Protein kinase Cα regulates the expression of complement receptor Ig in human monocyte-derived macrophages

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dc.contributor.authorMa, Y.
dc.contributor.authorUsuwanthim, K.
dc.contributor.authorMunawara, U.
dc.contributor.authorQuach, A.
dc.contributor.authorGorgani, N.
dc.contributor.authorAbbott, C.
dc.contributor.authorHii, C.
dc.contributor.authorFerrante, A.
dc.date.issued2015
dc.description.abstractThe complement receptor Ig (CRIg) is selectively expressed by macrophages. This receptor not only promotes the rapid phagocytosis of bacteria by macrophages but also has anti-inflammatory and immunosuppressive functions. Previous findings have suggested that protein kinase C (PKC) may be involved in the regulation of CRIg expression in human macrophages. We have now examined the role of PKCα in CRIg expression in human monocyte-derived macrophages (MDM). Macrophages nucleofected with plasmid containing short hairpin RNA against PKCα showed markedly reduced expression of PKCα, but normal PKCζ expression, by Western blotting analysis, and vice versa. PKCα-deficient MDM showed increased expression of CRIg mRNA and protein (both the long and short form), an increase in phagocytosis of complement-opsonized Candida albicans, and decreased production of TNF-α and IL-6. TNF-α caused a marked decrease in CRIg expression, and addition of anti-TNF mAb to the TNF-α-producing MDMs increased CRIg expression. PKCα-deficient macrophages also showed significantly less bacterial LPS-induced downregulation of CRIg. In contrast, cells deficient in PKCα showed decreased expression of CR type 3 (CR3) and decreased production of TNF-α and IL-6 in response to LPS. MDM developed under conditions that increased expression of CRIg over CR3 showed significantly reduced production of TNF-α in response to opsonized C. albicans. The findings indicate that PKCα promotes the downregulation of CRIg and upregulation of CR3 expression and TNF-α and IL-6 production, a mechanism that may promote inflammation.
dc.description.statementofresponsibilityYuefang Ma, Kanchana Usuwanthim, Usma Munawara, Alex Quach, Nick N. Gorgani, Catherine A. Abbott, Charles S. Hii, and Antonio Ferrante
dc.identifier.citationJournal of Immunology, 2015; 194(6):2855-2861
dc.identifier.doi10.4049/jimmunol.1303477
dc.identifier.issn0022-1767
dc.identifier.issn1550-6606
dc.identifier.orcidQuach, A. [0000-0003-1912-7581]
dc.identifier.orcidHii, C. [0000-0002-7107-8935]
dc.identifier.orcidFerrante, A. [0000-0002-2581-6407]
dc.identifier.urihttp://hdl.handle.net/2440/94323
dc.language.isoen
dc.publisherAmerican Association of Immunologists
dc.rightsCopyright © 2015 by The American Association of Immunologists, Inc.
dc.source.urihttps://doi.org/10.4049/jimmunol.1303477
dc.subjectMonocytes
dc.subjectCells, Cultured
dc.subjectMacrophages
dc.subjectHumans
dc.subjectCandida albicans
dc.subjectDexamethasone
dc.subjectLipopolysaccharides
dc.subjectTumor Necrosis Factor-alpha
dc.subjectMacrophage-1 Antigen
dc.subjectReceptors, Complement
dc.subjectAnti-Inflammatory Agents
dc.subjectInterleukin-6
dc.subjectBlotting, Western
dc.subjectReverse Transcriptase Polymerase Chain Reaction
dc.subjectCell Adhesion
dc.subjectGene Expression
dc.subjectDown-Regulation
dc.subjectRNA Interference
dc.subjectProtein Kinase C-alpha
dc.subjectInterleukin-1beta
dc.titleProtein kinase Cα regulates the expression of complement receptor Ig in human monocyte-derived macrophages
dc.title.alternativeProtein kinase C-alpha regulates the expression of complement receptor Ig in human monocyte-derived macrophages
dc.typeJournal article
pubs.publication-statusPublished

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