scholarly journals Coupling between inositol 1,4,5-trisphosphate receptors and human transient receptor potential channel 1 when intracellular Ca2+ stores are depleted

2000 ◽  
Vol 350 (3) ◽  
pp. 631-635 ◽  
Author(s):  
Juan A. ROSADO ◽  
Stewart O. SAGE
Keyword(s):  
Transient Receptor Potential ◽  
De Novo ◽  
Receptor Potential ◽  
Transient Receptor Potential Channel ◽  
Human Platelets ◽  
Ip3 Receptors ◽  
Inositol 1,4,5 Trisphosphate ◽  
Normal Human ◽  
Transient Receptor

In the present study we have investigated the role of inositol 1,4,5-trisphosphate (IP3), functional IP3 receptors (IP3Rs) and the human homologue of the Drosophila transient receptor potential (Trp) channel, human Trp1 (hTrp1), in store-mediated Ca2+ entry (SMCE) in human platelets. Inhibition of IP3 recycling using Li+, or the inhibition of IP3Rs using xestospongin C, both resulted in the inhibition of SMCE activation following Ca2+ store depletion using thapsigargin. Co-immunoprecipitation experiments indicated that endogenously expressed hTrp1 couples with IP3R type II, but not types I or III, in platelets with depleted intracellular Ca2+ stores, but not in control, undepleted cells. These results provide strong evidence for the activation of SMCE by conformational coupling involving de novo association between IP3Rs and a plasma membrane channel in normal human cells.

Activation of store-mediated calcium entry by secretion-like coupling between the inositol 1,4,5-trisphosphate receptor type II and human transient receptor potential (hTrp1) channels in human platelets

2001 ◽  
Vol 356 (1) ◽  
pp. 191-198 ◽  
Author(s):  
Juan A. ROSADO ◽  
Stewart O. SAGE
Keyword(s):  
Actin Filaments ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Human Platelets ◽  
Type Ii ◽  
Actin Network ◽  
Ip3 Receptors ◽  
Ip3 Receptor ◽  
Inositol 1,4,5 Trisphosphate ◽  
Transient Receptor

Physical coupling between inositol 1,4,5-trisphosphate (IP3) receptors and transient receptor potential (Trp) channels has been demonstrated in both transfected and normal cells as a candidate mechanism for the activation of store-mediated Ca2+ entry (SMCE). We have investigated the properties of the coupling between the type II IP3 receptor and naturally expressed human Trp1 (hTrp1) in human platelets. Treatment with xestospongin C, an inhibitor of IP3 receptor function, abolished SMCE and coupling between the IP3 receptor and hTrp1. The coupling was activated by depletion of the intracellular Ca2+ stores, and was reversed by refilling of the stores. We have also examined the role of actin filaments in the activation and maintenance of the coupling. Stabilization of the cortical actin network with jasplakinolide prevented the coupling, indicating that, as with secretion, the actin filaments at the cell periphery act as a negative clamp which prevents constitutive coupling. In addition, the actin cytoskeleton plays a positive role, since disruption of the actin network inhibited the coupling when the Ca2+ stores were depleted. These results provide strong evidence for the activation of SMCE by a secretion-like coupling mechanism involving a reversible association between IP3 receptors and hTrp1 in normal human cells.

Role of capacitative Ca2+ entry in bronchial contraction and remodeling

2002 ◽  
Vol 92 (4) ◽  
pp. 1594-1602 ◽  
Author(s):  
Michele Sweeney ◽  
Sharon S. McDaniel ◽  
Oleksandr Platoshyn ◽  
Shen Zhang ◽  
Ying Yu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Transient Receptor Potential ◽  
Bronchial Hyperresponsiveness ◽  
Receptor Potential ◽  
Transient Receptor Potential Channel ◽  
Wall Thickening ◽  
Bronchial Wall ◽  
Intracellular Ca ◽  
Transient Receptor

Asthma is characterized by airway inflammation, bronchial hyperresponsiveness, and airway obstruction by bronchospasm and bronchial wall thickening due to smooth muscle hypertrophy. A rise in cytosolic free Ca2+ concentration ([Ca2+]cyt) may serve as a shared signal transduction element that causes bronchial constriction and bronchial wall thickening in asthma. In this study, we examined whether capacitative Ca2+ entry (CCE) induced by depletion of intracellular Ca2+ stores was involved in agonist-mediated bronchial constriction and bronchial smooth muscle cell (BSMC) proliferation. In isolated bronchial rings, acetylcholine (ACh) induced a transient contraction in the absence of extracellular Ca2+ because of Ca2+ release from intracellular Ca2+ stores. Restoration of extracellular Ca2+in the presence of atropine, an M-receptor blocker, induced a further contraction that was apparently caused by a rise in [Ca2+]cyt due to CCE. In single BSMC, amplitudes of the store depletion-activated currents ( I SOC) and CCE were both enhanced when the cells proliferate, whereas chelation of extracellular Ca2+ with EGTA significantly inhibited the cell growth in the presence of serum. Furthermore, the mRNA expression of TRPC1, a transient receptor potential channel gene, was much greater in proliferating BSMC than in growth-arrested cells. Blockade of the store-operated Ca2+channels by Ni2+ decreased I SOC and CCE and markedly attenuated BSMC proliferation. These results suggest that upregulated TRPC1 expression, increased I SOC, enhanced CCE, and elevated [Ca2+]cyt may play important roles in mediating bronchial constriction and BSMC proliferation.

scholarly journals The Role of Transient Receptor Potential Channel 6 Channels in the Pulmonary Vasculature

2017 ◽  
Vol 8 ◽  
Author(s):  
Monika Malczyk ◽  
Alexandra Erb ◽  
Christine Veith ◽  
Hossein Ardeschir Ghofrani ◽  
Ralph T. Schermuly ◽  
...  
Keyword(s):  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor Potential Channel ◽  
Pulmonary Vasculature ◽  
Transient Receptor
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