Chloride Conductance Is Required for the Protein Kinase A and Rac1-dependent Phosphorylation of Moesin at Thr-558 by KCl in PC12 Cells

Abstract

Moesin is a member of the ERM family, a family of cross-linkers between the plasma membrane and the actin cytoskeleton, which are known to be activated by phosphorylation. Previously, we reported the RhoA and Rho kinase-dependent phosphorylation of moesin at Thr-558 in hippocampal neuronal cells by glutamate. Here we studied the induction of moesin phosphorylation by KCl (60 mM) in PC12 cells. Moesin phosphorylation at Thr-558 was increased after 2 min of KCl treatment, peaked at 5 min, and returned to the basal level by 60 min. KCl also activated Rac1, but not RhoA, in PC12 cells, and KCl-induced moesin phosphorylation was suppressed in dominant negative Rac1 (N17 Rac1)-expressed cells. The inhibition of protein kinase A (PKA), known as an upstream kinase of Rac1, abolished Rac1 activation and moesin phosphorylation by KCl. Interestingly, the phosphorylation of moesin by KCl was independent of KCl-induced membrane depolarization and calcium influx but was dependent on KCl-induced chloride conductance. 60 mM KCl induced chloride conductance in PC12 cells, and pretreatment with Cl ؊ channel blocker abolished Rac1 activation and moesin phosphorylation by KCl. These results suggest that the phosphorylation of moesin at Thr-558 in PC12 cells by KCl treatment is PKA-and Rac1-dependent and that KCl-induced chloride conductance is involved in the activation of this signaling system.

Quercetin Stimulates NGF-induced Neurite Outgrowth in PC12 Cells via Activation of Na⁺/K⁺/2Cl^- Cotransporter

“…Quercetin of 10 µM stimulated the NGF-induced neurite outgrowth in culture medium containing 61. 6 [31][32][33][34][35][36][37][38][39][40], gene expression of epithelial sodium channel via a PTK-dependent pathway [4], and cell migration via remodeling of cytoskeleton [41][42][43]. In addition, Menegazzi and colleagues [5,44] have reported that physiological functions of neutrophil (e.g.…”

The use of rodent models to investigate host–bacteria interactions related to periodontal diseases

“…The ability of P. gingivalis to establish an oral infection is facilitated by prior antibioticmediated suppression of the murine oral flora and may exploit inter-bacterial interactions with early colonizers as has been proposed for the human oral cavity (Daep, et al, 2006;Jeon, et al, 2005). Although vendors may claim that mice are pathogen-free, this does not necessarily mean that they are free of potential periodontal pathogens.…”

Stem cell factor induces ERM proteins phosphorylation through PI3K activation to mediate melanocyte proliferation and migration

“…In melanocytes, SCF‐induced lamellipodium formation is Rac1‐dependent (Ballestrem et al., 2000), suggesting that Rac may be a downstream mediator of PI3K stimulated by SCF in melanocytes. Recently, we reported that the KCl‐induced phosphorylation of moesin was Rac‐dependent in PC 12 cells (Jeon et al., 2005) and that nerve growth factor‐induced phosphorylation of moesin was mediated through PI3K/Rac/Akt activation in PC12 cells (S. Jeon, B. S. Koo, Y. S. Kim, C. D. Bae and J. Park, unpublished data), which suggest the possibility that the ERM (ezrin/radixin/moesin) proteins family could be a downstream target of Rac in SCF‐treated melanocytes.…”