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Article ; Online: Cannabinoid receptor 2 activation: a means to prevent monocyte-endothelium engagement.

Buch, Shilpa J

2013 Volume 183, Issue 5, Page(s) 1375–1377

Abstract: This Commentary highlights the article by Rom et al which shows that selective cannabinoid receptor 2 activation in leukocytes decreases key steps in monocyte-blood brain barrier engagement suppressing inflammatory leukocyte responses and preventing ... ...

Abstract	This Commentary highlights the article by Rom et al which shows that selective cannabinoid receptor 2 activation in leukocytes decreases key steps in monocyte-blood brain barrier engagement suppressing inflammatory leukocyte responses and preventing neuroinflammation.
MeSH term(s)	Animals ; Blood-Brain Barrier/metabolism ; Blood-Brain Barrier/pathology ; Endothelium/metabolism ; Humans ; Leukocytes/metabolism ; Receptor, Cannabinoid, CB2/metabolism
Chemical Substances	Receptor, Cannabinoid, CB2
Language	English
Publishing date	2013-11
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2013.08.003
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Article ; Online: Neuroimmune pharmacology as an emerging curriculum for pre-medical students.

Buch, Shilpa J

Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology

2010 Volume 6, Issue 1, Page(s) 68–70

Abstract: As science continues to evolve and expand some major areas of interest are now crossing boundaries to become multi-disciplinary in nature closely reflecting the biological processes of the organism as a whole. The fields of neuroscience, immunology, and ... ...

Abstract	As science continues to evolve and expand some major areas of interest are now crossing boundaries to become multi-disciplinary in nature closely reflecting the biological processes of the organism as a whole. The fields of neuroscience, immunology, and pharmacology are good examples of one such emerging inter-disciplinary area. This article is focused on developing a curriculum for undergraduate pre-medical students in the area of neuroimmune pharmacology (NIP) to empower them with the knowledge of neuroscience and its interaction with immune responses and drug interactions. This course is intended to amalgamate and put into perspective a large body of knowledge including: (1) brain function in health and disease, (2) cross talk between neural and immune responses, and (3) the pharmacology of drugs of abuse in the context of neurodegenerative diseases. The goal of this course is to expose pre-medical students to the field of NIP so that they are equipped with a solid foundation in these multidisciplinary fields for future clinical/academic careers.
MeSH term(s)	Allergy and Immunology/education ; Curriculum ; Education, Premedical/methods ; Humans ; Neurosciences/education ; Pharmacology/education ; Students, Premedical
Language	English
Publishing date	2010-07-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2227405-4
ISSN	1557-1904 ; 1557-1890
ISSN (online)	1557-1904
ISSN	1557-1890
DOI	10.1007/s11481-010-9229-4
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Article ; Online: HIV-1 Nef hijacks both exocytic and endocytic pathways of host intracellular trafficking through differential regulation of Rab GTPases.

Kumari, Sushila / Dash, Prasanta K / Kumari, Tripti / Guo, Ming-Lei / Ghosh, Jimut Kanti / Buch, Shilpa J / Tripathi, Raj Kamal

Biology of the cell

2022 Volume 114, Issue 10, Page(s) 276–292

Abstract: Background: HIV-1 Nef regulates several cellular functions in an infected cell which results in viral persistence and AIDS pathogenesis. The currently understood molecular mechanism(s) underlying Nef-dependent cellular function(s) are unable to explain ... ...

Abstract	Background: HIV-1 Nef regulates several cellular functions in an infected cell which results in viral persistence and AIDS pathogenesis. The currently understood molecular mechanism(s) underlying Nef-dependent cellular function(s) are unable to explain how events are coordinately regulated in the host cell. Intracellular membranous trafficking maintains cellular homeostasis and is regulated by Rab GTPases - a member of the Ras superfamily. Results: In the current study, we tried to decipher the role of Nef on the Rab GTPases-dependent complex and vesicular trafficking. Expression profiling of Rabs in Nef-expressing cells showed that Nef differentially regulates the expression of individual Rabs in a cell-specific manner. Further analysis of Rabs in HIV-1 Conclusion: This study demonstrates that Nef differentially regulates the expression of Rab proteins in HIV-1 infected cells to hijack the host intracellular trafficking, which augments viral replication and HIV-1 pathogenesis. Significance: Our study emphasized the indispensable role of HIV-1 protein Nef on various aspects of the intracellular trafficking regulated by Rabs GTPases, which explained how HIV-1 Nef may hijack membrane trafficking pathways in infected cells.
MeSH term(s)	HIV-1/physiology ; Membrane Proteins/metabolism ; Virion/chemistry ; Virion/metabolism ; nef Gene Products, Human Immunodeficiency Virus/analysis ; nef Gene Products, Human Immunodeficiency Virus/metabolism ; rab GTP-Binding Proteins/metabolism
Chemical Substances	Membrane Proteins ; nef Gene Products, Human Immunodeficiency Virus ; rab GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2022-08-07
Publishing country	England
Document type	Journal Article
ZDB-ID	245745-3
ISSN	1768-322X ; 0399-0311 ; 0248-4900
ISSN (online)	1768-322X
ISSN	0399-0311 ; 0248-4900
DOI	10.1111/boc.202100027
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Zs.A 758: Show issues

