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Metalloproteinases are enriched in microglia compared with leukocytes and they regulate cytokine levels in activated microglia
Glia, 2007-04, Vol.55 (5), p.516-526
Nuttall, Robert K.
Silva, Claudia
Hader, Walter
Bar-Or, Amit
Patel, Kamala D.
Edwards, Dylan R.
Yong, V. Wee
2007
Details
Autor(en) / Beteiligte
Nuttall, Robert K.
Silva, Claudia
Hader, Walter
Bar-Or, Amit
Patel, Kamala D.
Edwards, Dylan R.
Yong, V. Wee
Titel
Metalloproteinases are enriched in microglia compared with leukocytes and they regulate cytokine levels in activated microglia
Ist Teil von
Glia, 2007-04, Vol.55 (5), p.516-526
Ort / Verlag
Hoboken: Wiley Subscription Services, Inc., A Wiley Company
Erscheinungsjahr
2007
Link zum Volltext
Quelle
Wiley Online Library Journals Frontfile Complete
Beschreibungen/Notizen
Microglia are resident immune cells within the central nervous system (CNS). They become activated following neurological insults and increase their expression of cytokines. Also elevated in CNS injuries are proteases, including matrix metalloproteinases (MMPs) and A disintegrin and metalloproteinases (ADAMs). The spectrum of metalloproteinase members expressed by microglia and by the systemic leukocytes that infiltrate the injured CNS is unknown, as are their functions. We determined the levels of transcripts encoding all 24 MMPs, nine ADAMs, and their four physiological antagonists, tissue inhibitor of metalloproteinases (TIMPs), in human microglia, B and T cells, monocytes, and neutrophils. We found a distinct pattern for each immune subset and an enrichment of metalloproteinases in microglia compared with leukocytes. When microglia were activated, there was an upregulation of transcripts for nine metalloproteinases, and reduction of TIMP3. Activation of microglia also resulted in increased levels of tumor necrosis factor (TNF)‐α, interleukin (IL)‐1β, and IL‐10 protein in the conditioned media of cells. The amount of secreted TNF‐α, but not IL‐1β or IL‐10, was suppressed by BB94, a broad spectrum metalloproteinase inhibitor, and by TIMP3 but not TIMP1 or TIMP2. This inhibitory profile suggests the involvement of an ADAM member in TNF‐α secretion. We conclude that microglia bear a metalloproteinase signature distinct from systemic cells, and that following activation, microglia upregulate TNF‐α protein levels through a combination of elevated cytokine transcripts, increased metalloproteinase level and activity, and through the decrease of TIMP3. The results have implications for the regulation of neuroinflammation and its outcomes following CNS injuries. © 2007 Wiley‐Liss, Inc.
Sprache
Englisch
Identifikatoren
ISSN: 0894-1491
eISSN: 1098-1136
DOI: 10.1002/glia.20478
Titel-ID: cdi_proquest_miscellaneous_68965893
Format
–
Schlagworte
ADAM Proteins - classification
,
ADAM Proteins - genetics
,
ADAM Proteins - metabolism
,
Adult
,
cell activation
,
Cells, Cultured
,
Central Nervous System - injuries
,
cytokines
,
Cytokines - immunology
,
Cytokines - metabolism
,
Humans
,
Inflammation
,
Interleukin-10 - immunology
,
Interleukin-10 - metabolism
,
Interleukin-1beta - immunology
,
Interleukin-1beta - metabolism
,
Leukocytes - enzymology
,
Leukocytes - immunology
,
Lipopolysaccharides - immunology
,
Metalloproteases - classification
,
Metalloproteases - genetics
,
Metalloproteases - metabolism
,
metalloproteinases
,
microglia
,
Microglia - cytology
,
Microglia - enzymology
,
Microglia - immunology
,
RNA - analysis
,
RNA, Messenger - analysis
,
Tumor Necrosis Factor-alpha - immunology
,
Tumor Necrosis Factor-alpha - metabolism
,
Up-Regulation - physiology
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