NF-κB mediates the transcription of mouse calsarcin-1 gene, but not calsarcin-2, in C2C12 cells

BACKGROUND: The calsarcins comprise a novel family of muscle-specific calcineurin-interaction proteins that play an important role in modulating both the function and substrate specificity of calcineurin in muscle cells. The expression of calsarcin-1 (CS-1) is restricted to slow-twitch skeletal muscle fibres, whereas that of both calsarcin-2 (CS-2) and calsarcin-3 (CS-3) is enriched in fast-twitch fibres. However, the transcriptional control of this selective expression has not been previously elucidated. RESULTS: Our real-time RT-PCR analyses suggest that the expression of CS-1 and CS-2 is increased during the myogenic differentiation of mouse C2C12 cells. Promoter deletion analysis further suggests that an NF-κB binding site within the CS-1 promoter is responsible for the up-regulation of CS-1 transcription, but no similar mechanism was evident for CS-2. These findings are further supported by the results of EMSA analysis, as well as by overexpression and inhibition experiments in which NF-κB function was blocked by treatment with its inhibitor, PDTC. In addition, the overexpression of NFATc4 induces both the CS-1 and CS-2 promoters, whereas MEF2C only activates CS-1. CONCLUSION: Our present data suggest that NF-κB is required for the transcription of mouse CS-1 but not CS-2, and that the regulation of the calsarcins is mediated also by the NFAT and MEF2 transcription factors. These results provide new insights into the molecular mechanisms governing transcription in specific muscle fibre cells. The calsarcins may also serve as a valuable mechanistic tool to better understand the regulation of calcineurin signalling during muscle differentiation

Secure Multiple Amplify-and-Forward Relaying Over Correlated Fading Channels

This paper quantifies the impact of correlated fading on secure communication of multiple amplify-and-forward (AF) relaying networks. In such a network, the base station (BS) is equipped with multiple antennas and communicates with the destination through multiple AF relays, while the message from the relays can be overheard by an eavesdropper. We focus on the practical communication scenario, where the main and eavesdropper’s channels are correlated. In order to enhance the transmission security, transmit antenna selection (TAS) is performed at the BS, and the best relay is chosen according to the full or partial relay selection criterion, which relies on the dualhop relay channels or the second-hop relay channels, respectively. For these criteria, we study the impact of correlated fading on the network secrecy performance, by deriving an analytical approximation for the secrecy outage probability (SOP) and an asymptotic expression for the high main-to-eavesdropper ratio (MER). From these results, it is concluded that the channel correlation is always beneficial to the secrecy performance of full relay selection. However, it deteriorates the secrecy performance if partial relay selection is used, when the number of antennas at the BS is less than the number of relays.ARC Discovery Projects Grant DP150103905

Dual-factor Synergistically Activated ESIPT-based Probe:Differential Fluorescence Signals to Simultaneously Detect α-Naphthyl Acetate and Acid α-Naphthyl Acetate Esterase

[Image: see text] α-Naphthyl acetate esterase (α-NAE) and acid α-naphthyl acetate esterase (ANAE), a class of special esterases, are important for lymphocyte typing and immunocompetence-monitoring. As such, the simultaneous detection of α-NAE and ANAE has become a target to effectively improve the accuracy in lymphocyte typing. Therefore, we developed a dual-factor synergistically activated ESIPT-based probe (HBT-NA) to detect α-NAE and ANAE sensitively, rapidly, and simultaneously in a differential manner. HBT-NA exhibits differential fluorescence signal outputs toward small changes of α-NAE and ANAE activities. HBT-NA displays a weak fluorescence signal at 392 nm over a pH range from 6.0 to 7.4. However, when it interacts with α-NAE (0–25 U) at pH = 7.4, the fluorescence intensity at 392 nm enhanced linearly within 60 s (F(392 nm)/F0(392 nm) = 0.042 C(α-NAE) + 1.1, R(2) = 0.99). Furthermore, HBT-NA emits ratiometric fluorescence signals (F(505 nm)/F(392 nm)) for ANAE (0–25 U) at pH = 6.0 within 2.0 min, exhibiting a good linear relationship (F(505 nm)/F(392 nm) = 0.83C(ANAE) – 1.75, R(2) = 0.99). The differential fluorescence signals can be used to simultaneously detect the activities of α-NAE and ANAE in solutions and complex living organisms. More importantly, based on the differential fluorescence signals toward α-NAE and ANAE, T lymphocytes and B lymphocytes could be successfully typed and differentiated among nontyped lymphocytes, facilitating the real-time evaluation of their immune functions using flow cytometry. Hence, HBT-NA could be used for the ultrasensitive detection of the enzyme activities of α-NAE and ANAE, the real-time precise typing of lymphocytes, and the monitoring of immunocompetence

