Searching for just a few words should be enough to get started. If you need to make more complex queries, use the tips below to guide you.
Issue title: Memorial Issue dedicated to Oguz K. Baskurt
Article type: Research Article
Authors: Muravyov, Alexei; | Tikhomirova, Irina
Affiliations: Department of Medicine and Biology, State Pedagogical University, Yaroslavl, Russia
Note: [] Address for correspondence: Prof. Alexei Muravyov, Department of Medicine and Biology, State Pedagogical University, Respublikanskaya 108, Yaroslavl 150000, Russia. Fax.: +4852 30 55 96; E-mail: [email protected]
Abstract: The exposure of red blood cells (RBC) to some hormones (epinephrine, insulin and glucagon) and agonists of α- and β-adrenergic receptors (phenylephrine, clonidine and isoproterenol) may modify RBC aggregation (RBCA). Prostaglandin E1 (PGE1) significantly decreased RBCA, and PGE2 had a similar but lesser effect. Adenylyl cyclase (AC) stimulator forskolin added to RBC suspension, caused a decrease of RBCA. More marked lowering of RBCA occurred after RBC treatment by dB-cAMP. Phosphodiesterase (PDE) inhibitors markedly reduced RBCA. Ca2+ influx stimulated by A23187 was accompanied by an increase of RBCA. The blocking of Ca2+ entry into the RBC by verapamil or the chelation of Ca2+ by EGTA led to a significant RBCA decrease. Lesser changes of aggregation were found after RBC incubation with protein kinase C stimulator phorbol 12-myristate 13-acetate (PMA). A significant inhibitory effect of tyrosine protein kinase (TPK) activator cisplatin on RBCA was revealed, while selective TPK inhibitor, lavendustin, eliminated the above mentioned effect. Taken together, the data demonstrate that changes in RBCA are connected with activation of different intracellular signaling pathways. We suggest that alterations in RBCA are mainly associated with the crosstalk between the adenylyl cyclase-cAMP system and Ca2+ control mechanisms.
Keywords: Erythrocyte aggregation, adenylyl cyclase, phosphodiesterases, intracellular signaling pathways, intracellular calcium, protein kinases
DOI: 10.3233/BIR-140664
Journal: Biorheology, vol. 51, no. 2-3, pp. 135-145, 2014
IOS Press, Inc.
6751 Tepper Drive
Clifton, VA 20124
USA
Tel: +1 703 830 6300
Fax: +1 703 830 2300
[email protected]
For editorial issues, like the status of your submitted paper or proposals, write to [email protected]
IOS Press
Nieuwe Hemweg 6B
1013 BG Amsterdam
The Netherlands
Tel: +31 20 688 3355
Fax: +31 20 687 0091
[email protected]
For editorial issues, permissions, book requests, submissions and proceedings, contact the Amsterdam office [email protected]
Inspirees International (China Office)
Ciyunsi Beili 207(CapitaLand), Bld 1, 7-901
100025, Beijing
China
Free service line: 400 661 8717
Fax: +86 10 8446 7947
[email protected]
For editorial issues, like the status of your submitted paper or proposals, write to [email protected]
如果您在出版方面需要帮助或有任何建, 件至: [email protected]