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Article: Systems biology analyses reveal enhanced chronic morphine distortion of gut-brain interrelationships in simian human immunodeficiency virus infected rhesus macaques.

Olwenyi, Omalla A / Johnson, Samuel D / Bidokhti, Mehdi / Thakur, Vandana / Pandey, Kabita / Thurman, Michellie / Acharya, Arpan / Uppada, Srijayaprakash / Callen, Shannon / Giavedoni, Luis / Ranga, Udaykumar / Buch, Shilpa J / Byrareddy, Siddappa N

Frontiers in neuroscience

2022 Volume 16, Page(s) 1001544

Abstract: Background: Commonly used opioids, such as morphine have been implicated in augmented SIV/HIV persistence within the central nervous system (CNS). However, the extent of myeloid cell polarization and viral persistence in different brain regions remains ... ...

Abstract	Background: Commonly used opioids, such as morphine have been implicated in augmented SIV/HIV persistence within the central nervous system (CNS). However, the extent of myeloid cell polarization and viral persistence in different brain regions remains unclear. Additionally, the additive effects of morphine on SIV/HIV dysregulation of gut-brain crosstalk remain underexplored. Therefore, studies focused on understanding how drugs of abuse such as morphine affect immune dynamics, viral persistence and gut-brain interrelationships are warranted. Materials and methods: For a total of 9 weeks, rhesus macaques were ramped-up, and twice daily injections of either morphine ( Results: Flow Cytometry-based semi-supervised analysis revealed that morphine exposure led to exacerbated M1 (CD14/CD16)/M2 (CD163/CD206) polarization in activated microglia that spanned across diverse brain regions. This was accompanied by elevated SHIV DNA within the sites of neurogenesis-HIP and SVZ. HIP/SVZ CD16+ activated microglia positively correlated with SHIV DNA levels in the brain ( Conclusion: These findings are suggestive that morphine promotes CNS inflammation by altering receptor modulation, increasing myeloid brain activation, distorting gut-brain crosstalk, and causing selective enhancement of SHIV persistence in sites of neurogenesis.
Language	English
Publishing date	2022-10-13
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2022.1001544
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Article ; Online: Diminished Peripheral CD29hi Cytotoxic CD4+ T Cells Are Associated With Deleterious Effects During SIV Infection.

Olwenyi, Omalla A / Johnson, Samuel D / Pandey, Kabita / Thurman, Michellie / Acharya, Arpan / Buch, Shilpa J / Fox, Howard S / Podany, Anthony T / Fletcher, Courtney V / Byrareddy, Siddappa N

Frontiers in immunology

2021 Volume 12, Page(s) 734871

Abstract: Cytotoxic CD4+ T cells (CD4+ CTLs) limit HIV pathogenesis, as evidenced in elite controllers (a subset of individuals who suppress the virus without the need for therapy). CD4+ CTLs have also been shown to kill HIV-infected macrophages. However, little ... ...

