Hormonal regulation of ecdysis innate behavior in the hemimetabolous insect Rhodnius prolixus

In insects, ecdysis sequence is a series of stereotyped innate behaviors performed at the end of each molting period, in order to shed the old cuticle and to emerge as the following stage in the vital cycle. The hormonal regulation of ecdysis has been studied in holometabolous insects; it includes the participation of ecdysteroids and peptidic hormones. However, in spite of the fundamental differences in ecdysis between holometabolous and hemimetabolous, the hormonal regulation of this process has not been characterized in the latter.Facultad de Ciencias Exacta

Hormonal regulation of ecdysis innate behavior in the hemimetabolous insect Rhodnius prolixus

In insects, ecdysis sequence is a series of stereotyped innate behaviors performed at the end of each molting period, in order to shed the old cuticle and to emerge as the following stage in the vital cycle. The hormonal regulation of ecdysis has been studied in holometabolous insects; it includes the participation of ecdysteroids and peptidic hormones. However, in spite of the fundamental differences in ecdysis between holometabolous and hemimetabolous, the hormonal regulation of this process has not been characterized in the latter.Facultad de Ciencias Exacta

KCNK5 is Functionally Down-Regulated Upon Long-Term Hypotonicity in Ehrlich Ascites Tumor Cells

Background/Aims: Regulatory volume decrease (RVD) in response to acute cell swelling is well described and KCNK5 (also known as TASK-2 or K2P5.1) has been shown to be the volume sensitive K+ channel in Ehrlich cells. Very little is, on the other hand, known about the effects of long-term hypotonicity on expression and function of KCNK5, thus we have investigated the effect of long-term hypotonicity (24h - 48h) on KCNK5 in Ehrlich cells on the mRNA, protein and physiological levels. Methods: Physiological effects of long-term hypotonicity were measured using patch-clamp and Coulter counter techniques. Expression patterns of KCNK5 on mRNA and protein levels were established using real-time qPCR and western blotting respectively. Results: The maximum swelling-activated current through KCNK5 was significantly decreased upon 48h of hypotonicity and likewise the RVD response was significantly impaired after both 24 and 48h of hypotonic stimulation. No significant differences in the KCNK5 mRNA expression patterns between control and stimulated cells were observed, but a significant decrease in the KCNK5 protein level 48h after stimulation was found. Conclusion: The data suggest that the strong physiological impairment of KCNK5 in Ehrlich cells after long-term hypotonic stimulation is predominantly due to down-regulation of the KCNK5 protein synthesis

Theoretical Characterization of the Interface in a Nonequilibrium Lattice System

The influence of nonequilibrium bulk conditions on the properties of the interfaces exhibited by a kinetic Ising--like model system with nonequilibrium steady states is studied. The system is maintained out of equilibrium by perturbing the familiar spin--flip dynamics at temperature T with completely--random flips; one may interpret these as ideally simulating some (dynamic) impurities. We find evidence that, in the present case, the nonequilibrium mechanism adds to the basic thermal one resulting on a renormalization of microscopic parameters such as the probability of interfacial broken bonds. On this assumption, we develop theory for the nonequilibrium "surface tension", which happens to show a non--monotonous behavior with a maximum at some finite T. It ensues, in full agreement with Monte Carlo simulations, that interface fluctuations differ qualitatively from the equilibrium case, e.g., the interface remains rough at zero--T. We discuss on some consequences of these facts for nucleation theory, and make some explicit predictions concerning the nonequilibrium droplet structure.Comment: 10 pages, 7 figures, submitted to Phys. Re

KCa3.1 inhibition switches the phenotype of glioma-infiltrating microglia/macrophages

Among the strategies adopted by glioma to successfully invade the brain parenchyma is turning the infiltrating microglia/macrophages (M/MΦ) into allies, by shifting them toward an anti-inflammatory, pro-tumor phenotype. Both glioma and infiltrating M/MΦ cells express the Ca(2+)-activated K(+) channel (KCa3.1), and the inhibition of KCa3.1 activity on glioma cells reduces tumor infiltration in the healthy brain parenchyma. We wondered whether KCa3.1 inhibition could prevent the acquisition of a pro-tumor phenotype by M/MΦ cells, thus contributing to reduce glioma development. With this aim, we studied microglia cultured in glioma-conditioned medium or treated with IL-4, as well as M/MΦ cells acutely isolated from glioma-bearing mice and from human glioma biopsies. Under these different conditions, M/MΦ were always polarized toward an anti-inflammatory state, and preventing KCa3.1 activation by 1-[(2-Chlorophenyl)diphenylmethyl]-1H-pyrazole (TRAM-34), we observed a switch toward a pro-inflammatory, antitumor phenotype. We identified FAK and PI3K/AKT as the molecular mechanisms involved in this phenotype switch, activated in sequence after KCa3.1. Anti-inflammatory M/MΦ have higher expression levels of KCa3.1 mRNA (kcnn4) that are reduced by KCa3.1 inhibition. In line with these findings, TRAM-34 treatment, in vivo, significantly reduced the size of tumors in glioma-bearing mice. Our data indicate that KCa3.1 channels are involved in the inhibitory effects exerted by the glioma microenvironment on infiltrating M/MΦ, suggesting a possible role as therapeutic targets in glioma