[HTML][HTML] Rat glomerular epithelial cells produce and bear factor H on their surface that is up-regulated under complement attack

G Ren, M Doshi, BK Hack, JJ Alexander, RJ Quigg - Kidney international, 2003 - Elsevier
G Ren, M Doshi, BK Hack, JJ Alexander, RJ Quigg
Kidney international, 2003Elsevier
Rat glomerular epithelial cells produce and bear factor H on their surface that is up-
regulated under complement attack. Background Factor H is a potent complement inhibitory
molecule that is primarily produced by the liver and appears in plasma as a soluble protein.
Yet there is evidence that other cells, including those in the kidney, can produce factor H,
and that it can be cell-associated as well as present as a plasma protein. Here we studied
factor H in rat glomerular epithelial cells (GEC). Methods A polyclonal antibody to factor H …
Rat glomerular epithelial cells produce and bear factor H on their surface that is up-regulated under complement attack.
Background
Factor H is a potent complement inhibitory molecule that is primarily produced by the liver and appears in plasma as a soluble protein. Yet there is evidence that other cells, including those in the kidney, can produce factor H, and that it can be cell-associated as well as present as a plasma protein. Here we studied factor H in rat glomerular epithelial cells (GEC).
Methods
A polyclonal antibody to factor H was used to identify factor H protein. A polymerase chain reaction (PCR)-based strategy was utilized to clone the full-length cDNA of GEC factor H. The relative quantity of factor H mRNA was measured by quantitative reverse transcription (RT)-PCR in cultured GEC exposed to complement activation and in the passive Heymann nephritis (PHN) model of membranous nephropathy.
Results
By immunofluorescence microscopy, factor H protein was present on the plasma membranes of cultured GEC. Based upon Western blot studies, this appeared to be the full-length 150 kD factor H protein. Factor H cDNA cloned from GEC was identical to the newly deposited sequence for rat liver factor H cDNA. In cultured GEC in which complement was activated, factor H mRNA increased over time. Similarly, in the PHN model in which complement was activated on GEC in vivo, factor H mRNA and protein also increased over time.
Conclusion
Cultured GEC and glomeruli express factor H mRNA and protein. As modeled both in vitro and in vivo in the rat, factor H is up-regulated in membranous nephropathy. This is likely to be a direct response of GEC to complement attack and may represent a protective response of this cell.
Elsevier