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Published on: May 31, 2018
A novel CCCH-zinc finger protein family regulates proinflammatory activation of macrophages
Jian Liang1, Jing Wang, Asim Azfer
1Biomolecular Science Center, College of Medicine, University of Central Florida, 4000 Central Florida Boulevard, Orlando, FL 32816, USA.
Abstract:
Activated macrophages play an important role in many inflammatory diseases. However, the molecular mechanisms controlling macrophage activation are not completely understood. Here we report that a novel CCCH-zinc finger protein family, MCPIP1, 2, 3, and 4, encoded by four genes, Zc3h12a, Zc3h12b, Zc3h12c, and Zc3h12d, respectively, regulates macrophage activation. Northern blot analysis revealed that the expression of MCPIP1 and MCPIP3 was highly induced in macrophages in response to treatment with lipopolysaccharide (LPS). Although not affecting cell surface marker expression and phagocytotic function, overexpression of MCPIP1 significantly blunted LPS-induced inflammatory cytokine and NO(2)(.) production as well as their gene expression. Conversely, short interfering RNA-mediated reduction in MCPIP1 augmented LPS-induced inflammatory gene expression. Further studies demonstrated that MCPIP1 did not directly affect the mRNA stability of tumor necrosis factor alpha and monocyte chemoattractant protein 1 (MCP-1) but strongly inhibited LPS-induced tumor necrosis factor alpha and inducible nitric-oxide synthase promoter activation. Moreover, we found that forced expression of MCPIP1 significantly inhibited LPS-induced nuclear factor-kappaB activation. These results identify MCP-induced proteins, a novel CCCH-zinc finger protein family, as negative regulators in macrophage activation and may implicate them in host immunity and inflammatory diseases.
Insights
Novel CCCH-zinc finger proteins, MCPIP1-4, regulate macrophage activation. MCPIP1 acts as a negative regulator, inhibiting inflammatory responses and nuclear factor-kappaB activation, suggesting roles in immunity and inflammatory diseases.
Area of Science:
- Immunology
- Molecular Biology
- Cell Biology
Background:
- Activated macrophages are central to inflammatory diseases.
- Molecular mechanisms governing macrophage activation require further elucidation.
Purpose of the Study:
- To investigate the role of a novel CCCH-zinc finger protein family (MCPIP1-4) in regulating macrophage activation.
- To identify the specific functions of MCPIP1 in inflammatory responses.
Main Methods:
- Northern blot analysis to assess gene expression.
- Overexpression and short interfering RNA (siRNA) knockdown of MCPIP1.
- Assays for inflammatory cytokine and nitric oxide (NO2-) production.
- Reporter assays to evaluate promoter activation (TNF-alpha, iNOS).
- Analysis of nuclear factor-kappaB (NF-κB) activation.
Main Results:
- MCPIP1 and MCPIP3 expression were induced by lipopolysaccharide (LPS) in macrophages.
- MCPIP1 overexpression suppressed LPS-induced inflammatory cytokine and NO2- production and gene expression.
- MCPIP1 knockdown enhanced LPS-induced inflammatory gene expression.
- MCPIP1 inhibited LPS-induced activation of TNF-alpha and iNOS promoters.
- MCPIP1 significantly inhibited LPS-induced NF-κB activation.
Conclusions:
- The MCPIP family, particularly MCPIP1, acts as a negative regulator of macrophage activation.
- MCPIP1 functions by inhibiting inflammatory gene promoter activation and NF-κB signaling.
- These findings implicate MCPIP proteins in host immunity and the pathogenesis of inflammatory diseases.
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