PMID- 23784603
OWN - NLM
STAT- MEDLINE
DCOM- 20140403
LR  - 20220408
IS  - 2567-689X (Electronic)
IS  - 0340-6245 (Linking)
VI  - 110
IP  - 2
DP  - 2013 Aug
TI  - Contact- and agonist-regulated microvesiculation of human platelets.
PG  - 331-9
LID - 10.1160/TH12-11-0853 [doi]
AB  - After exposure to an agonist, platelets are activated and become aggregated. They 
      also shed membrane microparticles that participate in the pathogenesis of 
      thrombosis, hyper-coagulation and inflammation. However, microvesiculation can 
      potentially disrupt the integrity of platelet aggregation by shedding the 
      membrane receptors and phosphatidylserine critical for forming and stabilising a 
      platelet clot. We tested the hypothesis that adhesion and microvesiculation are 
      functions of different subsets of platelets at the time of haemostasis by 
      real-time monitoring of agonist-induced morphological changes and 
      microvesiculation of human platelets.We identified two types of platelets that 
      are adherent to fibrinogen: a high density bubble shape (HDBS) and low-density 
      spread shape (LDSS). Adenosine diphosphate (ADP) predominantly induced HDBS 
      platelets to vesiculate, whereas LDSS platelets were highly resistant to such 
      vesiculation. Thrombin-receptor activating peptide (TRAP) stabilised platelets 
      against microvesiculation by promoting a rapid HDBS-to-LDSS morphological 
      transition. These activities of ADP and TRAP were reversed for platelets in 
      suspension, independent of an engagement integrin alphaIIbbeta3. As the result of 
      membrane contact, LDSS platelets inhibited the microvesiculation of HDBS 
      platelets in response to ADP. Aspirin and clopidogrel inhibited ADP-induced 
      microvesiculation through different mechanisms. These results suggest that 
      platelet aggregation and microvesiculation occur in different subsets of 
      platelets and are differently regulated by agonists, platelet-platelets and 
      platelet-fibrinogen interactions.
FAU - Zhang, Yanjun
AU  - Zhang Y
AD  - Department of Neurosurgery, University General Hospital, Tianjin Medical 
      University, 154 Anshan Road, Tianjin, China. jianningzhang@hotmail.com
FAU - Liu, Xiao
AU  - Liu X
FAU - Liu, Li
AU  - Liu L
FAU - Zaske, Ana-Maria
AU  - Zaske AM
FAU - Zhou, Zhou
AU  - Zhou Z
FAU - Fu, Yuanyuan
AU  - Fu Y
FAU - Yang, Xi
AU  - Yang X
FAU - Conyers, Jodie L
AU  - Conyers JL
FAU - Li, Min
AU  - Li M
FAU - Dong, Jing-fei
AU  - Dong JF
FAU - Zhang, Jianning
AU  - Zhang J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130620
PL  - Germany
TA  - Thromb Haemost
JT  - Thrombosis and haemostasis
JID - 7608063
RN  - 0 (Peptide Fragments)
RN  - 0 (Platelet Aggregation Inhibitors)
RN  - 145229-76-1 (thrombin receptor peptide SFLLRNP)
RN  - 61D2G4IYVH (Adenosine Diphosphate)
RN  - 9001-32-5 (Fibrinogen)
RN  - A74586SNO7 (Clopidogrel)
RN  - OM90ZUW7M1 (Ticlopidine)
RN  - R16CO5Y76E (Aspirin)
SB  - IM
MH  - Adenosine Diphosphate/blood/pharmacology
MH  - Aspirin/pharmacology
MH  - Blood Platelets/*drug effects/*physiology/ultrastructure
MH  - Cell Shape/drug effects/physiology
MH  - Cell-Derived Microparticles/drug effects/ultrastructure
MH  - Clopidogrel
MH  - Fibrinogen/physiology
MH  - Humans
MH  - Microscopy, Atomic Force
MH  - Peptide Fragments/blood/pharmacology
MH  - Platelet Aggregation/drug effects/physiology
MH  - Platelet Aggregation Inhibitors/pharmacology
MH  - Ticlopidine/analogs & derivatives/pharmacology
EDAT- 2013/06/21 06:00
MHDA- 2014/04/04 06:00
CRDT- 2013/06/21 06:00
PHST- 2012/11/21 00:00 [received]
PHST- 2013/04/23 00:00 [accepted]
PHST- 2013/06/21 06:00 [entrez]
PHST- 2013/06/21 06:00 [pubmed]
PHST- 2014/04/04 06:00 [medline]
AID - 12-11-0853 [pii]
AID - 10.1160/TH12-11-0853 [doi]
PST - ppublish
SO  - Thromb Haemost. 2013 Aug;110(2):331-9. doi: 10.1160/TH12-11-0853. Epub 2013 Jun 
      20.