Given the potential clinical benefit of inhibiting Na+/Ca2+ exchanger (NCX) activity dur ing myocardial ischemia reperfusion (I/R), pharmacological approaches have been pursued to both inhibit and clarify the importance of this exchanger. SEA0400 was reported to have a potent NCX selectivity. Thus, we examined the effect of SEA0400 on NCX currents and I/R induced intracellular Ca2+ overload in mouse ventricular myocytes using patch clamp techniques and fluorescence measurements. Ischemia significantly inhibited inward and outward NCX current (from -0.04±0.01nA to 0 nA at -100 mV; from 0.23±0.08 nA to 0.11±0.03 nA at +50 mV, n=7). Subsequent reperfusion not only restored the current rapidly but enhanced the current amplitude obviously, especially the outward currents (from 0.23±0.08 nA to 0.49±0.12 nA at +50 mV, n=7). [Ca2+]i, expressed as the ratio of Fura-2 fluorescence intensity, increased to 138±7 % (P<0.01) during ischemia and to 210±11 % (P<0.01) after reperfusion. The change of NCX current and the increase of [Ca 2+]i during I/R can be blocked by SEA0400 in a dose-dependent manner with an EC50 value of 31 nM and 28 nM for the inward and outward NCX current, respectively. The results suggested that SEA0400 is a potent NCX inhibitor, which can protect mouse cardiac myocytes from Ca2+ overload during I/R injuries., J. Wang, Z. Zhang, Y. Hu, X. Hou, Q. Cui, Y. Zang, C. Wang., and Obsahuje bibliografii a bibliografické odkazy
How the photosynthetic characteristics of insect-resistant transgenic cotton (Gossypium hirsutum L.) respond to light or whether this genetic transformation could result in unintended effects on their photosynthetic and physiological processes is not well known. Two experiments were conducted to investigate the shapes of net photosynthetic rate (P N), stomatal conductance (g s), apparent light use efficiency (LUEapp) and water use efficiency (WUE) light-response curves for single leaves of Bt (Bacillus thuringiensis) and Bt+CpTI (cowpea trypsin inhibitor) transgenic cotton plants and their non-transgenic counterparts, respectively. Results showed that the significant difference in response of P N and WUE to light between transgenic cotton and non-transgenic cotton occured but not always throughout the growing season or in different experiments or for all transgenic cotton lines. It was highly dependent on growth stage, culture condition and variety, but no obvious difference between any transgenic cotton and non-transgenic cotton in the shapes of g s and LUEapp light-response curves was observed in two experiments at different growth stages. In the field experiments, transgenic Bt+CpTI cotton was less sensitive to response of P N to high irradiance at the boll-opening stage. In pot experiments, WUE light-response curves of both Bt transgenic cotton and Bt+CpTI transgenic cotton progressively decreased whereas non-transgenic cotton slowly reached a maximum at high irradiance at boll-opening stage. We supposed that culture environment could affect the photosynthesis of transgenic cotton both directly and indirectly through influencing either foreign genes expression or growth and physiological processes. and C. X. Sun ... [et al.].
Spontaneously hypertensive rats (SHR/NIH strain) harbor a deletion variant in the Cd36 fatty acid transporter and display defective fatty acid metabolism, insulin resistance and hypertension. Transgenic rescue of Cd36 in SHR ameliorates insulin resistance and improves dyslipidemia. However, the role of Cd36 in blood pressure regulation remains controversial due to inconsistent blood pressure effects that were observed with transgenic expression of Cd36 on the SHR background. In the current studies, we developed two new SHR transgenic lines, which express wild type Cd36 under the control of the universal Ef-1 promoter, and examined the effects of transgenic expression of wild type Cd36 on selected metabolic and cardiovascular phenotypes. Transgenic expression of Cd36 in the new lines was associated with significantly decreased serum fatty acids, amelioration of insulin resistance and glucose intolerance but failed to induce any consistent changes in blood pressure as measured by radiotelemetry. The current findings confirm the genetic association of defective Cd36 with disordered insulin action and fatty acid metabolism in the SHR/NIH strain and suggest that Cd36 is linked to other gene(s) on rat chromosome 4 that regulate blood pressure., M. Pravenec, V. Landa, V. Zídek, A. Musilová, L. Kazdová, N. Qi, J. Wang, E. St.Lezin, T. W. Kurtz., and Obsahuje bibliografii