Pregled bibliografske jedinice broj: 643813
The effects of guanylat cyclase A agonists on the bradykinin signaling pathway after ischemic mouse brain injury
The effects of guanylat cyclase A agonists on the bradykinin signaling pathway after ischemic mouse brain injury // Periodicum biologorum
Zagreb: Croatian Society of Natural Sciences, 2013. str. 25-25 (predavanje, međunarodna recenzija, sažetak, znanstveni)
CROSBI ID: 643813 Za ispravke kontaktirajte CROSBI podršku putem web obrasca
Naslov
The effects of guanylat cyclase A agonists on the bradykinin signaling pathway after ischemic mouse brain injury
Autori
Dobrivojević, Marina ; Špiranec, Katarina ; Erjavec, Igor ; Gorup, Dunja ; Habek, Nikola ; Hirsch, Jochen R ; Forssmann, Wolf-Georg ; Schlatter, Eberhard ; Sinđić, Aleksandra
Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni
Izvornik
Periodicum biologorum
/ - Zagreb : Croatian Society of Natural Sciences, 2013, 25-25
Skup
Treći Kongres Hrvatskog društva fiziologa i prvi Regionalni kongres fizioloških društava
Mjesto i datum
Rijeka, Hrvatska, 13.09.2013. - 15.09.2013
Vrsta sudjelovanja
Predavanje
Vrsta recenzije
Međunarodna recenzija
Ključne riječi
bradykinin; guanylat cyclase A; mouse; ischemic injury
Sažetak
Bradykinin is involved in the formation of cerebral edema after ischemic brain injury increasing the size of brain. Furthmore, it is known that natriuretic peptides are involved in decreasing cerebral edema via still unknown mechanisms. First, we examined the effects of natriuretic peptides and bradykinin in vitro in HEK-293 cells, primary isolated neurons and astrocytes using the whole cell patch clamp technique and by measuring the intracellular calcium concentration. In a mouse model of ischemic brain injury, we measured the size of the ischemic lesion and edema using microCT. In HEK- 293 cells, ligands of GC-A, but not GC-B, inhibit the bradykinin signaling pathway by activating RGS protein which is responsible for inactivation of G coupled protein. Our preliminary results show that the same inhibition exists in primary isolated mouse neurons. In in vivo experiments, when urodilatin, agonist of GC-A was applied, no brain lesion was detected by microCT scanning. When only bradykinin was applied, brain damage increased. Applying a combination of natriuretic peptides with bradykinin the size of the lesion and the brain edema decreased. The results indicated the existence of an endogenous antagonist of the bradykinin signaling pathway and a possible protective role of natriuretic peptides during stroke.
Izvorni jezik
Engleski
Znanstvena područja
Temeljne medicinske znanosti
POVEZANOST RADA
Ustanove:
Zdravstveno veleučilište, Zagreb
Profili:
Dunja Gorup
(autor)
Katarina Špiranec
(autor)
Aleksandra Sinđić
(autor)
Nikola Habek
(autor)
Igor Erjavec
(autor)
Marina Radmilović
(autor)
Citiraj ovu publikaciju:
Časopis indeksira:
- Web of Science Core Collection (WoSCC)
- Science Citation Index Expanded (SCI-EXP)
- SCI-EXP, SSCI i/ili A&HCI
- Scopus