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New insights into the complex physiologic role of the cilium in secretory epithelia
Author(s) -
Satlin Lisa
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.78.3
Subject(s) - cilium , microbiology and biotechnology , biology
The cortical collecting duct (CCD) of the distal nephron is a major site for the final renal regulation of K homeostasis. Within this segment, principal cells (PCs) possess a single apical cilium whereas the surfaces of adjacent intercalated cells (ICs), devoid of cilia, are decorated with abundant microvilli and microplicae.Increases in tubular (urinary) flow rate, induced by volume expansion, diuretics, or a high K diet, subject CCD cells to hydrodynamic forces (fluid shear stress, circumferential stretch, and drag/torque on apical cilia and presumably microvilli/microplicae) that are transduced into increases in PC and IC cytoplasmic Ca 2+ concentration that activate apical voltage‐, stretch‐ and Ca 2+ ‐activated BK channels, which mediate flow‐induced K secretion (FIKS). Functional and immunoreactive apical BK channels are more abundant in ICs than PCs, but appear to be constitutively closed under low flow conditions in a cell‐specific manner by PKA/AKAP and MAPK elements in PCs, and WNK4 in ICs. We have recently identified a high density of immunoreactive and conducting BK channels in PC cilia. Pharmacologic deciliation of CCDs does not affect FIKS, leading us to conclude thatBK channels in PC cilia do not mediate FIKS. We speculate that cilia BK channels are responsible for localized hyperpolarization of membrane potential, facilitating sustained mechanoinduced Ca 2+ entry through TRPP Ca 2+ ‐selective channels in this organelle and subsequent autocrine/paracrine signaling events.