Abstract	Cytotoxic CD4+ T cells (CD4+ CTLs) limit HIV pathogenesis, as evidenced in elite controllers (a subset of individuals who suppress the virus without the need for therapy). CD4+ CTLs have also been shown to kill HIV-infected macrophages. However, little is known about their contribution towards HIV persistence, how they are affected following exposure to immune modulators like morphine, and what factors maintain their frequencies and function. Further, the lack of robust markers to identify CD4+ CTLs in various animal models limits understanding of their role in HIV pathogenesis. We utilized various PBMC samples obtained from SIV infected and cART treated rhesus macaques exposed to morphine or saline and subjected to flow cytometry evaluations. Thereafter, we compared and correlated the expression of CD4+ CTL-specific markers to viral load and viral reservoir estimations in total CD4+ T cells. We found that CD29 could be reliably used as a marker to identify CD4+ CTLs in rhesus macaques since CD29hi CD4+ T cells secrete higher cytotoxic and proinflammatory cytokines following PMA/ionomycin or gag stimulation. In addition, this immune cell subset was depleted during untreated SIV infection. Strikingly, we also observed that early initiation of cART reconstitutes depleted CD29hi CD4+ T cells and restores their function. Furthermore, we noted that morphine exposure reduced the secretion of proinflammatory cytokines/cytotoxic molecules in CD29hi CD4+ T cells. Lastly, increased functionality of CD29hi CD4+ T cells as depicted by elevated levels of either IL-21 or granzyme B hi T Bet+ gag specific responses were linked to limiting the size of the replication-competent reservoir during cART treatment. Collectively, our data suggest that CD4+ CTLs are crucial in limiting SIV pathogenesis and persistence.
MeSH term(s)	Animals ; Anti-Retroviral Agents/pharmacology ; Cells, Cultured ; Cytokines/metabolism ; Cytotoxicity, Immunologic ; Disease Models, Animal ; Host-Pathogen Interactions ; Integrin beta1/metabolism ; Macaca mulatta ; Morphine/pharmacology ; Phenotype ; Simian Acquired Immunodeficiency Syndrome/drug therapy ; Simian Acquired Immunodeficiency Syndrome/immunology ; Simian Acquired Immunodeficiency Syndrome/metabolism ; Simian Acquired Immunodeficiency Syndrome/virology ; Simian Immunodeficiency Virus/drug effects ; Simian Immunodeficiency Virus/growth & development ; Simian Immunodeficiency Virus/immunology ; T-Lymphocytes, Cytotoxic/drug effects ; T-Lymphocytes, Cytotoxic/immunology ; T-Lymphocytes, Cytotoxic/metabolism ; T-Lymphocytes, Cytotoxic/virology ; Viral Load ; Virus Replication
Chemical Substances	Anti-Retroviral Agents ; Cytokines ; Integrin beta1 ; Morphine (76I7G6D29C)
Language	English
Publishing date	2021-10-13
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.734871
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Article ; Online: Chronic morphine administration differentially modulates viral reservoirs in SIVmac251 infected rhesus macaque model.

Acharya, Arpan / Olwenyi, Omalla A / Thurman, Michellie / Pandey, Kabita / Morsey, Brenda M / Lamberty, Benjamin / Ferguson, Natasha / Callen, Shannon / Fang, Qiu / Buch, Shilpa J / Fox, Howard S / Byrareddy, Siddappa N

Journal of virology

2020 Volume 95, Issue 5

Abstract: HIV persists in cellular reservoirs despite effective combined antiretroviral therapy (cART) and there is viremia flare up upon therapy interruption. Opioids modulate the immune system and suppress antiviral gene responses, which significantly impact ... ...

Abstract	HIV persists in cellular reservoirs despite effective combined antiretroviral therapy (cART) and there is viremia flare up upon therapy interruption. Opioids modulate the immune system and suppress antiviral gene responses, which significantly impact people living with HIV (PLWH). However, the effect of opioids on viral reservoir dynamics remain elusive. Herein, we developed a morphine dependent SIVmac251 infected
Language	English
Publishing date	2020-12-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.01657-20
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Zs.A 609: Show issues

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Article ; Online: Chronic SIV and morphine treatment increases heat shock protein 5 expression at the synapse.

Pendyala, Gurudutt / Periyasamy, Palsamy / Callen, Shannon / Fox, Howard S / Lisco, Steven J / Buch, Shilpa J

Journal of neurovirology

2015 Volume 21, Issue 5, Page(s) 592–598

Abstract: The abuse of opiates such as morphine in synergy with HIV infection accelerates neurocognitive impairments and neuropathology in the CNS of HIV-infected subjects, collectively referred to as HAND. To identify potential pathogenic markers associated with ... ...

Abstract	The abuse of opiates such as morphine in synergy with HIV infection accelerates neurocognitive impairments and neuropathology in the CNS of HIV-infected subjects, collectively referred to as HAND. To identify potential pathogenic markers associated with HIV and morphine in perturbing the synaptic architecture, we performed quantitative mass spectrometry proteomics on purified synaptosomes isolated from the caudate of two groups of rhesus macaques chronically infected with SIV differing by one regimen-morphine treatment. The upregulation of heat shock 70-kDa protein 5 in the SIV + morphine group points to increased cellular stress during SIV/morphine interaction thus leading to CNS dysfunction.
MeSH term(s)	Analgesics, Opioid/toxicity ; Animals ; Blotting, Western ; Cell Line ; Heat-Shock Proteins/biosynthesis ; Humans ; Macaca mulatta ; Morphine/toxicity ; Neurons/drug effects ; Proteomics/methods ; Real-Time Polymerase Chain Reaction ; Simian Acquired Immunodeficiency Syndrome/metabolism ; Simian Acquired Immunodeficiency Syndrome/pathology ; Simian Immunodeficiency Virus ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; Synapses/drug effects ; Synapses/metabolism ; Synaptosomes/drug effects ; Synaptosomes/metabolism ; Up-Regulation
Chemical Substances	Analgesics, Opioid ; Heat-Shock Proteins ; molecular chaperone GRP78 ; Morphine (76I7G6D29C)
Language	English
Publishing date	2015-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1283265-0
ISSN	1538-2443 ; 1355-0284
ISSN (online)	1538-2443
ISSN	1355-0284
DOI	10.1007/s13365-015-0356-9
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Article ; Online: HIV-1 Tat-mediated neurotoxicity in retinal cells.

