| Multi-pathway network analysis of mammalian epithelial cell responses in inflammatory environments. | |
| | |
MedLine Citation:
|
PMID: 22260679 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
|
Inflammation is a key physiological response to infection and injury and, although usually beneficial, it can also be damaging to the host. The liver is a prototypical example in this regard because inflammation helps to resolve liver injury, but it also underlies the aetiology of pathologies such as fibrosis and hepatocellular carcinoma. Liver cells sense their environment, including the inflammatory environment, through the activities of receptor-mediated signal transduction pathways. These pathways are organized in a complex interconnected network, and it is becoming increasingly recognized that cellular adaptations result from the quantitative integration of multi-pathway network activities, rather than isolated pathways causing particular phenotypes. Therefore comprehending liver cell signalling in inflammation requires a scientific approach that is appropriate for studying complex networks. In the present paper, we review our application of systems analyses of liver cell signalling in response to inflammatory environments. Our studies feature broad measurements of cell signalling and phenotypes in response to numerous experimental perturbations reflective of inflammatory environments, the data from which are analysed using Boolean and fuzzy logic models and regression-based methods in order to quantitatively relate the phenotypic responses to cell signalling network states. Our principal biological insight from these studies is that hepatocellular carcinoma cells feature uncoupled inflammatory and growth factor signalling, which may underlie their immune evasion and hyperproliferative properties. |
| | |
Authors:
|
David C Clarke; Douglas A Lauffenburger |
Related Documents
:
|
15371279 - Interaction between no and cox pathways in retinal cells exposed to elevated glucose an... 18640269 - Prostaglandin e(2)-loaded microspheres as strategy to inhibit phagocytosis and modulate... 9428719 - Prostaglandin e2 biphasic control of lymphocyte proliferation: inhibition by picomolar ... 19534809 - Deoxycholate induces cox-2 expression via erk1/2-, p38-mapk and ap-1-dependent mechanis... 21715489 - Nf-kappab protects human papillomavirus type 38 e6/e7-immortalized human keratinocytes ... 22262759 - Pretreatment with carbon monoxide releasing molecules suppresses hepcidin expression du... 16084019 - Bax-regulated mitochondria-mediated apoptosis is responsible for the in vitro ischemia ... 16982929 - Novel approach to inhibit asthma-mediated lung inflammation using anti-cd147 intervention. 12844389 - The oral immunogenicity of bioprotein, a bacterial single-cell protein, is affected by ... |
Publication Detail:
|
Type: Journal Article |
Journal Detail:
|
Title: Biochemical Society transactions Volume: 40 ISSN: 1470-8752 ISO Abbreviation: Biochem. Soc. Trans. Publication Date: 2012 Feb |
Date Detail:
|
Created Date: 2012-01-20 Completed Date: - Revised Date: - |
Medline Journal Info:
|
Nlm Unique ID: 7506897 Medline TA: Biochem Soc Trans Country: England |
Other Details:
|
Languages: eng Pagination: 133-8 Citation Subset: IM |
Affiliation:
|
Department of Biological Engineering and the Center for Cellular Decision Processes, Massachusetts Institute of Technology, 77 Mass Ave., Cambridge, MA 02139, U.S.A. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Cell migration and invasion in human disease: the Tks adaptor proteins.
Next Document: Cross-talk between mitogenic Ras/MAPK and survival PI3K/Akt pathways: a fine balance.