W
William C. Parks
Researcher at Cedars-Sinai Medical Center
Publications - 247
Citations - 25887
William C. Parks is an academic researcher from Cedars-Sinai Medical Center. The author has contributed to research in topics: Matrix metalloproteinase & Extracellular matrix. The author has an hindex of 77, co-authored 240 publications receiving 24092 citations. Previous affiliations of William C. Parks include Washington University in St. Louis & Harborview Medical Center.
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Journal ArticleDOI
Matrix metalloproteinases as modulators of inflammation and innate immunity
TL;DR: Recent findings indicate that matrix metalloproteinases act on pro-inflammatory cytokines, chemokines and other proteins to regulate varied aspects of inflammation and immunity.
Journal ArticleDOI
Regulation of Intestinal α-Defensin Activation by the Metalloproteinase Matrilysin in Innate Host Defense
Carole L. Wilson,Andre J. Ouellette,Donald P. Satchell,Tokiyoshi Ayabe,Yolanda S. López-Boado,Jennifer L. Stratman,Scott J. Hultgren,Lynn M. Matrisian,William C. Parks +8 more
TL;DR: This article showed that matrilysin functions in intestinal mucosal defense by regulating the activity of defensins, which may be a common role for this metalloproteinase in its numerous epithelial sites of expression.
Journal ArticleDOI
Secretion of microbicidal alpha-defensins by intestinal Paneth cells in response to bacteria.
Tokiyoshi Ayabe,Donald P. Satchell,Carole L. Wilson,William C. Parks,Michael E. Selsted,Andre J. Ouellette +5 more
TL;DR: Paneth cells in mouse small intestinal crypts secrete granules rich in microbicidal peptides when exposed to bacteria or bacterial antigens as discussed by the authors, and alpha-defensins or cryptdins account for 70% of the released bactericidal peptide activity.
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Induction and evasion of host defenses by type 1-piliated uropathogenic Escherichia coli.
Matthew A. Mulvey,Yolanda S. López-Boado,Carole L. Wilson,Robyn Roth,William C. Parks,John E. Heuser,Scott J. Hultgren +6 more
TL;DR: Bacterial attachment resulted in exfoliation of host bladder epithelial cells as part of an innate host defense system through a rapid apoptosis-like mechanism involving caspase activation and host DNA fragmentation.
Journal ArticleDOI
Matrilysin shedding of syndecan-1 regulates chemokine mobilization and transepithelial efflux of neutrophils in acute lung injury.
TL;DR: Impaired transepithelial migration was accompanied by a lack of both shed syndecan-1, a heparan sulfate proteoglycan, and KC, a CXC chemokine, in the alveolar fluid.