Influence of acrylamide on ROS, Hsp27 and NF-kB in bone marrow mesenchymal stem cells

The bone marrow mesenchymal stem cells (BM-MSCs) treated with acrylamide (ACR) were used to make out the immune response to ROS, interleukin-8 and phosphorylated Hsp27 of ACR. ACR was reported as a probable human carcinogen, neurotoxic and mutagenic. BMMSCs have the capability of immunoregulation, and participate in the process of multiple immune response. It has attracted the attention of researchers that these cells have priority to move to the damaged tissue, as a kind of potential therapeutic tool for tissue repair. ACR and BMMSCs are related to immune reactions, especially those involving in tumours and cancers. However, the interaction between ACR and BMMSCs is still poorly understood. In present study, we report the influence of ACR on BMMSCs. At first, BMMSCs were disposed with 0.5mM ACR for 72 h, and then the secretion of ROS, interleukin-8, phospho- Hsp27 and NF-kB activities, apoptosis and cell cycle, respectively, were determined. The results showed that the secretion of ROS, interleukin-8 and phosph-Hsp27 increased and NF-kB was activated, while the apoptosis and cell cycle have no obvious alteration. In conclusion, ACR probably activated the NF-kB pathway in BMMSCs via oxidative stress, which may provide new insights to study the immune response and the influence mechanism of ACR

Fully Band Resolved Scattering Rate in MgB2 Revealed by Nonlinear Hall Effect and Magnetoresistance Measurements

We have measured the normal state temperature dependence of the Hall effect and magnetoresistance in epitaxial MgB2 thin films with variable disorders characterized by the residual resistance ratio RRR ranging from 4.0 to 33.3. A strong nonlinearity of the Hall effect and magnetoresistance have been found in clean samples, and they decrease gradually with the increase of disorders or temperature. By fitting the data to the theoretical model based on the Boltzmann equation and ab initio calculations for a four-band system, for the first time, we derived the scattering rates of these four bands at different temperatures and magnitude of disorders. Our method provides a unique way to derive these important parameters in multiband systems.Comment: 4 pages, 4 figure

Effect of Corilagin on the Proliferation and NF- κ

Background. This study is to explore the effect of corilagin on the proliferation and NF-κB signaling pathway in U251 glioblastoma cells and U251 glioblastoma stem-like cells. Methods. CD133 positive U251 glioblastoma cells were separated by immunomagnetic beads to isolate glioblastoma stem-like cells. U251 cells and stem-like cells were intervened by different corilagin concentrations (0, 25, 50, and 100 μg/mL) for 48 h, respectively. Cell morphology, cell counting kit-8 assay, flow cytometry, dual luciferase reporter assay, and a western blot were used to detect and analyze the cell proliferation and cell cycle and investigate the expression of IKBα protein in cytoplasm and NF-κB/p65 in nucleus. Results. Corilagin inhibited the cell proliferation of U251 cells and their stem-like cells and the inhibition role was stronger in U251 stem-like cells (P<0.05). The cell cycle was arrested at G2/M phase in the U251 cells following corilagin intervention; the proportion of cells in G2/M phase increased as the concentration of corilagin increased (P<0.05). The U251 stem-like cells were arrested at the S phase following treatment with corilagin; the proportion of cells in the S phase increased as the concentration of corilagin increased (P<0.05). The ratio of dual luciferase activities of U251 stem-like cells was lower than that of U251 cells in the same corilagin concentration. With increasing concentrations of corilagin, the IKBα expression in cytoplasm of U251 cells and U251 stem-like cells was increased, but the p65 expression in nucleus of U251 cells and U251 stem-like cells was decreased (P<0.05). Conclusion. Corilagin can inhibit the proliferation of glioblastoma cells and glioblastoma stem-like cells; the inhibition on glioblastoma stem-like cell proliferation is stronger than glioblastoma cells. This different result indicates that the effect of corilagin on U251 cells and U251 stem-like cells may have close relationships with mechanism of cell cycle and NF-κB signaling pathway; however, the real antitumor mechanism of corilagin is not yet clear and requires further study