“
“Interaction of cationic phenosafranin (PSF), anionic 8-anilino-1-naphthalene sulfonate (ANS) and nonionic nile red (NR) have been studied with the zwitterionic phospholipid, egg yolk L-alpha-phosphatidylcholine (EYPC). The study reveals discernible binding interactions of the three fluorescent probes with CA3 inhibitor the EYPC lipid vesicle. Once the binding of the probes with the lipid is established, the effect of cyclic oligosaccharide, beta-cyclodextrin (beta-CD), on these lipid bound probes has been investigated. Different fluorometric techniques

suggest that addition of beta-CD to the probe-lipid complexes leads to the release of the probes from the lipid medium through the formation of probe-beta-CD inclusion complexes. A competitive binding of the probes between beta-cyclodextrin and the lipid is ascribed to be responsible for the effect. This provides an easy avenue Selleckchem DAPT for the removal of the probe molecules from the lipid environment. Extension of this work with drug molecules in cell membranes is expected to give rise to a strategy for the removal of adsorbed drugs from the cell membranes by the use of non-toxic beta-cyclodextrin. (C)

2015 Elsevier B.V. All rights reserved.”
“Yamak A, Temsah R, Maharsy W, Caron S, Paradis P, Aries A, Nemer M. Cyclin D-2 rescues size and function of GATA4 haplo-insufficient hearts. Am J Physiol Heart Circ Physiol 303: H1057-H1066, 2012. First published August 24, 2012; doi:10.1152/ajpheart.00250.2012.-Transcription factor GATA4 is a key regulator of cardiomyocyte growth, and differentiation

and 50% reduction in GATA4 levels results in hypoplastic hearts. Search for GATA4 targets/effectors revealed cyclin D-2 (CD2), a member of the D-type cyclins (D-1, D-2, and D-3) that play a vital role in cell growth and differentiation as a direct transcriptional target and a mediator of GATA4 growth in postnatal cardiomyocytes. GATA4 associates with the CD2 promoter in cardiomyocytes and is sufficient to induce endogenous CD2 transcription and to dose-dependently activate the CD2 promoter in heterologous cells. Z VAD FMK Cardiomyocyte-specific overexpression of CD2 results in enhanced postnatal cardiac growth because of increased cardiomyocyte proliferation. When these transgenic mice are crossed with Gata4 heterozygote mice, they rescue the hypoplastic cardiac phenotype of Gata4(+/-) mice and enhance cardiomyocyte survival and heart function. The data uncover a role for CD2 in the postnatal heart as an effector of GATA4 in myocyte growth and survival. The finding that postnatal upregulation of a cell-cycle gene in GATA4 haplo-insufficient hearts may be protective opens new avenues for maintaining or restoring cardiac function in GATA4-dependent cardiac disease.