Rat glomerular epithelial cells produce and bear factor H on their surface that is up-regulated under complement...

Area of Science:

• Nephrology
• Immunology
• Complement System Biology

Background:

• Factor H is a key complement inhibitor, primarily synthesized by the liver.
• While known as a plasma protein, Factor H can also be cell-associated and produced by non-hepatic cells.
• This study investigates Factor H expression and regulation within rat glomerular epithelial cells (GEC).

Purpose of the Study:

• To determine if rat GEC express Factor H.
• To investigate the regulation of Factor H in GEC under conditions of complement activation.
• To explore the role of Factor H in the context of membranous nephropathy.

Main Methods:

• Immunofluorescence microscopy and Western blotting to detect Factor H protein in GEC.
• Polymerase chain reaction (PCR) and quantitative reverse transcription (RT-PCR) to analyze Factor H cDNA and mRNA.
• In vitro studies using cultured GEC with complement activation and in vivo studies using the passive Heymann nephritis (PHN) rat model.

Main Results:

• Factor H protein was localized to the plasma membrane of cultured GEC, consistent with the full-length 150 kD protein.
• Cloned GEC Factor H cDNA was identical to rat liver Factor H cDNA.
• Both cultured GEC and GEC in the PHN model showed increased Factor H mRNA and protein levels upon complement activation.

Conclusions:

• Rat GEC and glomeruli express Factor H mRNA and protein.
• Factor H is upregulated in GEC during membranous nephropathy, both in vitro and in vivo.
• This upregulation is a likely direct response to complement attack, potentially serving a protective function for GEC.