| Role of neurogenic substance P in overexpression of alveolar macrophages' neurokinin 1 receptor in mice exposed to cigarette smoke. | |
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MedLine Citation:
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PMID: 20426532 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Neurokinin 1 receptors (NK1Rs) in alveolar macrophages (AMs) are overexpressed by cigarette smoke (CS) in vivo and substance P (SP) in vitro. Because CS could stimulate pulmonary C-fibers (PCFs) to release SP, we asked whether this neurogenic SP was responsible for AMs' NK1R overexpression during CS. We compared pulmonary SP and AMs' NK1R gene and protein levels in intact and PCF-degenerated mice exposed to filtered air (FA) and CS. Pulmonary SP was increased by CS but almost eliminated by PCF degeneration, which closely correlated to the changes in AMs' NK1R expression. Moreover, SP was higher in the PCF-degenerated mice exposed to CS than FA. To evaluate the direct effects of CS and SP on the NK1R expression and the involvement of nuclear factor (NF)-kappaB, macrophages were exposed to CS condensate (CSC) and/or SP without or with blocking NK1R or inhibiting NF-kappaB activation in vitro. CSC itself induced a moderate secretion of SP from macrophages, and amplified NK1R responses to SP that were completely eliminated by blocking NK1R, and substantially reduced after inhibiting NF-kappaB. Our results suggest that CS produces AMs' NK1R overexpression primarily by both promoting neurogenic SP release and synergizing NK1R response to neurogenic SP largely via activating NF-kappaB pathway. |
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Authors:
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Junyang Xu; Fadi Xu |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Experimental lung research Volume: 36 ISSN: 1521-0499 ISO Abbreviation: Exp. Lung Res. Publication Date: 2010 May |
Date Detail:
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Created Date: 2010-04-29 Completed Date: 2010-08-10 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8004944 Medline TA: Exp Lung Res Country: England |
Other Details:
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Languages: eng Pagination: 243-54 Citation Subset: IM |
Affiliation:
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Pathophysiology Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87108, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Dose-Response Relationship, Drug Lung / drug effects*, metabolism Macrophages, Alveolar / drug effects*, metabolism Mice Mice, Inbred C3H NF-kappa B / metabolism Receptors, Neurokinin-1 / metabolism* Receptors, Tachykinin / metabolism Substance P / metabolism* Tobacco Smoke Pollution / adverse effects* Up-Regulation |
| Grant Support | |
ID/Acronym/Agency:
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74183//PHS HHS |
| Chemical | |
Reg. No./Substance:
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0/NF-kappa B; 0/Receptors, Neurokinin-1; 0/Receptors, Tachykinin; 0/Tobacco Smoke Pollution; 33507-63-0/Substance P |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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