Вплив делеції гена β-катеніну на морфологію та фізіологію кардіоміоцитів за умов дії стимуляторів гіпертрофії
Aim. The investigation of β–catenin signaling function during cardiomyocyte hypertrophy development under the one allele of β–catenin conditional cardiospecific knock-out condition was the aim of present work. Methods. The heart of new-born trangenic and wild-type animals were used for the primary culture isolation. The physiological activity was evaluated with MTT-test. The primary cardiomyocytes were H&E stained and morphological parameters were measured. Results. The physiological activity elevation was detected for wild-type and haploinsufficient animals after lithium chloride treatment comparing to control cells in MTT-test. The inhibition of physiological activity was detected for all genotypes comparing to controls. The binucleated cells distribution was shown to differ between the control and LiCl-treated cells. Also the frequency of binucleated cells tended to increase for mutants comparing to controls after canonical Wnt stimulation with LiCl. Conclusions. The deletion of β–catenin leads to disruptions in cell morphology and physiology in postnatal cardiovyocytes and attenuated cell hypertrophy development possibly due to canonical Wnt-signaling inhibition.
Keywords: hypertrophic stimuli, β–catenin haploinsufficiency, β–catenin deletion, canonical Wnt signaling.