Pentraxin-2 suppresses c-Jun/AP-1 signaling to inhibit progressive fibrotic disease
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Pentraxin-2 (PTX-2), also known as serum amyloid P component (SAP/APCS), is a constitutive, antiinflammatory, innate immune plasma protein whose circulating level is decreased in chronic human fibrotic diseases. Here we show that recombinant human PTX-2 (rhPTX-2) retards progression of chronic kidney disease in Col4a3 mutant mice with Alport syndrome, reducing blood markers of kidney failure, enhancing lifespan by 20%, and improving histological signs of disease. Exogenously delivered rhPTX-2 was detected in macrophages but also in tubular epithelial cells, where it counteracted macrophage activation and was cytoprotective for the epithelium. Computational analysis of genes regulated by rhPTX-2 identified the transcriptional regulator c-Jun along with its activator protein–1 (AP-1) binding partners as a central target for the function of rhPTX-2. Accordingly, PTX-2 attenuates c-Jun and AP-1 activity, and reduces expression of AP-1–dependent inflammatory genes in both monocytes and epithelium. Our studies therefore identify rhPTX-2 as a potential therapy for chronic fibrotic disease of the kidney and an important inhibitor of pathological c-Jun signaling in this setting.
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Integration of multi-modal single-cell technologies and global initiatives such as the Human Cell Atlas represents an opportunity to decode cellular and molecular mechanisms of fibrosis at high resolution.
“The convergence and integration of these multi-modal single-cell technologies20,180, alongside global initiatives such as the Human Cell Atlas181, represent an extraordinary opportunity to decode the cellular and molecular mechanisms of fibrosis at unprecedented resolution”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [180]
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- Authors
- Nakagawa, N., Barron, L., Gomez, I. G., Johnson, B. G., Roach, A. M., Kameoka, S., Jack, R. M., Lupher, M. L., Gharib, S. A., & Duffield, J. S.
- Affiliations
- Asahikawa Medical University (JP)
- Biogen (United States) (US)
- Promedior Inc., Lexington, Massachusetts, USA.
- University of Washington (US)
- ORCID
- Venue
- JCI Insight
- Published
- 2016-12-08
- Volume
- 1
- Issue
- 20
- Pages
- e87446-e87446
- ISSN
- 2379-3708 (ISSN-L)
- PMC
- PMC5135274
- OpenAlex
- W2559836007
- Cited by
- 59
- References
- 74
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 6 · 2023: 15 · 2022: 6 · 2021: 9 · 2020: 7 · 2019: 5 · 2018: 3 · 2017: 3
- FWCI
- 2.22
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- JCI Insight (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Heart Association (12040023)
- Biogen (DK094768, DK093493)
- University of Washington
- Asahikawa Medical University
- National Institutes of Health (UH2TR000504, UH3TR000504, TR000504)
- National Institute of Diabetes and Digestive and Kidney Diseases (RC1DK087389, R24DK094768, R01DK093493)
- National Center for Advancing Translational Sciences
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Biomarkers in Disease Mechanisms
- Health Sciences › Medicine › Nephrology › Renal Diseases and Glomerulopathies
- Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
- Keywords
- serum amyloid P component, c-Jun, AP-1 signaling, chronic kidney disease, Alport syndrome, renal fibrosis, macrophage activation, tubular epithelial cells, inflammatory gene expression, lifespan extension
- MeSH terms
- Pentraxins, Animals, C-Reactive Protein, Cells, Cultured, Fibrosis, Humans, Kidney, Macrophage Activation, Monocytes, Nephritis, Hereditary, Nerve Tissue Proteins, Recombinant Proteins, Signal Transduction, Proto-Oncogene Proteins c-jun, Mice, Knockout, Transcription Factor AP-1, Mice, Mice, 129 Strain
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