Complement activation dramatically accelerates blood plasma fouling on antifouling poly(2-hydroxyethyl methacrylate) brush surfaces

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61389013%3A_____%2F22%3A00555739" target="_blank" >RIV/61389013:_____/22:00555739 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00023736:_____/22:00013361

Výsledek na webu

<a href="https://onlinelibrary.wiley.com/doi/10.1002/mabi.202100460" target="_blank" >https://onlinelibrary.wiley.com/doi/10.1002/mabi.202100460</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1002/mabi.202100460" target="_blank" >10.1002/mabi.202100460</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Complement activation dramatically accelerates blood plasma fouling on antifouling poly(2-hydroxyethyl methacrylate) brush surfaces

Popis výsledku v původním jazyce

Non-specific protein adsorption (fouling) triggers a number of deleterious events in the application of biomaterials. Antifouling polymer brushes successfully suppress fouling, however for some coatings an extremely high variability of fouling for different donors remains unexplained. The authors report that in the case of poly(2-hydroxyethyl methacrylate) (poly(HEMA)) this variability is due to the complement system activation that causes massive acceleration in the fouling kinetics of blood plasma. Using plasma from various donors, the fouling kinetics on poly(HEMA) is analyzed and correlated with proteins identified in the deposits on the surface and with the biochemical compositions of the plasma. The presence of complement components in fouling deposits and concentrations of C3a in different plasmas indicate that the alternative complement pathway plays a significant role in the fouling on poly(HEMA) through the “tick-over” mechanism of spontaneous C3 activation. The generated C3b binds to the poly(HEMA) surface and amplifies complement activation locally. Heat-inactivated plasma prevents accelerated fouling kinetics, confirming the central role of complement activation. The results highlight the need to take into account the variability between individuals when assessing interactions between biomaterials and blood plasma, as well as the importance of the mechanistic insight that can be gained from protein identification.

Název v anglickém jazyce

Complement activation dramatically accelerates blood plasma fouling on antifouling poly(2-hydroxyethyl methacrylate) brush surfaces

Popis výsledku anglicky

Non-specific protein adsorption (fouling) triggers a number of deleterious events in the application of biomaterials. Antifouling polymer brushes successfully suppress fouling, however for some coatings an extremely high variability of fouling for different donors remains unexplained. The authors report that in the case of poly(2-hydroxyethyl methacrylate) (poly(HEMA)) this variability is due to the complement system activation that causes massive acceleration in the fouling kinetics of blood plasma. Using plasma from various donors, the fouling kinetics on poly(HEMA) is analyzed and correlated with proteins identified in the deposits on the surface and with the biochemical compositions of the plasma. The presence of complement components in fouling deposits and concentrations of C3a in different plasmas indicate that the alternative complement pathway plays a significant role in the fouling on poly(HEMA) through the “tick-over” mechanism of spontaneous C3 activation. The generated C3b binds to the poly(HEMA) surface and amplifies complement activation locally. Heat-inactivated plasma prevents accelerated fouling kinetics, confirming the central role of complement activation. The results highlight the need to take into account the variability between individuals when assessing interactions between biomaterials and blood plasma, as well as the importance of the mechanistic insight that can be gained from protein identification.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10610 - Biophysics

Projekt

<a href="/cs/project/GA20-10845S" target="_blank" >GA20-10845S: Individuální variabilita a patofyziologie krevní plasmy a jejich vliv na interakci s umělými povrchy potlačujícími nespecifické interakce</a><br>

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2022

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Macromolecular Bioscience

ISSN

1616-5187

e-ISSN

1616-5195

Svazek periodika

22

Číslo periodika v rámci svazku

3

Stát vydavatele periodika

DE - Spolková republika Německo

Počet stran výsledku

8

Strana od-do

2100460

Kód UT WoS článku

000738641200001

EID výsledku v databázi Scopus

2-s2.0-85122330307