Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/94323
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Type: Journal article
Title: Protein kinase Cα regulates the expression of complement receptor Ig in human monocyte-derived macrophages
Other Titles: Protein kinase C-alpha regulates the expression of complement receptor Ig in human monocyte-derived macrophages
Author: Ma, Y.
Usuwanthim, K.
Munawara, U.
Quach, A.
Gorgani, N.
Abbott, C.
Hii, C.
Ferrante, A.
Citation: Journal of Immunology, 2015; 194(6):2855-2861
Publisher: American Association of Immunologists
Issue Date: 2015
ISSN: 0022-1767
1550-6606
Statement of
Responsibility: 
Yuefang Ma, Kanchana Usuwanthim, Usma Munawara, Alex Quach, Nick N. Gorgani, Catherine A. Abbott, Charles S. Hii, and Antonio Ferrante
Abstract: The 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.
Keywords: Monocytes
Cells, Cultured
Macrophages
Humans
Candida albicans
Dexamethasone
Lipopolysaccharides
Tumor Necrosis Factor-alpha
Macrophage-1 Antigen
Receptors, Complement
Anti-Inflammatory Agents
Interleukin-6
Blotting, Western
Reverse Transcriptase Polymerase Chain Reaction
Cell Adhesion
Gene Expression
Down-Regulation
RNA Interference
Protein Kinase C-alpha
Interleukin-1beta
Rights: Copyright © 2015 by The American Association of Immunologists, Inc.
DOI: 10.4049/jimmunol.1303477
Published version: http://dx.doi.org/10.4049/jimmunol.1303477
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