Monokine-induced gene expression of a human endothelial cell-derived neutrophil chemotactic factor
dc.contributor.author | Strieter, Robert M. | en_US |
dc.contributor.author | Kunkel, Steven L. | en_US |
dc.contributor.author | Showell, J. J. (Henry J.) | en_US |
dc.contributor.author | Marks, Rory M. | en_US |
dc.date.accessioned | 2006-04-07T20:08:47Z | |
dc.date.available | 2006-04-07T20:08:47Z | |
dc.date.issued | 1988-11-15 | en_US |
dc.identifier.citation | Strieter, R.M., Kunkel, S.L., Showell, H.J., Marks, R.M. (1988/11/15)."Monokine-induced gene expression of a human endothelial cell-derived neutrophil chemotactic factor." Biochemical and Biophysical Research Communications 156(3): 1340-1345. <http://hdl.handle.net/2027.42/27070> | en_US |
dc.identifier.uri | http://www.sciencedirect.com/science/article/B6WBK-4G3D5KD-136/2/655e04f809d5989eca7e048739afda38 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/27070 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=3263857&dopt=citation | en_US |
dc.description.abstract | Monokines have been increasingly recognized as communication signals that interact with both immune and non-immune cells during inflammation. Specifically, interleukin-1alpha (IL-lalpha), interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) possess potent effector activities on various cell types. We present novel data demonstrating that human endothelial cells are a major source of a neutrophil chemotactic factor (NCF) synthesized upon stimulation with either IL-1alpha, IL-1beta, or TNF-alpha; but not with interleukin-6 (IL-6). Northern blot analysis demonstrated that 20 ng/ml of either IL-1 or TNF-alpha could induce endothelial cells to express significant levels of NCF mRNA, while IL-6 was not active in this system. These data demonstrate that monokines play an important role in mediating acute inflammation via induction of an endothelial cell-derived NCF. | en_US |
dc.format.extent | 368464 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Elsevier | en_US |
dc.title | Monokine-induced gene expression of a human endothelial cell-derived neutrophil chemotactic factor | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Natural Resources and Environment | en_US |
dc.subject.hlbsecondlevel | Molecular, Cellular and Developmental Biology | en_US |
dc.subject.hlbsecondlevel | Ecology and Evolutionary Biology | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, The University of Michigan Medical School, Ann Arbor, Michigan, USA. | en_US |
dc.contributor.affiliationum | Department of Pathology, The University of Michigan Medical School, Ann Arbor, Michigan, USA | en_US |
dc.contributor.affiliationum | Department of Pathology, The University of Michigan Medical School, Ann Arbor, Michigan, USA | en_US |
dc.contributor.affiliationother | Department of Immunology, Pfizer Central Research, Groton, Connecticut, USA | en_US |
dc.identifier.pmid | 3263857 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/27070/1/0000060.pdf | en_US |
dc.identifier.source | Biochemical and Biophysical Research Communications | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
Files in this item
Remediation of Harmful Language
The University of Michigan Library aims to describe library materials in a way that respects the people and communities who create, use, and are represented in our collections. Report harmful or offensive language in catalog records, finding aids, or elsewhere in our collections anonymously through our metadata feedback form. More information at Remediation of Harmful Language.
Accessibility
If you are unable to use this file in its current format, please select the Contact Us link and we can modify it to make it more accessible to you.