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231224s2017 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2017.01.002
|2 doi
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|a pubmed24n0893.xml
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|a (DE-627)NLM268056242
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|a (NLM)28093362
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|a (PII)S1521-6616(16)30537-X
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|a DE-627
|b ger
|c DE-627
|e rakwb
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| 041 |
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|a eng
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| 100 |
1 |
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|a Dewitz, Carola
|e verfasserin
|4 aut
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| 245 |
1 |
0 |
|a Hypoxia-inducible factor-1α inhibition modulates airway hyperresponsiveness and nitric oxide levels in a BALB/c mouse model of asthma
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|c 2017
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| 336 |
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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| 338 |
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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| 500 |
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|a Date Completed 05.06.2017
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|a Date Revised 14.12.2018
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Published by Elsevier Inc.
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|a Hypoxia-inducible factor (HIF)-1α is a master regulator of inflammation and is upregulated in alveolar macrophages and lung parenchyma in asthma. HIF-1α regulates select pathways in allergic inflammation, and thus may drive particular asthma phenotypes. This work examines the role of pharmacologic HIF-1α inhibition in allergic inflammatory airway disease (AIAD) pathogenesis in BALB/c mice, which develop an airway hyperresponsiveness (AHR) asthma phenotype. Systemic treatment with HIF-1α antagonist YC-1 suppressed the increase in HIF-1α expression seen in control AIAD mice. Treatment with YC-1 also decreased AHR, blood eosinophilia, and allergic inflammatory gene expression: IL-5, IL-13, myeloperoxidase and iNOS. AIAD mice had elevated BAL levels of NO, and treatment with YC-1 eliminated this response. However, YC-1 did not decrease BAL, lung or bone marrow eosinophilia. We conclude that HIF-1α inhibition in different genetic backgrounds, and thus different AIAD phenotypes, decreases airway resistance and markers of inflammation in a background specific manner
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| 520 |
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|a CAPSULE SUMMARY: Asthma is a common disease that can be difficult to control with current therapeutics. We describe how pharmacologic targeting of a specific transcription factor, HIF-1α, suppresses asthmatic airway reactivity and inflammation
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|a Journal Article
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|a Research Support, U.S. Gov't, Non-P.H.S.
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|a Research Support, Non-U.S. Gov't
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| 650 |
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|a Allergic inflammation
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| 650 |
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4 |
|a Asthma
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| 650 |
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4 |
|a Eosinophils
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| 650 |
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4 |
|a Hypoxia inducible factor (HIF)-1α
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| 650 |
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4 |
|a Nitric oxide
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| 650 |
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4 |
|a YC-1
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| 650 |
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7 |
|a Hypoxia-Inducible Factor 1, alpha Subunit
|2 NLM
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| 650 |
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7 |
|a Interleukin-13
|2 NLM
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| 650 |
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7 |
|a Interleukin-5
|2 NLM
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| 650 |
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7 |
|a Nitric Oxide
|2 NLM
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| 650 |
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7 |
|a 31C4KY9ESH
|2 NLM
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| 650 |
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7 |
|a Nitric Oxide Synthase Type II
|2 NLM
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| 650 |
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7 |
|a EC 1.14.13.39
|2 NLM
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| 700 |
1 |
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|a McEachern, Elisa
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Shin, Stephanie
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Akong, Kathryn
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Nagle, Dale G
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Broide, David H
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Akuthota, Praveen
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Crotty Alexander, Laura E
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 176(2017) vom: 01. März, Seite 94-99
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
1 |
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|g volume:176
|g year:2017
|g day:01
|g month:03
|g pages:94-99
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| 856 |
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|u http://dx.doi.org/10.1016/j.clim.2017.01.002
|3 Volltext
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|a AR
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|d 176
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