West Virginia, United States of America.
[Ti] Título:Vascular endothelial overexpression of human CYP2J2 (Tie2-CYP2J2 Tr) modulates cardiac oxylipin profiles and enhances coronary reactive hyperemia in mice.
[So] Source:PLoS One;12(3):e0174137, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Arachidonic acid is metabolized to epoxyeicosatrienoic acids (EETs) by cytochrome (CYP) P450 epoxygenases, and to ω-terminal hydroxyeicosatetraenoic acids (HETEs) by ω-hydroxylases. EETs and HETEs often have opposite biologic effects; EETs are vasodilatory and protect against ischemia/reperfusion injury, while ω-terminal HETEs are vasoconstrictive and cause vascular dysfunction. Other oxylipins, such as epoxyoctadecaenoic acids (EpOMEs), hydroxyoctadecadienoic acids (HODEs), and prostanoids also have varied vascular effects. Post-ischemic vasodilation in the heart, known as coronary reactive hyperemia (CRH), protects against potential damage to the heart muscle caused by ischemia. The relationship among CRH response to ischemia, in mice with altered levels of CYP2J epoxygenases has not yet been investigated. Therefore, we evaluated the effect of endothelial overexpression of the human cytochrome P450 epoxygenase CYP2J2 in mice (Tie2-CYP2J2 Tr) on oxylipin profiles and CRH. Additionally, we evaluated the effect of pharmacologic inhibition of CYP-epoxygenases and inhibition of ω-hydroxylases on CRH. We hypothesized that CRH would be enhanced in isolated mouse hearts with vascular endothelial overexpression of human CYP2J2 through modulation of oxylipin profiles. Similarly, we expected that inhibition of CYP-epoxygenases would reduce CRH, whereas inhibition of ω-hydroxylases would enhance CRH. Compared to WT mice, Tie2-CYP2J2 Tr mice had enhanced CRH, including repayment volume, repayment duration, and repayment/debt ratio (P < 0.05). Similarly, inhibition of ω-hydroxylases increased repayment volume and repayment duration, in Tie2-CYP2J2 Tr compared to WT mice (P < 0.05). Endothelial overexpression of CYP2J2 significantly changed oxylipin profiles, including increased EETs (P < 0.05), increased EpOMEs (P < 0.05), and decreased 8-iso-PGF2α (P < 0.05). Inhibition of CYP epoxygenases with MS-PPOH attenuated CRH (P < 0.05). Ischemia caused a decrease in mid-chain HETEs (5-, 11-, 12-, 15-HETEs P < 0.05) and HODEs (P < 0.05). These data demonstrate that vascular endothelial overexpression of CYP2J2, through changing the oxylipin profiles, enhances CRH. Inhibition of CYP epoxygenases decreases CRH, whereas inhibition of ω-hydroxylases enhances CRH.
[Mh] Termos MeSH primário: Sistema Enzimático do Citocromo P-450/metabolismo
Endotélio Vascular/metabolismo
Hiperemia/metabolismo
Oxilipinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Ácido Araquidônico/metabolismo
Citocromo P-450 CYP4A/metabolismo
Dinoprosta/análogos & derivados
Dinoprosta/metabolismo
Feminino
Coração/fisiologia
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Miocárdio/metabolismo
Traumatismo por Reperfusão/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Oxylipins); 27415-26-5 (8-epi-prostaglandin F2alpha); 27YG812J1I (Arachidonic Acid); 9035-51-2 (Cytochrome P-450 Enzyme System); B7IN85G1HY (Dinoprost); EC 1.14.14.1 (arachidonate epoxygenase); EC 1.14.15.3 (Cytochrome P-450 CYP4A)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170323
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0174137


  8 / 782 MEDLINE  
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[PMID]:28220441
[Au] Autor:Long H; Wang Y; Chang S; Liu G; Chen T; Huo G; Zhang W; Wu X; Tai X; Sun L; Zhang B
[Ad] Endereço:College of Bioscience and Bioengineering, Jiangxi Agricultural University, Nanchang, Jiangxi, 330045, China.
[Ti] Título:Diversity of crude oil-degrading bacteria and alkane hydroxylase (alkB) genes from the Qinghai-Tibet Plateau.
[So] Source:Environ Monit Assess;189(3):116, 2017 Mar.
[Is] ISSN:1573-2959
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to survey the response of the microbial community to crude oil and the diversity of alkane hydroxylase (alkB) genes in soil samples from the Qinghai-Tibet Plateau (QTP). The enrichment cultures and clone libraries were used. Finally, 53 isolates and 94 alkB sequences were obtained from 10 pristine soil samples after enrichment at 10 °C with crude oil as sole carbon source. The isolates fell into the phyla Proteobacteria, Actinobacteria, and Bacteroidetes, with the dominance of Pseudomonas and Acinetobacter. The composition of degraders was different from polar habitats where Acinetobacter sp. is not a predominant responder of alkane degradative microbial communities. Phylogenetic analysis showed that the alkB genes from isolates and enrichment communities formed eight clusters and mainly related with alkB genes of Pseudomonas, Rhodococcus, and Acinetobacter. The alkB gene diversity in the QTP was lower than marine environments and polar soil samples. In particular, a total of 10 isolates exhibiting vigorous growth with crude oil could detect no crude oil degradation-related gene sequences, such as alkB, P450, almA, ndoB, and xylE genes. The Shannon-Wiener index of the alkB clone libraries from the QTP ranged from 1.00 to 2.24 which is similar with polar pristine soil samples but lower than that of contaminated soils. These results indicated that the Pseudomonas, Acinetobacter, and Rhodococcus genera are the candidate for in situ bioremediation, and the environment of QTP may be still relatively uncontaminated by crude oil.
[Mh] Termos MeSH primário: Bactérias/classificação
Citocromo P-450 CYP4A/genética
Microbiologia do Solo
[Mh] Termos MeSH secundário: Biodegradação Ambiental
Monitoramento Ambiental
Genes Bacterianos
Petróleo
Filogenia
Tibet
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Petroleum); EC 1.14.15.3 (Cytochrome P-450 CYP4A)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170222
[St] Status:MEDLINE
[do] DOI:10.1007/s10661-017-5798-5


