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Renal Epithelial Complement C3 Expression Affects Kidney Fibrosis Progression.

Ganna Stepanova1, Anna Manzéger1,2, Miklós M Mózes1,2

  • 1Institute of Translational Medicine, Semmelweis University, Nagyvárad tér 4, 1089 Budapest, Hungary.

International Journal of Molecular Sciences
|December 17, 2024
PubMed
Summary

De novo kidney complement component 3 (C3) synthesis is linked to faster fibrosis progression in mice and human kidney disease. This C3 overproduction may drive chronic kidney disease progression through local pro-fibrotic effects.

Keywords:
FSGScomplementgene expressionprogressiontubulointerstitial fibrosis

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Area of Science:

  • Nephrology
  • Immunology
  • Molecular Biology

Background:

  • Kidney fibrosis is a common outcome in chronic kidney diseases.
  • Genetic factors and complement component 3 (C3) are implicated in fibrosis, but the specific role of renal C3 production in fibrosis progression and epithelial-to-mesenchymal transition (EMT) is unclear.

Purpose of the Study:

  • To investigate the role of renal C3 production in genetically determined kidney fibrosis progression.
  • To explore the impact of C3 on epithelial-to-mesenchymal transition (EMT) and its association with fibrosis in mouse models and human kidney disease.

Main Methods:

  • Unilateral ureteral obstruction (UUO) model in fibrosis-resistant (C57Bl/6J) and fibrosis-prone (CBA/J, BALB/cJ) mice.
  • Analysis of kidney tissue for C3, collagen, and other fibrotic markers at different time points.
  • In vitro studies using mouse primary tubular epithelial cells (PTECs) treated with TGFβ or C3a agonist.
  • Examination of human focal segmental glomerulosclerosis (FSGS) and healthy kidney samples.

Main Results:

  • Fibrosis-prone mice showed early renal C3 messenger RNA (mRNA) induction and faster fibrosis progression compared to resistant mice.
  • CBA mice exhibited the highest expression of C3, lipocalin-2 (Lcn2), Tgfb1, and Ccl2.
  • Human FSGS kidneys displayed C3 mRNA over-expression and significant tubular C3 staining.
  • In PTECs, C3a agonist treatment induced pro-fibrotic EGR1 and EMT, independent of TGFβ.

Conclusions:

  • De novo renal tubular C3 synthesis is associated with the rate of genetically determined kidney fibrosis progression in mice.
  • Tubular C3 overproduction plays a role in the pathogenesis of FSGS in humans.
  • Local pro-fibrotic effects of tubular C3 may influence the progression of chronic kidney disease.