Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Formation of the Platelet Plug01:22

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
Dipeptidyl Peptidase 4 Inhibitors01:23

Dipeptidyl Peptidase 4 Inhibitors

Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a significant...
Oral Hypoglycemic Agents: α-Glucosidase Inhibitors01:19

Oral Hypoglycemic Agents: α-Glucosidase Inhibitors

α-glucosidase inhibitors, including acarbose (Precose), miglitol (Glyset), and voglibose (Voglib) (primarily available in Asia), are drugs that control blood sugar levels by delaying the digestion of starch and disaccharides. They achieve this by inhibiting α-glucosidase enzymes in the intestine, which slow the absorption of carbohydrates in the intestine, which in turn leads to a prolonged release of the glucoregulatory hormone GLP-1 from intestinal L-cells.
Acarbose and miglitol are typically...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Fatty acid profile driven by maternal diet is associated with the composition of human milk microbiota.

Frontiers in microbiomes·2026
Same author

Corrigendum: Fatty acid profile driven by maternal diet is associated with the composition of human milk microbiota.

Frontiers in microbiomes·2026
Same author

Regulation of hepatic Sirt1 expression and lipid metabolism through TNF receptor signaling.

Frontiers in immunology·2025
Same author

Endoscopic papillectomy for laterally spreading lesions of the papilla: a propensity score-matched analysis.

Endoscopy·2025
Same author

Development and validation of the SDLD score: a simplified tool to predict successful endoscopic papillectomy in ampullary lesions.

Gastrointestinal endoscopy·2025
Same author

Endoscopic papillectomy versus surgical ampullectomy for adenomas and early cancers of the papilla: a retrospective Pancreas2000/European Pancreatic Club analysis.

Gut·2024

Related Experiment Video

Updated: May 17, 2026

Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells
10:10

Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells

Published on: October 27, 2009

Glycine reduces platelet aggregation.

Peter Schemmer1, Zhi Zhong, Uwe Galli

  • 1Department of General and Transplant Surgery, Ruprecht-Karls-University, Im Neuenheimer Feld 110, 69120 Heidelberg, Germany. Peter.Schemmer@med.uni-heidelberg.de

Amino Acids
|November 9, 2012
PubMed
Summary
This summary is machine-generated.

Dietary glycine significantly prolonged bleeding time and inhibited platelet aggregation in rats and humans. Glycine acts through glycine receptors to prevent platelet aggregation, offering potential therapeutic benefits.

More Related Videos

Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation
09:13

Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation

Published on: April 6, 2017

Related Experiment Videos

Last Updated: May 17, 2026

Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells
10:10

Platelet Adhesion and Aggregation Under Flow using Microfluidic Flow Cells

Published on: October 27, 2009

Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation
09:13

Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation

Published on: April 6, 2017

Area of Science:

  • Pharmacology
  • Hematology
  • Neuroscience

Background:

  • Glycine-gated chloride channels are present in various immune cells, including macrophages and neutrophils.
  • Glycine binding to its receptor causes chloride influx, leading to membrane hyperpolarization and preventing calcium influx.
  • Platelet aggregation is a calcium-dependent process crucial for hemostasis.

Purpose of the Study:

  • To investigate the hypothesis that glycine inhibits platelet aggregation.
  • To determine the role of glycine receptors in this inhibitory effect.
  • To assess the effect of dietary glycine on bleeding time and platelet aggregation.

Main Methods:

  • Rats were fed diets supplemented with glycine or valine for five days.
  • Bleeding time and platelet aggregation induced by ADP and collagen were measured.
  • Glycine was added in vitro to assess its direct effect on platelet aggregation, with and without strychnine (a glycine receptor antagonist).
  • Western blotting was used to detect glycine receptors in rat and human platelets.

Main Results:

  • Dietary glycine significantly increased bleeding time twofold compared to controls.
  • Platelet aggregation induced by ADP or collagen was reduced by over 50% in rats fed glycine.
  • In vitro glycine addition dose-dependently inhibited rat platelet aggregation.
  • Strychnine abolished the inhibitory effect of glycine in vitro, indicating a role for glycine receptors.
  • Glycine also inhibited human platelet aggregation, and glycine receptors were detected in both rat and human platelets.

Conclusions:

  • Glycine effectively prevents platelet aggregation in a dose-dependent manner.
  • This effect is mediated through glycine receptors present on platelets.
  • Glycine holds potential for therapeutic applications in conditions involving excessive platelet aggregation.