  9 / 782 MEDLINE  
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[PMID]:27745913
[Au] Autor:Gandolfi I; Canedoli C; Imperato V; Tagliaferri I; Gkorezis P; Vangronsveld J; Padoa Schioppa E; Papacchini M; Bestetti G; Franzetti A
[Ad] Endereço:Dept. of Earth and Environmental Sciences, University of Milano-Bicocca, Milan, Italy. Electronic address: isabella.gandolfi@unimib.it.
[Ti] Título:Diversity and hydrocarbon-degrading potential of epiphytic microbial communities on Platanus x acerifolia leaves in an urban area.
[So] Source:Environ Pollut;220(Pt A):650-658, 2017 Jan.
[Is] ISSN:1873-6424
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Plants and their associated bacteria have been suggested to play a role in air pollution mitigation, especially in urban areas. Particularly, epiphytic bacteria might be able to degrade atmospheric hydrocarbons. However, phyllospheric bacterial communities are highly variable depending on several factors, e.g. tree species, leaf age and physiology, environmental conditions. In this work, bacterial communities hosted by urban Platanus x acerifolia leaves were taxonomically characterized using high throughput sequencing of 16S rRNA gene, and their temporal and spatial variability was assessed by comparing samples collected from different locations in the city of Milan (Italy) and in different months. The diversity of alkane hydroxylase (alkB) phylotypes harboured by phyllospheric bacteria associated to urban Platanus trees was also evaluated. Results revealed that temporal changes, which are related to seasonality, acted as a stronger driver both on Platanus phyllospheric community structure and on alkB phylotype diversity than sampling location. Biodiversity of bacterial communities decreased along the growing season, leading to a strong dominance by the genus Stenotrophomonas. On the contrary, diversity of hydrocarbon-degrading populations increased over the months, although it resulted lower than that reported for other habitats. It was therefore hypothesized that atmospheric hydrocarbons might play a key role in the selection of phyllospheric populations in urban areas.
[Mh] Termos MeSH primário: Poluentes Atmosféricos/metabolismo
Hidrocarbonetos/metabolismo
Magnoliopsida/microbiologia
Folhas de Planta/microbiologia
Stenotrophomonas/classificação
Stenotrophomonas/metabolismo
Árvores/microbiologia
[Mh] Termos MeSH secundário: Biodegradação Ambiental
Biodiversidade
Citocromo P-450 CYP4A/genética
Itália
Filogenia
RNA Ribossômico 16S/genética
Estações do Ano
Stenotrophomonas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Air Pollutants); 0 (Hydrocarbons); 0 (RNA, Ribosomal, 16S); EC 1.14.15.3 (Cytochrome P-450 CYP4A)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161018
[St] Status:MEDLINE


  10 / 782 MEDLINE  
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[PMID]:27435360
[Au] Autor:Uehara S; Uno Y; Ishii S; Inoue T; Sasaki E; Yamazaki H
[Ad] Endereço:a Laboratory of Drug Metabolism and Pharmacokinetics , Showa Pharmaceutical University , Machida , Tokyo , Japan.
[Ti] Título:Marmoset cytochrome P450 4A11, a novel arachidonic acid and lauric acid ω-hydroxylase expressed in liver and kidney tissues.
[So] Source:Xenobiotica;47(7):553-561, 2017 Jul.
[Is] ISSN:1366-5928
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:1. A cDNA encoding novel cytochrome P450 (P450) 4A enzyme was cloned from marmoset livers by reverse transcription (RT)-polymerase chain reaction (PCR) based on the marmoset genome sequences. The amino acid sequence deduced from P450 4A11 cDNA contained consensus sequences of six substrate recognition sites and one heme-binding domain. 2. Marmoset P450 4A11, highly identical (85-88%) to cynomolgus monkey and human P450 4A enzymes, was grouped into the same cluster as cynomolgus monkey and human P450 4A enzymes by phylogenetic analysis. 3. The tissue distribution analyses by real-time RT PCR and immunoblotting demonstrated that marmoset P450 4A11 mRNA and proteins were expressed in kidneys and livers. Marmoset P450 4A11 enzyme heterologously expressed in Escherichia coli preferentially catalyzed the ω-hydroxylation of arachidonic acid and lauric acid, similar to cynomolgus monkey and human P450 4A11 enzymes. However, lauric acid ω-hydroxylation activity of marmoset P450 4A11 was low compared with those of marmoset liver microsomes. 4. These results indicated that novel marmoset P450 4A11 was also a fatty acid ω-hydroxylase expressed in kidneys and livers, with the same regioselectivity (at ω-position of fatty acid) as cynomolgus monkey and human P450 4A enzymes.
[Mh] Termos MeSH primário: Citocromo P-450 CYP4A/metabolismo
Rim/metabolismo
Fígado/metabolismo
[Mh] Termos MeSH secundário: Animais
Ácido Araquidônico
Callithrix
Macaca fascicularis/metabolismo
Microssomos Hepáticos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
27YG812J1I (Arachidonic Acid); EC 1.14.15.3 (Cytochrome P-450 CYP4A)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160721
[St] Status:MEDLINE
[do] DOI:10.1080/00498254.2016.1206673



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