Role molecular signaling pathways in changes of red blood cell deformability.
作者： Alexei V. Muravyov , Irina A. Tikhomirova
DOI: 10.3233/CH-2012-1575
关键词:
摘要: This study was designed to investigate the dependency of red blood cell deformability upon activation extra- and intracellular signaling pathways. Exposures cells (RBCs) catecholamines insulin led positive change in RBC deformability. When forskolin, a stimulator adenylyl cyclase (AC), added suspension, increased. Somewhat more significant rise appeared after incubation with dB-AMP. The inhibitors phosphodiesterase (PDE) activity increased These results revealed considerable role AC-cAMP system regulation Ca 2+ influx, stimulated by mechanical loading or A23187 accompanied marked lowering At same time blocking entry into verapamil chelating EGTA rise. comparison effect different protein kinases on showed that it altered under PKA forskolin dB-cAMP than other kinases. There lesser but quite statistically tyrosine kinase (TPK) microrheology. Whereas microrheological PKC not so considerable. problem short-term microrheology is examined. latter includes: modes molecular pathways, ligand - receptor interaction, second messengers, membrane phosphorylation. On whole total data clearly show changes are connected extra It seems reasonable suppose were mainly associated AC-cAMP-PKA pathway, decrease cells.
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