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1 U478, INSERM, Paris, 75018, France
2 laboratoire de Radiobiologie Digestive, Institut de Protection et de Surete Nucleaire, Fontenay aux Roses, 92265, France
* To whom correspondence should be addressed. E-mail: farman{at}bichat.inserm.fr.
Aldosterone classically modulates sodium transport in tight epithelia such as the renal collecting duct (CD) through the transcellular route, but it is not known whether the hormone could also affect paracellular permeability. Such permeability is controlled by tight junctions (TJ) that form a size- and charge-selective barrier. Among TJ proteins, claudin 4 has been highlighted as a key element to control paracellular charge selectivity. In RCCD2 CD cells grown on filters, we have identified novel early aldosterone effects on TJ. Endogenous claudin 4 abundance or cellular localization were unaltered by aldosterone. However the hormone promoted rapid (within 15-20 min) and transient phosphorylation of endogenous claudin 4 on threonine residues, without affecting tyrosine or serine; this event was fully developed at 10 nM aldosterone and appeared specific for aldosterone (as it is not observed after dexamethasone treatment and as it depends on mineralocorticoid receptor occupancy). Within the same delay, aldosterone also promoted an increased apical to basal passage of 125Iodine (a substitute for chloride) while 22Na passage was unaffected; paracellular permeability to 3H mannitol was also reduced. Later on (45 min), a fall in transepithelial resistance was observed. These data indicate that aldosterone modulates TJ properties in renal epithelial cells.
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