Chatterjee, Nivedita / Callen, Shannon / Seigel, Gail M / Buch, Shilpa J

Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology

2011 Volume 6, Issue 3, Page(s) 399–408

Abstract: The current study was aimed at investigating the effect of HIV-1 protein Tat on the retinal neurosensory cell line R28. Exposure of Tat resulted in induction of pro-inflammatory mediators such as CXCL10 and TNF-α in addition to the activation marker GFAP ...

Abstract	The current study was aimed at investigating the effect of HIV-1 protein Tat on the retinal neurosensory cell line R28. Exposure of Tat resulted in induction of pro-inflammatory mediators such as CXCL10 and TNF-α in addition to the activation marker GFAP in these cells. Conditioned media from Tat-treated R28 cells was able to induce monocyte migration, an effect that was blocked by CXCR3 antagonist. Complementary studies in the HIV-1 Tat-transgenic mice, showed a complete absence of the nuclear layer and the outer photoreceptor segments of the retina with a concomitant increase in glial activation. These findings lend support to the observation in post-HAART era of increased incidence of immune response-mediated retinal degeneration. These findings have direct relevance to diseases such as immune response uveitis and patients recovering from CMV retinitis.
MeSH term(s)	Animals ; Cell Line ; Cell Proliferation ; Cell Survival/drug effects ; Chemokine CXCL10/biosynthesis ; Immunohistochemistry ; Mice ; Mice, Transgenic ; Photoreceptor Cells, Vertebrate/drug effects ; Photoreceptor Cells, Vertebrate/metabolism ; Photoreceptor Cells, Vertebrate/virology ; RNA, Messenger/analysis ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction ; Tumor Necrosis Factor-alpha/biosynthesis ; tat Gene Products, Human Immunodeficiency Virus/metabolism ; tat Gene Products, Human Immunodeficiency Virus/pharmacology
Chemical Substances	Chemokine CXCL10 ; RNA, Messenger ; Tumor Necrosis Factor-alpha ; tat Gene Products, Human Immunodeficiency Virus
Language	English
Publishing date	2011-01-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2227405-4
ISSN	1557-1904 ; 1557-1890
ISSN (online)	1557-1904
ISSN	1557-1890
DOI	10.1007/s11481-011-9257-8
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Article ; Online: HIV-1 transgenic rats display mitochondrial abnormalities consistent with abnormal energy generation and distribution.

Villeneuve, Lance M / Purnell, Phillip R / Stauch, Kelly L / Callen, Shannon E / Buch, Shilpa J / Fox, Howard S

Journal of neurovirology

2016 Volume 22, Issue 5, Page(s) 564–574

Abstract: With the advent of the combination antiretroviral therapy era (cART), the development of AIDS has been largely limited in the USA. Unfortunately, despite the development of efficacious treatments, HIV-1-associated neurocognitive disorders (HAND) can ... ...

