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Updated: May 8, 2026

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
Published on: June 8, 2022
Ficolin-1 is up-regulated in leukocytes and glomeruli from microscopic polyangiitis patients
Eri Muso1, Daisuke Okuzaki, Shigeto Kobayashi
1Division of Nephrology and Hemodialysis, Kitano Hospital, The Tazuke Kofukai Medical Research Institute , Osaka 538-8480 , Japan .
Abstract:
Microscopic polyangiitis (MPA) is a systemic autoimmune disease that often has a fatal outcome. Although delineating the molecular pathogenesis is essential for its remedy, an understanding of its molecular mechanism has remained elusive. To search for new markers of active lesions that might help better understand the molecular basis of MPA and aid in its diagnosis, we here performed DNA microarray analysis with peripheral blood mononuclear cells (PBMCs). Compared to normal control, several genes were up- or down-regulated in MPA patients, including up-regulation of the mRNA level of ficolin-1 (FCN1 or M-ficolin), an innate pattern recognition complement molecule. The amount of ficolin-1, as detected by immunohistochemistry, was higher in the glomeruli of another group of MPA patients than in the glomeruli of control patients who harbored almost normal glomeruli. Many of the ficolin-1 dots were also positive for CD68, suggesting that the ficolin-1-positive cells were monocytes, such as macrophages or dendritic cells. This is not due to the difference in the number of neutrophil or monocytes in the blood samples of MPA and control patients. Taken together, we conclude that increased ficolin-1 expression could serve as a new marker for the characterization of MPA, especially when it is associated with local active lesions.
Insights
Microscopic polyangiitis (MPA) is a serious autoimmune disease. Increased ficolin-1 (FCN1) in kidney lesions may serve as a diagnostic marker for active MPA.
Area of Science:
- Immunology
- Nephrology
- Molecular Biology
Background:
- Microscopic polyangiitis (MPA) is a systemic autoimmune disease with a high fatality rate.
- The molecular mechanisms underlying MPA remain poorly understood, hindering effective treatment.
- Identifying novel biomarkers is crucial for diagnosing and understanding active MPA lesions.
Purpose of the Study:
- To identify novel molecular markers associated with active lesions in microscopic polyangiitis (MPA).
- To investigate the potential role of ficolin-1 (FCN1) as a biomarker in MPA.
- To enhance the understanding of MPA's molecular pathogenesis.
Main Methods:
- DNA microarray analysis of peripheral blood mononuclear cells (PBMCs) from MPA patients and controls.
- Immunohistochemical detection of ficolin-1 (FCN1) in kidney glomeruli.
- Co-localization studies using CD68 marker to identify ficolin-1-positive cells.
Main Results:
- DNA microarray analysis revealed differential gene expression in MPA patients compared to controls.
- Upregulation of ficolin-1 (FCN1) mRNA levels was observed in MPA patients.
- Elevated ficolin-1 (FCN1) protein levels were detected in the glomeruli of MPA patients, primarily within CD68-positive cells (monocytes/macrophages).
Conclusions:
- Increased ficolin-1 (FCN1) expression is a potential novel marker for characterizing microscopic polyangiitis (MPA).
- Ficolin-1 (FCN1) may be particularly useful for identifying active lesions in MPA.
- These findings contribute to a better understanding of MPA's molecular basis and diagnosis.
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