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Apolipoprotein B release from activated human platelets.
Atherosclerosis
|September 1, 1986
Summary
Human platelets release apolipoprotein B (apoB) upon activation. This release, measured by ELISA, is similar to beta-thromboglobulin (beta-TG) release and is inhibited by carbacyclin.
Area of Science:
- Biochemistry
- Hematology
- Immunology
Background:
- Platelets play a crucial role in hemostasis and thrombosis.
- Apolipoprotein B (apoB) is a major component of low-density lipoproteins (LDL).
- The presence and release of apoB from platelets are not well understood.
Purpose of the Study:
- To investigate the release of apolipoprotein B (apoB) from activated human platelets.
- To characterize the conditions and mechanisms of apoB release.
Main Methods:
- Washed human platelets were activated using various agonists (thrombin, Ca2+-ionophore A23187, U46619).
- Apolipoprotein B (apoB) release was quantified using enzyme-linked immunosorbent assay (ELISA).
- Density gradient ultracentrifugation was employed to determine the density of released apoB.
Main Results:
- Platelet activation with thrombin, A23187, or U46619 stimulated the release of approximately 20 ng apoB/10(8) platelets.
- Thrombin-induced apoB release was inhibited by the prostacyclin analogue carbacyclin.
- The dose-response curves for apoB and beta-thromboglobulin (beta-TG) release were similar, as was the inhibition by carbacyclin.
- Density gradient ultracentrifugation showed that released apoB was primarily in the LDL density range.
- Heparin treatment did not affect apoB levels or thrombin-induced release.
Conclusions:
- Human platelets contain immunoreactive apolipoprotein B (apoB).
- Platelet activation triggers the release of apoB, suggesting its involvement in platelet function.
- The release mechanism shares similarities with that of beta-thromboglobulin (beta-TG).