Abstract	With the advent of the combination antiretroviral therapy era (cART), the development of AIDS has been largely limited in the USA. Unfortunately, despite the development of efficacious treatments, HIV-1-associated neurocognitive disorders (HAND) can still develop, and as many HIV-1 positive individuals age, the prevalence of HAND is likely to rise because HAND manifests in the brain with very low levels of virus. However, the mechanism producing this viral disorder is still debated. Interestingly, HIV-1 infection exposes neurons to proteins including Tat, Nef, and Vpr which can drastically alter mitochondrial properties. Mitochondrial dysfunction has been posited to be a cornerstone of the development of numerous neurodegenerative diseases. Therefore, we investigated mitochondria in an animal model of HAND. Using an HIV-1 transgenic rat model expressing seven of the nine HIV-1 viral proteins, mitochondrial functional and proteomic analysis were performed on a subset of mitochondria that are particularly sensitive to cellular changes, the neuronal synaptic mitochondria. Quantitative mass spectroscopic studies followed by statistical analysis revealed extensive proteome alteration in this model paralleling mitochondrial abnormalities identified in HIV-1 animal models and HIV-1-infected humans. Novel mitochondrial protein changes were discovered in the electron transport chain (ETC), the glycolytic pathways, mitochondrial trafficking proteins, and proteins involved in various energy pathways, and these findings correlated well with the function of the mitochondria as assessed by a mitochondrial coupling and flux assay. By targeting these proteins and proteins upstream in the same pathway, we may be able to limit the development of HAND.
Language	English
Publishing date	2016-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	1283265-0
ISSN	1538-2443 ; 1355-0284
ISSN (online)	1538-2443
ISSN	1355-0284
DOI	10.1007/s13365-016-0424-9
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Zs.A 4426: Show issues

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Article ; Online: Reactive Oxygen Species/Hypoxia-Inducible Factor-1α/Platelet-Derived Growth Factor-BB Autocrine Loop Contributes to Cocaine-Mediated Alveolar Epithelial Barrier Damage.

Yang, Lu / Chen, Xufeng / Simet, Samantha M / Hu, Guoku / Cai, Yu / Niu, Fang / Kook, Yeonhee / Buch, Shilpa J

American journal of respiratory cell and molecular biology

2016 Volume 55, Issue 5, Page(s) 736–748

Abstract: Abuse of psychostimulants, such as cocaine, has been shown to be closely associated with complications of the lung, such as pulmonary hypertension, edema, increased inflammation, and infection. However, the mechanism by which cocaine mediates impairment ... ...

Abstract	Abuse of psychostimulants, such as cocaine, has been shown to be closely associated with complications of the lung, such as pulmonary hypertension, edema, increased inflammation, and infection. However, the mechanism by which cocaine mediates impairment of alveolar epithelial barrier integrity that underlies various pulmonary complications has not been well determined. Herein, we investigate the role of cocaine in disrupting the alveolar epithelial barrier function and the associated signaling cascade. Using the combinatorial electric cell-substrate impedance sensing and FITC-dextran permeability assays, we demonstrated cocaine-mediated disruption of the alveolar epithelial barrier, as evidenced by increased epithelial monolayer permeability with a concomitant loss of the tight junction protein zonula occludens-1 (Zo-1) in both mouse primary alveolar epithelial cells and the alveolar epithelial cell line, L2 cells. To dissect the signaling pathways involved in this process, we demonstrated that cocaine-mediated induction of permeability factors, platelet-derived growth factor (PDGF-BB) and vascular endothelial growth factor, involved reactive oxygen species (ROS)-dependent induction of hypoxia-inducible factor (HIF)-1α. Interestingly, we demonstrated that ROS-dependent induction of another transcription factor, nuclear factor erythroid-2-related factor-2, that did not play a role in cocaine-mediated barrier dysfunction. Importantly, this study identifies, for the first time, that ROS/HIF-1α/PDGF-BB autocrine loop contributes to cocaine-mediated barrier disruption via amplification of oxidative stress and downstream signaling. Corroboration of these cell culture findings in vivo demonstrated increased permeability of the alveolar epithelial barrier, loss of expression of Zo-1, and a concomitantly increased expression of both HIF-1α and PDGF-BB. Pharmacological blocking of HIF-1α significantly abrogated cocaine-mediated loss of Zo-1. Understanding the mechanism(s) by which cocaine mediates barrier dysfunction could provide insights into the development of potential therapeutic targets for cocaine-mediated pulmonary hypertension.
MeSH term(s)	Alveolar Epithelial Cells/drug effects ; Alveolar Epithelial Cells/metabolism ; Alveolar Epithelial Cells/pathology ; Animals ; Autocrine Communication ; Cell Membrane Permeability/drug effects ; Cocaine/adverse effects ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Mice, Inbred C57BL ; NF-E2-Related Factor 2/metabolism ; Proto-Oncogene Proteins c-sis/metabolism ; Reactive Oxygen Species/metabolism ; Vascular Endothelial Growth Factor A/metabolism
Chemical Substances	Hypoxia-Inducible Factor 1, alpha Subunit ; NF-E2-Related Factor 2 ; Nfe2l2 protein, mouse ; Proto-Oncogene Proteins c-sis ; Reactive Oxygen Species ; Vascular Endothelial Growth Factor A ; becaplermin (1B56C968OA) ; Cocaine (I5Y540LHVR)
Language	English
Publishing date	2016-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2016-0096OC
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