Role of ERK and JNK pathways in regulating cell motility and matrix metalloproteinase 9 production in growth factor-stimulated human epidermal keratinocytes
dc.contributor.author | Zeigler, Mary E. | en_US |
dc.contributor.author | Chi, Yiqing | en_US |
dc.contributor.author | Schmidt, Tanja | en_US |
dc.contributor.author | Varani, James | en_US |
dc.date.accessioned | 2006-04-19T13:34:30Z | |
dc.date.available | 2006-04-19T13:34:30Z | |
dc.date.issued | 1999-08 | en_US |
dc.identifier.citation | Zeigler, Mary E.; Chi, Yiqing; Schmidt, Tanja; Varani, James (1999)."Role of ERK and JNK pathways in regulating cell motility and matrix metalloproteinase 9 production in growth factor-stimulated human epidermal keratinocytes." Journal of Cellular Physiology 180(2): 271-284. <http://hdl.handle.net/2027.42/34441> | en_US |
dc.identifier.issn | 0021-9541 | en_US |
dc.identifier.issn | 1097-4652 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/34441 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=10395297&dopt=citation | en_US |
dc.description.abstract | Invasion is an essential cellular response that plays an important role in a number of physiological and pathological processes. Matrix metalloproteinase (MMP) production and cell movement are diverse cellular responses integral to the process of invasion. The complexity of the invasive process suggests the necessity of coordinate activation of more than one signaling pathway in order to activate specific factors responsible for regulating these cellular responses. In this report, we demonstrate that cell movement and MMP-9 production are both directly dependent on the activation of endogenous ERK signaling in hepatocyte growth factor (HGF)-or epidermal growth factor (EGF)-stimulated human epidermal keratinocytes. The kinetic profiles of endogenous MEK and ERK activity suggest that prolonged activation of these signal transducers is an underlying mechanism involved in stimulating cell motility and MMP-9 production. In support of this finding, a transient MEK/ERK signal elicited by keratinocyte growth factor (KGF) or insulin-like growth factor-1 (IGF-1) fails to stimulate these invasion-related responses. Specific inhibition of MEK leads to suppression of ERK activation, marked reduction in steady-state levels of c-Fos, and inhibition of cell movement and MMP-9 production. This occurs despite continued activation of JNK and c-Jun signaling in the presence of MEK-specific inhibition. In contrast, when JNK activity is specifically inhibited in HGF-stimulated cells, AP-1 activity is suppressed but cell motility is not affected. This evidence suggests that while ERK and JNK activity are necessary for AP-1 activation, ERK but not JNK is sufficient in stimulating cell motility. J. Cell. Physiol. 180:271–284, 1999. © 1999 Wiley-Liss, Inc. | en_US |
dc.format.extent | 299397 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | John Wiley & Sons, Inc. | en_US |
dc.subject.other | Life and Medical Sciences | en_US |
dc.subject.other | Cell & Developmental Biology | en_US |
dc.title | Role of ERK and JNK pathways in regulating cell motility and matrix metalloproteinase 9 production in growth factor-stimulated human epidermal keratinocytes | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Molecular, Cellular and Developmental Biology | en_US |
dc.subject.hlbsecondlevel | Kinesiology and Sports | 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 | Department of Pathology, The University of Michigan Medical School, Ann Arbor, Michigan ; Department of Pathology, University of Michigan, MS I, Box 0602, 1301 Catherine Road, Ann Arbor, MI 48109 | en_US |
dc.contributor.affiliationum | Department of Pathology, The University of Michigan Medical School, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Department of Pathology, The University of Michigan Medical School, Ann Arbor, Michigan | en_US |
dc.contributor.affiliationum | Department of Pathology, The University of Michigan Medical School, Ann Arbor, Michigan | en_US |
dc.identifier.pmid | 10395297 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/34441/1/15_ftp.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1002/(SICI)1097-4652(199908)180:2<271::AID-JCP15>3.0.CO;2-D | en_US |
dc.identifier.source | Journal of Cellular Physiology | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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