Abstract
Previous studies indicate that the kidney PT is involved in body Fe homeostasis: 1) Fe is filtered and reabsorbed by the kidney PT; 2) The divalent metal transporter DMT1 is expressed in lysosomes of PT cells where its expression is responsive to systemic Fe levels. Here we show by immunostaining that the iron exporter ferroportin‐1 (FPN‐1) is expressed in rat kidney cortex and localized to PT cells. FPN‐1 is also expressed in a cell line derived from the S1‐segment of rat PT at the mRNA and protein level. Fe over‐load with ferric ammonium citrate (FAC) or depletion with desferrioxamine (DF) do not change overall FPN‐1 protein expression in cultured PT cells, as evidenced by immunoblotting. However, immunofluorescence staining shows increased cell surface expression of FPN‐1 in FAC treated cells. This was confirmed using cell surface biotinylation and immunoprecipitation of FPN‐1. The results indicate that FPN‐1 is expressed intracellularly and in plasma membranes of kidney PT cells. Fe overload may induce redistribution of intracellular FPN‐1 to the plasma membrane, possibly to increase Fe exit from PT cells. The expression of Fe transport proteins, such as DMT1 and FPN‐1, that are regulated by Fe suggest that the kidney PT is involved in Fe homeostasis. Supported by DFG & Wellcome Trust.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
