A thrombocyta mint gyulladásos sejt = The platelet as an inflammatory cell

A kutatast az alabbi negy fokuszteruleten vegeztuk: 1. A P-selectin glycoprotein ligand-1 (PSGL-1) knock out, modellben leirtuk, hogy a PSGL-1 hianya protektiv szereppel bir a thrombosis kialakulasa soran es megallapitottuk, hogy a PSGL-1 hianyaban a myeloid sejtek es azok prekurzorai szignifikansan magasabb szamban szabadulnak fel, G-CSF hatasara (kozles alatt). 2. A thrombocyta aktivacio modulacio teren megallapitottuk, hogy a calyculin-A (CLA) hatasara jelentősen csokken a thromin receptor anragonista peptid (TRAP) aktivacio altal letrehozott valasz. Valamint leirtuk, hogy a hagyomanyos anti-platelet kezeles mellett a P-selectin, a PF4, valamint a CD40L receptorokon keresztul milyen modon befolyasolhato a thrombocyta műkodes. 3. Az inlammatorikus stimulusok kozul megallapitottuk, hogy a lipopoliszacharid (LPS) formak kozul kizarolag az Re-LPS formanak van hatasa a thrombocyta aktivacio bizonyos parametereire. 4. A klinikai kollaboracios vizsgalatok teren a thrombocyta rendellenessegek kozul kollaboracios vizsgalataink soran meghataroztuk, hogy Glanzmann thrombasthenia eseten a thrombocyta felszini receptorok expressziojat es leirtuk ezek TRAP aktivacio utan megjelenő szintjet. Tovabbi klinikai kollaboracios vizsgalataink eredmenyekent ket beteg populacioban (obesitas es PAD) mutattunk ki jelentős verlemezke aktivaciot illetve ezek osszefuggeset a betegseg alatti egyeb valtozokkal. | The research activity was carried out in 4 focus areas: 1. In P-selectin glycoprotein ligand-1 (PSGL-1) knock out mice we verified, that PSGL-1 is protective against thrombosis in a murine model (Miszti-Blasius et al, 2011), and we found that in the absence of PSGL-1 mature and precursor myeloid cells are released earlier upon G-CSF treatment (submitted). 2. Studying the modulation of platelet activation we proved that calyculin-A (CLA) inhibits TRAP elicited platelet activation parallel with its phosphatase inhibitor activity. (Simon Z et al, 2010) In case of conventional anti-platelet treatment we described the modulation of platelet fuction via P-selectin, PF4 and CD40L receptors (Nagy B Jr et al, 2012) 3. We investigated the effect of lipopolysaccharide and (LPS). We found that out of the LPS isoforms only the Re-LPS but not the S-LPS is capable of mediating platelet activation (Kappelmayer et al, 2012, under revision) 4. In case of clinical collaborations on platelets, we determined platelet surface glycoprotein expressions in Glanzmann thrombastenia and described their expression levels after TRAP activation. Further collaborative studies proved considerable platelet activation in obese and peripheral arterial disease patients (Csongradi et al 2011, Shemirani et al, 2011)