Research ExplorerPublicationsInsulin inhibition of platelet-endothelial interaction is me...

Insulin inhibition of platelet-endothelial interaction is mediated by insulin effects on endothelial cells without direct effects on platelets

Standard

Insulin inhibition of platelet-endothelial interaction is mediated by insulin effects on endothelial cells without direct effects on platelets. / Rauchfuss, S; Geiger, J; Walter, U; Renne, T; Gambaryan, S.

In: J THROMB HAEMOST, Vol. 6, No. 5, 01.05.2008, p. 856-64.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Rauchfuss, S, Geiger, J, Walter, U, Renne, T & Gambaryan, S 2008, 'Insulin inhibition of platelet-endothelial interaction is mediated by insulin effects on endothelial cells without direct effects on platelets', J THROMB HAEMOST, vol. 6, no. 5, pp. 856-64. https://doi.org/10.1111/j.1538-7836.2008.02925.x

APA

Rauchfuss, S., Geiger, J., Walter, U., Renne, T., & Gambaryan, S. (2008). Insulin inhibition of platelet-endothelial interaction is mediated by insulin effects on endothelial cells without direct effects on platelets. J THROMB HAEMOST, 6(5), 856-64. https://doi.org/10.1111/j.1538-7836.2008.02925.x

Vancouver

Rauchfuss S, Geiger J, Walter U, Renne T, Gambaryan S. Insulin inhibition of platelet-endothelial interaction is mediated by insulin effects on endothelial cells without direct effects on platelets. J THROMB HAEMOST. 2008 May 1;6(5):856-64. https://doi.org/10.1111/j.1538-7836.2008.02925.x

Bibtex

@article{1667f03cd45348d1abe21c2a0a828930,
title = "Insulin inhibition of platelet-endothelial interaction is mediated by insulin effects on endothelial cells without direct effects on platelets",
abstract = "OBJECTIVES: Platelet hyperreactivity contributes to adverse vascular events in diabetes mellitus. It is unclear whether platelet hyperreactivity is due to impaired insulin effects directly on platelets and /or originates from endothelial cells. Here, acute effects of insulin on platelet activation and platelet-endothelial cell interactions were analyzed.METHODS AND RESULTS: Washed human platelets were treated with insulin alone or in combinations with thrombin, collagen and ADP. Insulin signaling was analyzed by intracellular phosphorylation markers of platelet activation (ERK, p38 MAPK, PKB) or inhibition (VASP), platelet aggregation, intracellular Ca(2+) levels, and platelet adhesion to collagen coated surfaces and endothelial cells under flow. Insulin up to 100 nm for 5 min did not change phosphorylation status of VASP, p38, ERK or PKB in platelets. Integrin alpha(IIb)beta(3) activation, P-selectin expression, aggregation, and platelet adhesion to collagen coated surfaces and endothelial cells under flow were not altered by insulin. An insulin receptor was detected on endothelial cells but not on human platelets. Insulin treatment decreased platelet adhesion to endothelial cells through insulin stimulation of endothelial NO production and NOS inhibition interfered with this process.CONCLUSIONS: Insulin exerts no direct acute effects on platelet function but inhibits platelet-endothelial interaction by insulin stimulation of endothelial NO production.",
keywords = "Blood Platelets, Endothelial Cells, Humans, Insulin, Nitric Oxide, Phosphorylation, Platelet Activation, Platelet Adhesiveness, Receptor, Insulin, Signal Transduction",
author = "S Rauchfuss and J Geiger and U Walter and T Renne and S Gambaryan",
year = "2008",
month = may,
day = "1",
doi = "10.1111/j.1538-7836.2008.02925.x",
language = "English",
volume = "6",
pages = "856--64",
journal = "J THROMB HAEMOST",
issn = "1538-7933",
publisher = "Wiley-Blackwell",
number = "5",

}

RIS

TY - JOUR

T1 - Insulin inhibition of platelet-endothelial interaction is mediated by insulin effects on endothelial cells without direct effects on platelets

AU - Rauchfuss, S

AU - Geiger, J

AU - Walter, U

AU - Renne, T

AU - Gambaryan, S

PY - 2008/5/1

Y1 - 2008/5/1

N2 - OBJECTIVES: Platelet hyperreactivity contributes to adverse vascular events in diabetes mellitus. It is unclear whether platelet hyperreactivity is due to impaired insulin effects directly on platelets and /or originates from endothelial cells. Here, acute effects of insulin on platelet activation and platelet-endothelial cell interactions were analyzed.METHODS AND RESULTS: Washed human platelets were treated with insulin alone or in combinations with thrombin, collagen and ADP. Insulin signaling was analyzed by intracellular phosphorylation markers of platelet activation (ERK, p38 MAPK, PKB) or inhibition (VASP), platelet aggregation, intracellular Ca(2+) levels, and platelet adhesion to collagen coated surfaces and endothelial cells under flow. Insulin up to 100 nm for 5 min did not change phosphorylation status of VASP, p38, ERK or PKB in platelets. Integrin alpha(IIb)beta(3) activation, P-selectin expression, aggregation, and platelet adhesion to collagen coated surfaces and endothelial cells under flow were not altered by insulin. An insulin receptor was detected on endothelial cells but not on human platelets. Insulin treatment decreased platelet adhesion to endothelial cells through insulin stimulation of endothelial NO production and NOS inhibition interfered with this process.CONCLUSIONS: Insulin exerts no direct acute effects on platelet function but inhibits platelet-endothelial interaction by insulin stimulation of endothelial NO production.

AB - OBJECTIVES: Platelet hyperreactivity contributes to adverse vascular events in diabetes mellitus. It is unclear whether platelet hyperreactivity is due to impaired insulin effects directly on platelets and /or originates from endothelial cells. Here, acute effects of insulin on platelet activation and platelet-endothelial cell interactions were analyzed.METHODS AND RESULTS: Washed human platelets were treated with insulin alone or in combinations with thrombin, collagen and ADP. Insulin signaling was analyzed by intracellular phosphorylation markers of platelet activation (ERK, p38 MAPK, PKB) or inhibition (VASP), platelet aggregation, intracellular Ca(2+) levels, and platelet adhesion to collagen coated surfaces and endothelial cells under flow. Insulin up to 100 nm for 5 min did not change phosphorylation status of VASP, p38, ERK or PKB in platelets. Integrin alpha(IIb)beta(3) activation, P-selectin expression, aggregation, and platelet adhesion to collagen coated surfaces and endothelial cells under flow were not altered by insulin. An insulin receptor was detected on endothelial cells but not on human platelets. Insulin treatment decreased platelet adhesion to endothelial cells through insulin stimulation of endothelial NO production and NOS inhibition interfered with this process.CONCLUSIONS: Insulin exerts no direct acute effects on platelet function but inhibits platelet-endothelial interaction by insulin stimulation of endothelial NO production.

KW - Blood Platelets

KW - Endothelial Cells

KW - Humans

KW - Insulin

KW - Nitric Oxide

KW - Phosphorylation

KW - Platelet Activation

KW - Platelet Adhesiveness

KW - Receptor, Insulin

KW - Signal Transduction

U2 - 10.1111/j.1538-7836.2008.02925.x

DO - 10.1111/j.1538-7836.2008.02925.x

M3 - SCORING: Journal article

C2 - 18284601

VL - 6

SP - 856

EP - 864

JO - J THROMB HAEMOST

JF - J THROMB HAEMOST

SN - 1538-7933

IS - 5

ER -