TY - JOUR
T1 - Mechanism of Cytoplasmic Calcium Changes in Platelets in Contact with Polystyrene and Poly(Acrylamide-Co-Methacrylic Acid) Surfaces
AU - Yui, Nobuhiko
AU - Suzuki, Ken
AU - Okano, Teruo
AU - Sakurai, Yasuhisa
AU - Ishikawa, Chikako
AU - Fujimoto, Keiji
AU - Kawaguchi, Haruma
N1 - Funding Information:
The authors are grateful to Dr David W. Grainger, Oregon Graduate Institute of Science and Technology, USA, for his valuable discussion, and to Sekisul Chemical Co., Japan, for their supply of polystyrene microsphere particles. This research was financially supported by a Grant-in-Aid from the Ministry of Education, Science and Culture, Japan.
PY - 1993
Y1 - 1993
N2 - Changes in cytoplasmic free calcium levels ([Ca2+]i) in platelets in contact with polystyrene (PSt) and poly(acrylamide-co-methacrylic acid) (PAAmMAc) particles were evaluated and results were compared with those from two representative biological calcium agonists; thrombin and calcium ionophore A23187. PSt particles stimulated a steep increase in cytoplasmic calcium levels in platelets as much as thrombin and A23187. Serratia protease-treated platelets showed a steep increase in [Ca2+]i) by PSt particles, suggesting that PSt surfaces can initiate platelet activation independent of a glycoprotein Ib (GPIb)-mediated pathway. By contrast, dibucaine-treated platelets showed little increase in [Ca2+]i by PSt particles, indicating that microfilament assembly, including binding of GPIb with actin binding protein, should be required for platelet activation in contact with PSt surfaces. PAAmMAc particles induced little increase in cytoplasmic calcium levels in platelets. However, PAAmMAc particle-treated platelets demonstrated little response to thrombin in terms of an increase in [Ca2+]i and ATP release, suggesting the possibility that PAAmMAc surfaces may regulate [Ca2+]i by influencing platelet metabolism. Furthermore, sodium azide-treated platelets showed an increase in [Ca2+]i in platelets when contacting PAAmMAc particles, supporting the suggestion that PAAmMAc surfaces could regulate platelet functions. Fluorescence polarization measurements using 1, 6-diphenyl-l, 3, 5-hexatriene-loaded platelets revealed that PAAmMAc particles increased membrane fluidity in platelets, which may be due to physicochemical interaction with PAAmMAc surfaces.
AB - Changes in cytoplasmic free calcium levels ([Ca2+]i) in platelets in contact with polystyrene (PSt) and poly(acrylamide-co-methacrylic acid) (PAAmMAc) particles were evaluated and results were compared with those from two representative biological calcium agonists; thrombin and calcium ionophore A23187. PSt particles stimulated a steep increase in cytoplasmic calcium levels in platelets as much as thrombin and A23187. Serratia protease-treated platelets showed a steep increase in [Ca2+]i) by PSt particles, suggesting that PSt surfaces can initiate platelet activation independent of a glycoprotein Ib (GPIb)-mediated pathway. By contrast, dibucaine-treated platelets showed little increase in [Ca2+]i by PSt particles, indicating that microfilament assembly, including binding of GPIb with actin binding protein, should be required for platelet activation in contact with PSt surfaces. PAAmMAc particles induced little increase in cytoplasmic calcium levels in platelets. However, PAAmMAc particle-treated platelets demonstrated little response to thrombin in terms of an increase in [Ca2+]i and ATP release, suggesting the possibility that PAAmMAc surfaces may regulate [Ca2+]i by influencing platelet metabolism. Furthermore, sodium azide-treated platelets showed an increase in [Ca2+]i in platelets when contacting PAAmMAc particles, supporting the suggestion that PAAmMAc surfaces could regulate platelet functions. Fluorescence polarization measurements using 1, 6-diphenyl-l, 3, 5-hexatriene-loaded platelets revealed that PAAmMAc particles increased membrane fluidity in platelets, which may be due to physicochemical interaction with PAAmMAc surfaces.
KW - ATP release
KW - Polystyrene
KW - cytoplasmic free calcium level
KW - glycoprotein
KW - membrane fluidity
KW - poly(acrylamide-co-methacrylic acid)
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U2 - 10.1163/156856293X00528
DO - 10.1163/156856293X00528
M3 - Article
C2 - 8476791
AN - SCOPUS:0027345256
VL - 4
SP - 199
EP - 215
JO - Journal of Biomaterials Science, Polymer Edition
JF - Journal of Biomaterials Science, Polymer Edition
SN - 0920-5063
IS - 3
ER -