TY  - JOUR
A1  - Loeffler, Claudia
A1  - Loeffler, Jürgen
A1  - Kobsar, Anna
A1  - Speer, Christian P.
A1  - Eigenthaler, Martin
T1  - Septic Vs Colonizing Group B Streptococci Differentially Regulate Inflammation and Apoptosis in Human Coronary Artery Endothelial Cells - a Pilot Study
JF  - Journal of Pediatrics and Neonatal Care
N2  - In this pilot study, we exemplify differences between a septic and a colonizing GBS strain during their interaction with Endothelial Cells by evaluating cytokine levels, surface and apoptosis-related molecules. These preliminary results indicate that in vitro infection using an exemplary septic GBS strain results in diminished activation of the innate immune response.
KW  - streptococci
KW  - apoptosis
KW  - inflammation
KW  - endothelial cells
KW  - innate immunity
KW  - early onset sepsis
Y1  - 2015
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-125596
VL  - 2
IS  - 2
ER  - 
TY  - JOUR
A1  - Rukoyatkina, N.
A1  - Mindukshev, I.
A1  - Walter, U.
A1  - Gambaryan, S.
T1  - Dual role of the p38 \(MAPK/cPLA_2\) pathway in the regulation of platelet apoptosis induced by ABT-737 and strong platelet agonists
JF  - Cell Death & Disease
N2  - p38 Mitogen-activated protein (MAP) kinase is involved in the apoptosis of nucleated cells. Although platelets are anucleated cells, apoptotic proteins have been shown to regulate platelet lifespan. However, the involvement of p38 MAP kinase in platelet apoptosis is not yet clearly defined. Therefore, we investigated the role of p38 MAP kinase in apoptosis induced by a mimetic of BH3-only proteins, ABT-737, and in apoptosis-like events induced by such strong platelet agonists as thrombin in combination with convulxin (Thr/Cvx), both of which result in p38 MAP kinase phosphorylation and activation. A p38 inhibitor (SB202190) inhibited the apoptotic events induced by ABT-737 but did not influence those induced by Thr/Cvx. The inhibitor also reduced the phosphorylation of cytosolic phospholipase \(A_2\) (cPLA2), an established p38 substrate, induced by ABT-737 or Thr/Cvx. ABT-737, but not Thr/Cvx, induced the caspase 3-dependent cleavage and inactivation of cPLA2. Thus, p38 MAPK promotes ABT-737-induced apoptosis by inhibiting the cPLA2/arachidonate pathway. We also show that arachidonic acid (AA) itself and in combination with Thr/Cvx or ABT-737 at low concentrations prevented apoptotic events, whereas at high concentrations it enhanced such events. Our data support the hypothesis that the p38 MAPK-triggered arachidonate pathway serves as a defense mechanism against apoptosis under physiological conditions.
KW  - cPLA2
KW  - platelet
KW  - apoptosis
KW  - p38 MAP kinase
Y1  - 2013
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-128783
VL  - 4
IS  - e931
ER  -