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Mechanical Stimulation-induced Calcium Wave Propagation in Cell Monolayers: The Example of Bovine Corneal Endothelial Cells
Published on: July 16, 2013
Cytosolic calcium as a second messenger for collagen-induced platelet responses
J B Smith1, M A Selak, C Dangelmaier
1Department of Pharmacology, Temple University Medical School, Philadelphia, PA 19140.
Collagen-induced platelet responses like arachidonic acid liberation and dense granule secretion require increased intracellular calcium (Ca2+). However, this calcium increase is not essential for protein kinase C pathway activation during platelet adhesion to collagen.
Area of Science:
- Biochemistry
- Cell Biology
- Hematology
Background:
- Platelet activation by collagen is a critical step in hemostasis.
- Previous studies indicated collagen-induced platelet activation involves cytosolic free Ca2+ concentration ([Ca2+]i) increase, but its necessity for adhesion was unclear.
Purpose of the Study:
- To investigate the role of intracellular calcium ([Ca2+]i) in collagen-induced platelet activation pathways.
- To determine if [Ca2+]i is required for specific platelet responses beyond adhesion.
Main Methods:
- Platelets were loaded with the calcium chelator BAPTA or a non-chelating control (diazo-3).
- Collagen was used to stimulate platelets, and responses like arachidonic acid liberation, myosin phosphorylation, 5-hydroxytryptamine secretion, phosphatidic acid formation, and pleckstrin phosphorylation were measured.
Main Results:
- Collagen-induced arachidonic acid liberation, myosin phosphorylation, and 5-hydroxytryptamine secretion were significantly inhibited by BAPTA.
- BAPTA partially inhibited collagen-induced phosphatidic acid formation but had minimal impact on pleckstrin phosphorylation.
- The non-chelating control (diazo-3) did not inhibit these responses.
Conclusions:
- Increases in intracellular calcium ([Ca2+]i) are essential for collagen-induced dense granule secretion and arachidonic acid liberation in platelets.
- [Ca2+]i is not required for the stimulation of the protein kinase C pathway during collagen-induced platelet activation.
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