PMID- 15657298
OWN - NLM
STAT- MEDLINE
DCOM- 20050613
LR  - 20181113
IS  - 0022-1295 (Print)
IS  - 1540-7748 (Electronic)
IS  - 0022-1295 (Linking)
VI  - 125
IP  - 2
DP  - 2005 Feb
TI  - Ca(2+)- and volume-sensitive chloride currents are differentially regulated by 
      agonists and store-operated Ca2+ entry.
PG  - 197-211
AB  - Using patch-clamp and calcium imaging techniques, we characterized the effects of 
      ATP and histamine on human keratinocytes. In the HaCaT cell line, both receptor 
      agonists induced a transient elevation of [Ca2+]i in a Ca(2+)-free medium 
      followed by a secondary [Ca2+]i rise upon Ca2+ readmission due to store-operated 
      calcium entry (SOCE). In voltage-clamped cells, agonists activated two 
      kinetically distinct currents, which showed differing voltage dependences and 
      were identified as Ca(2+)-activated (I(Cl(Ca))) and volume-regulated (I(Cl, 
      swell)) chloride currents. NPPB and DIDS more efficiently inhibited I(Cl(Ca)) and 
      I(Cl, swell), respectively. Cell swelling caused by hypotonic solution invariably 
      activated I(Cl, swell) while regulatory volume decrease occurred in intact cells, 
      as was found in flow cytometry experiments. The PLC inhibitor U-73122 blocked 
      both agonist- and cell swelling-induced I(Cl, swell), while its inactive analogue 
      U-73343 had no effect. I(Cl(Ca)) could be activated by cytoplasmic calcium 
      increase due to thapsigargin (TG)-induced SOCE as well as by buffering [Ca2+]i in 
      the pipette solution at 500 nM. In contrast, I(Cl, swell) could be directly 
      activated by 1-oleoyl-2-acetyl-sn-glycerol (OAG), a cell-permeable DAG analogue, 
      but neither by InsP3 infusion nor by the cytoplasmic calcium increase. PKC also 
      had no role in its regulation. Agonists, OAG, and cell swelling induced I(Cl, 
      swell) in a nonadditive manner, suggesting their convergence on a common pathway. 
      I(Cl, swell) and I(Cl(Ca)) showed only a limited overlap (i.e., simultaneous 
      activation), although various maneuvers were able to induce these currents 
      sequentially in the same cell. TG-induced SOCE strongly potentiated I(Cl(Ca)), 
      but abolished I(Cl, swell), thereby providing a clue for this paradox. Thus, we 
      have established for the first time using a keratinocyte model that I(Cl, swell) 
      can be physiologically activated under isotonic conditions by receptors coupled 
      to the phosphoinositide pathway. These results also suggest a novel function for 
      SOCE, which can operate as a "selection" switch between closely localized 
      channels.
FAU - Zholos, Alexander
AU  - Zholos A
AD  - Laboratoire de Physiologie Cellulaire, INSERM EMI 0228, Universite des Sciences 
      et Technologie de Lille, 59655 Villeneuve d'Ascq, France.
FAU - Beck, Benjamin
AU  - Beck B
FAU - Sydorenko, Vadym
AU  - Sydorenko V
FAU - Lemonnier, Loic
AU  - Lemonnier L
FAU - Bordat, Pascal
AU  - Bordat P
FAU - Prevarskaya, Natalia
AU  - Prevarskaya N
FAU - Skryma, Roman
AU  - Skryma R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20050118
PL  - United States
TA  - J Gen Physiol
JT  - The Journal of general physiology
JID - 2985110R
RN  - 0 (Chloride Channels)
RN  - 0 (Receptors, Cytoplasmic and Nuclear)
RN  - 0 (Receptors, Histamine)
RN  - 0 (phosphatidylinositol receptors)
RN  - 820484N8I3 (Histamine)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Adenosine Triphosphate/*pharmacology
MH  - Calcium/*pharmacokinetics
MH  - Cell Line
MH  - Cell Size
MH  - Chloride Channels/*physiology
MH  - Electrophysiology
MH  - Flow Cytometry
MH  - Histamine/*pharmacology
MH  - Humans
MH  - Keratinocytes
MH  - Patch-Clamp Techniques
MH  - Receptors, Cytoplasmic and Nuclear/physiology
MH  - Receptors, Histamine/physiology
PMC - PMC2217498
EDAT- 2005/01/20 09:00
MHDA- 2005/06/14 09:00
PMCR- 2005/08/01
CRDT- 2005/01/20 09:00
PHST- 2005/01/20 09:00 [pubmed]
PHST- 2005/06/14 09:00 [medline]
PHST- 2005/01/20 09:00 [entrez]
PHST- 2005/08/01 00:00 [pmc-release]
AID - jgp.200409161 [pii]
AID - 200409161 [pii]
AID - 10.1085/jgp.200409161 [doi]
PST - ppublish
SO  - J Gen Physiol. 2005 Feb;125(2):197-211. doi: 10.1085/jgp.200409161. Epub 2005 Jan 
      18.