Down-regulation of nestin in mesenchymal stem cells derived from peripheral blood through blocking bone morphogenesis pathway

Different signaling pathways are implicated in proliferation and differentiation of stem cells. Bone Morphogenesis Pathway (BMP) signaling was known to display an important function in osteogenic and adipogenic differentiation of mesenchymal stem cells (MSCs). In the present study, the authors investigated whether blocking BMP signaling was associated with down regulation of Nestin expression as neural stem cell marker in peripheral blood derived mesenchymal stem cells (PB-MSCs). At first, MSCs were isolated from peripheral blood by plastic adherent ability and flow cytometry analysis. After reaching the confluence, the cells were treated with medium containing Noggin as antagonist of BMP signaling upon 8 days. Real time PCR analysis indicated that the expression of Nestin was diminished in PB-MSCs by attenuating BMP signaling. The obtained results suggested that BMP signaling might have a regulatory function on the Nestin expression in mesenchymal stem cells.     

Subcellular localization of EGFR in esophageal carcinoma cell lines

Background: The EGF receptor is a therapeutic target in cancer cells, whereby mutations of EGFR and/or signalling members act as predictive markers. EGFR however also exhibits dynamic changes of subcellular localization, leading to STAT5 complex formation, nuclear translocation and induction of Aurora-A expression in squamous cancer cells. We previously described high EGFR and Aurora-A expression in esophageal cancer cells. Here, we investigated subcellular localization of EGFR and STAT5 in esophageal cancer cells. Results: Quantitative immunofluorescence analyses of four esophageal cancer cell lines reflecting esophageal squamous cell carcinomas (ESCC) and esophageal adenocarcinomas (EAC) revealed that the subcellular localization of EGFR was shifted from a membranous to cytoplasmic localization upon EGF-stimulation in OE21 (ESCC) cells. Thereby, EGFR in part co-localized with E-Cadherin. In parallel, phosphorylated STAT5-Tyr694 appeared to increase in the nucleus and to decrease at the cell membrane. In three additional cell lines, EGFR was only marginally (Kyse-410/ESCC; OE19/EAC) and weakly (OE33, EAC) detectable at the cell membrane. Partial co-localization of EGFR and E-Cadherin occurred in OE33 cells. Post EGF-stimulation, EGFR was detected in the cytoplasm, resembling endosomal compartments. Furthermore, OE19 and OE33 exhibited nuclear STAT5-Tyr694 phosphorylation upon EGF-stimulation. None of the four cell lines showed nuclear EGFR expression and localization. Conclusion: In contrast to other (squamous) cancer cells, activation of EGFR in esophageal squamous cancer cells does not result in nuclear translocation of EGFR. Still, the subcellular localization of EGFR may influence STAT5-associated signaling pathways in esophageal cancer cells and hence possibly also the responses to ErbB, respective EGFR-targeted therapies.     

What if we lose a hub? Experimental testing of pollination network resilience to removal of keystone floral resources

On the basis of theoretical predictions, pollination networks seem to be resilient to random node elimination but sensitive to targeted exclusion. However, such predictions have a very weak empirical basis. In order to test the robustness of the pollination network to short-term disturbances, we removed inflorescences of the most connected species occurring in a lowland meadow network using the before–after approach and compared the result with that obtained by network modelling. The manipulated network showed no significant differences for the most commonly used metrics, but was more generalized than control networks, owing to a change in the preferences of pollinators. Furthermore, no secondary extinctions (emigrations) were found, owing to the considerable natural variation found among insect species assemblages. Following elimination of the most linked plant species, a new hub was detected in the experimental meadow, the hub node being a plant species with a similar inflorescence to that removed, and formerly playing the role of a peripheral node. We conclude that exclusion of the main food source forced insects to change their specialized preferences to other plant species that were available. Mostly, these had inflorescences similar to those that were removed.     

Interspecific differences in milkweeds alter predator density and the strength of trophic cascades

Trophic cascades occur when predators benefit plants by consuming herbivores, but the overall strength of a trophic cascade depends upon the way species interactions propagate through a system. For example, plant resistance to, or tolerance of, herbivores reduces the potential magnitude of a trophic cascade. At the same time, plants can also affect predator foraging or consumption in ways that either increase or decrease the strength of trophic cascades. In this study, we investigated the effects of plant variation on cascade strength by manipulating predator access to aphid populations on two species of milkweed: the slower-growing, putatively more-defended Asclepias syriaca and the faster-growing, putatively less-defended Asclepias incarnata. Predatory insects increased plant growth and survival for both species, but the strength of these trophic cascades was greater on A. incarnata, which supported more aphid growth early in the season than did A. syriaca. More predators were observed per aphid on A. incarnata, and cage treatments generated significant patterns consistent with predator aggregation on A. incarnata, but not A. syriaca. Although predators strongly affected aphids, this effect did not differ consistently between milkweed species. Plant tolerance to herbivory may therefore be the primary driver of the difference in trophic cascade strength observed. Importantly, we observed that the timing of predator exclusion affected plant growth and survival differently, indicating that measures of “cascade strength” may change with phenology and plant physiological responses. Together, our results suggest a mechanism by which differences in resource allocation patterns could explain differences in growth, phenology, and cascade strength between species.     

Cul3-KLHL20 ubiquitin ligase: physiological functions,stress responses,and disease implications

Cullin-RING ubiquitin ligases are the largest Ubiquitin ligase family in eukaryotes and are multi-protein complexes. In these complexes, the Cullin protein serves as a scaffold to connect two functional modules of the ligases, the catalytic subunit and substrate-binding subunit. KLHL20 is a substrate-binding subunit of Cullin3 (Cul3) ubiquitin ligase. Recent studies have identified a number of substrates of KLHL20-based ubiquitin ligase. Through ubiquitination of these substrates, KLHL20 elicits diverse cellular functions, some of which are associated with human diseases. Furthermore, the functions, subcellular localizations, and expression of KLHL20 are regulated by several physiological and stressed signals, which allow KLHL20 to preferentially act on certain substrates to response to these signals. Here, we provide a summary of the functions and regulations of KLHL20 in several physiological processes and stress responses and its disease implications.