Platelet-Rich Plasma Influences Expansion and Paracrine Function of Adipose-Derived Stromal Cells in a Dose-Dependent Fashion

2016 ◽  
Vol 137 (3) ◽  
pp. 554e-565e ◽  
Author(s):  
Joep C. N. Willemsen ◽  
Maroesjka Spiekman ◽  
H. P. Jeroen Stevens ◽  
Berend van der Lei ◽  
Martin C. Harmsen
1981 ◽  
Author(s):  
D Aharonv ◽  
J B Smith ◽  
M J Silver

The arachidonate hydroperoxides 12-HPETE and 15-HPETE were biosynthesized from arachidonic acid using partially purified human platelet lipoxygenase or soybean lipoxidase respectively, and isolated by thin layer chromatography. Both compounds inhibited the arachidonic acid- induced aggregation of washed human platelets, suspended in calcium-free Krebs Henseleit solution, in a dose dependent fashion at concentrations between 1 and 50 uM. No inhibition was seen with up to 100 uM of these hydroperoxides when platelet -rich plasma was used. 12-HPETE (in micromolar concentrations) inhibited the formation of both thromboxane B2 (radioimmunoassay) and malonyldialdehyde (spectrophotometrie assay) when washed platelets were incubated with arachidonic acid. The 12-hydroxide, 12-HETE also inhibited platelet aggregation and thromboxane formation, but was less potent than 12-HPETE. We suggest that arachidonate hydroperoxide generated in platelets via the lipoxygenase pathway modulates platelet aggregation induced by arachidonic acid by inhibiting thromboxane formation.


2019 ◽  
Vol 229 (4) ◽  
pp. S108
Author(s):  
Raquel Araujo-Gutierrez ◽  
Jeffrey L. Van Eps ◽  
Fernando J. Cabrera ◽  
Keith A. Youker ◽  
Joseph S. Fernandez-Moure

Biomaterials ◽  
2008 ◽  
Vol 29 (23) ◽  
pp. 3338-3345 ◽  
Author(s):  
Yunsong Liu ◽  
Yongsheng Zhou ◽  
Hailan Feng ◽  
Gui-e Ma ◽  
Yongwei Ni

2013 ◽  
Vol 22 (3) ◽  
pp. 437-445 ◽  
Author(s):  
Suk Ho Bhang ◽  
Jooyeon Park ◽  
Hee Seok Yang ◽  
Jaehoon Shin ◽  
Byung-Soo Kim

1987 ◽  
Author(s):  
C Cordova ◽  
F Violi ◽  
D Praticò ◽  
A Ghiselli ◽  
C Alessandri ◽  
...  

Low doses of aspirin (20 mg/day) were previously reported to be uneffective in preventing platelet aggregation (PA) induced by pairs of aggregating agents such as PAF and adrenalin.This was in part attributed to the inability of such treatment to inhibit lipo oxygenase-dependent PA.The latter can be observed in vitro in"aspl rinated"platelets stimulated with high quantities of aggregating -agents.The aim of this study was to evaluate if the lipooxygenase-dependent PA was influenced by aspirin in a dose-dependent fashion. PA was studied in platelet rich plasma (PRP)(Born's method) by using threshold doses of aggregating agents (TDA) such as PAF(4-75 nM),epinephrine(0.6-2 μM) and collagen(2-4 μg/ml).PA performed in PRP pretrated with 100μM aspirin was fully prevented;in the same samples thromboxane (Tx) A2 evaluated by its metabolite Tx B2 was almost absent.Increasing amount of PAF(20 fold TDA),epinephrine(20 fold TDA) and collagen (36 fold TDA) do aggregate"aspirinated"pla telets;similarly"aspirinated"platelets aggregate when stimulated-with a pair of aggregating agents (TDA of PAF+epinephrine).This phenomenon was not detected if platelets were incubated with higher amounts of aspirin (250-500 μM).The study suggests that aspirin could influence lipooxygenase-dependent PA.This hypothesis is sup ported by a research showing the aspirin inhibits dose-dependently platelet HETE formation.A further study is now in progress to eva luate the influence of high doses of aspirin on cyclooxygenase-i"n dependent PA in vivo.


2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Himanshu Bansal ◽  
Kristin Comella ◽  
Jerry Leon ◽  
Poonam Verma ◽  
Diwaker Agrawal ◽  
...  

This article has been retracted. Please see the Retraction Notice for more detail: https://doi.org/10.1186/s12967-021-02852-z


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