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Complement expression profiles in human glomerular mesangial cells, endothelial cells, podocytes and proximal tubular epithelial cells.

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Title: Complement expression profiles in human glomerular mesangial cells, endothelial cells, podocytes and proximal tubular epithelial cells.
Authors: Gao Y; Department of Nephrology, Peking University Third Hospital, Beijing, China., Li Q; Department of Nephrology, Peking University Third Hospital, Beijing, China., Wang Y; Department of Nephrology, Peking University Third Hospital, Beijing, China., Deng Z; Department of Nephrology, Peking University Third Hospital, Beijing, China.
Source: Frontiers in immunology [Front Immunol] 2026 Sep 01; Vol. 17, pp. 1881549. Date of Electronic Publication: 2026 Sep 01 (Print Publication: 2026).
Publication Type: Journal Article
Language: English
Journal Info: Publisher: Frontiers Research Foundation] Country of Publication: Switzerland NLM ID: 101560960 Publication Model: eCollection Cited Medium: Internet ISSN: 1664-3224 (Electronic) Linking ISSN: 16643224 NLM ISO Abbreviation: Front Immunol Subsets: MEDLINE
Imprint Name(s): Original Publication: [Lausanne : Frontiers Research Foundation]
MeSH Terms: Mesangial Cells*/immunology , Mesangial Cells*/metabolism , Podocytes*/immunology , Podocytes*/metabolism , Complement System Proteins*/genetics , Complement System Proteins*/metabolism , Complement System Proteins*/immunology , Endothelial Cells*/metabolism , Endothelial Cells*/immunology , Kidney Tubules, Proximal*/immunology , Kidney Tubules, Proximal*/cytology , Kidney Tubules, Proximal*/metabolism , Epithelial Cells*/metabolism , Epithelial Cells*/immunology, Humans ; Complement Activation ; Cells, Cultured ; Single-Cell Gene Expression Analysis ; Gene Expression Profiling ; Transcriptome
Abstract: Background: Local expression of complement components in the kidney has been reported sporadically in both diseased and normal kidneys. This study aimed to comprehensively characterize the expression of complement components in human glomerular mesangial cells (GMCs), glomerular endothelial cells (GECs), podocytes, and proximal tubular epithelial cells (PTECs) in non-diseased renal tissue.
Methods: Complement expression in cultured human renal intrinsic cells was initially evaluated using reverse transcription polymerase chain reaction and immunofluorescence staining. These findings were further examined using publicly available single-cell RNA-sequencing datasets and 10×Genomics single-cell RNA sequencing of non-diseased human kidney tissue. The analyses focused on complement components involved in the initiation of the classical, lectin, and alternative pathways, as well as components shared among these activation pathways, terminal pathway components, complement regulators, and complement receptors.
Results: Complement components unique to the initial phase for classical pathway (C1S, C1R, C2, C4), lectin pathway (MBL2, FCN1, MASP1), alternative pathway (CFB, CFD), and the C3 component shared by the three activation pathways were detected in these cells. The components shared by the terminal pathways including C5, C6, C7, C8 and C9 exhibited lower expression, while complement regulators (CFH, CFI, CD55/DAF, CD46/MCP, CD59, C4BPB, PROS1/Protein S) or receptors (CD93/C1QR1, CR1), particularly membrane-bound proteins, such as DAF, MCP and CD59, which inhibit complement activation and the formation of the membrane attack complex, showed relatively high expression.
Conclusion: These results showed that all four types of intrinsic renal cells expressed multiple complement components associated with the classical, lectin, and alternative pathways. In non-diseased kidney tissue, complement regulatory molecules involved in the control of complement activation showed relatively higher expression, whereas components of the terminal complement pathway were expressed at relatively lower levels, suggesting that renal intrinsic cells maintain a locally poised but tightly regulated complement system.
(Copyright © 2026 Gao, Li, Wang and Deng.)
Competing Interests: The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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Contributed Indexing: Keywords: complement; endothelial cells; mesangial cells; podocytes; proximal tubular epithelial cells
Substance Nomenclature: 9007-36-7 (Complement System Proteins)
Entry Date(s): Date Created: 20260916 Date Completed: 20260916 Latest Revision: 20260917
Update Code: 20260917
PubMed Central ID: PMC13574829
DOI: 10.3389/fimmu.2026.1881549
PMID: 42746023
Database: MEDLINE
Description
ISSN:1664-3224
DOI:10.3389/fimmu.2026.1881549