Cardioprotective role of extracellular vesicles: A highlight on exosome beneficial effects in cardiovascular diseases

Extracellular vesicles (EVs) are nano-sized vesicles, released from many cell types including cardiac cells, have recently emerged as intercellular communication tools in cell dynamics. EVs are an important mediator of signaling within cells that influencing the functional behavior of the target cells. In heart complex, cardiac cells can easily use EVs to transport bioactive molecules such as proteins, lipids, and RNAs to the regulation of neighboring cell function. Cross-talk between intracardiac cells plays pivotal roles in the heart homeostasis and in adaptive responses of the heart to stress. EVs were released by cardiomyocytes under baseline conditions, but stress condition such as hypoxia intensifies secretome capacity. EVs secreted by cardiac progenitor cells and cardiosphere-derived cells could be pinpointed as important mediators of cardioprotection and cardiogenesis. Furthermore, EVs from many different types of stem cells could potentially exert a therapeutic effect on the damaged heart. Recent evidence shows that cardiac-derived EVs are rich in microRNAs, suggesting a key role in the controlling of cellular processes. EVs harboring exosomes may be clinically useful in cell-free therapy approaches and potentially act as prognosis and diagnosis biomarkers of cardiovascular diseases.     

High-Quantum Efficiency of the Plasmonic Photodetectors-Based on Coupling Between Ag Nanoparticles and Ag Nanograting Electrodes

The plasmonic effects due to the coupling of silver spherical nanoparticles with silver nanograting electrodes on active medium of the photo detector are investigated. Calculations show that the coupling of nanoparticles and nanograting electrodes at the surface of active medium lead to reflection wave into the active medium, and electrodes can participate in the absorption and quantum efficiency. Calculations show that the addition of nanograting electrodes to the structure can lead to increase the absorption coefficient up to 120% respect to the plasmonic structure containing only nanoparticles and about 4.5 times that of conventional (metal-semiconductor -metal ) MSM photo detectors.

     

Ultra-compact Spatial Terahertz Switch Based on Graphene Plasmonic-Coupled Waveguide

We are proposing graphene (G)-based multilayered plasmonic spatial switch, operating at 10 THz. It is composed of hBN/Ag/hBN/G/hBN/G/hBN/SiO₂/p⁺-Si multilayers. When a 10-THz transverse magnetic (TM)-polarized signal is normally incident upon the structure top surface, the nanoaperture devised in the Ag nanolayer, acting as a grating, excites surface plasmons at the top graphene micro-ribbons/hBN interface. These surface plasmons depending on the graphenes chemical potentials can be coupled to the lower-right or left graphene micro-ribbons and continue to propagate laterally towards the corresponding output port. Numerical simulations show that a change of ∆V_G ≈ ± 2.7 V in the voltage, applied to the gated micro-ribbons, can modulate their chemical potentials sufficiently to switch the right (left) output port from ON (OFF) to OFF(ON) and vice versa. Besides its low power consumption, the switch ultra-small dimensions make it a potential spatial router suitable for THz-integrated circuit applications.

     

Let-7e enhances the radiosensitivity of colorectal cancer cells by directly targeting insulin-like growth factor 1 receptor

Abnormal expression of various microRNAs (miRNAs), as regulators of biological signaling pathways, has a strong association with cancer resistance to chemotherapy and radiotherapy. The let-7 family of miRNAs as tumor suppressors have shown to be downregulated in different types of human malignancies including colorectal cancer (CRC). However, the biological function of let-7 members in the processes of resistance to radiation in CRC has not yet been completely elucidated. Insulin-like growth factor 1 receptor (IGF-1R) signaling pathway is amplified in CRC and leads to its progression, development, and also radiation resistance. So, it seems like an attractive target for anticancer therapy. In this study, by using bioinformatics analysis, it has been revealed that IGF-1R is a direct target of the let-7e member. Consistent with this, we identified that increased levels of let-7e in CRC cells reduced IGF-1R protein level and subsequently its downstream signaling pathways, which resulted in the G1 cell cycle arrest and a significant reduction in the proliferation, survival and also resistance to radiation of CRC cells. Altogether, these results suggested that let-7e by targeting the IGF-1R signaling pathway might serve as therapeutics in anticancer therapy.     

Curcumin: A new candidate for retinal disease therapy?

The retina is the neural portion and light-sensitive layer of the eye, which has been observed in most of the vertebrates. The retina is composed of light-sensitive cells that absorb light and convert it into neural signals. These signals are sent to the brain for visual recognition. It has been shown that many pathogenesis conditions, including inflammation, angiogenesis, oxidative stress, and imbalanced histone modifications in the retina are associated with initiation and progression of retinal diseases (ie, glaucoma, diabetic retinopathy, and age-related macular degeneration). Currently available treatments include laser surgery, freezing, stem-cell therapy, shrinking abnormal blood vessels. It has some limitations, such as invasive methods, high costs, and many side effects. Hence, finding a new therapeutic platform for stopping or slowing of the disease progression is required. Curcumin is a natural product, which is associated with a wide range of properties, such as antioxidant, anti-inflammatory, antiangiogenic, and antitumor activates. It exerts therapeutic effects via activation/inhibition cellular and molecular targets involved in various diseases, such as retinal diseases. Increasing evidence revealed that curcumin can be used as a therapeutic option in the treatment of different retinal diseases. Here, we summarized various clinical and preclinical studies that used curcumin as a therapeutic agent in the treatment of retinal disorders.     

HIV-1 Vpr Modulates Macrophage Metabolic Pathways: A SILAC-Based Quantitative Analysis

Human immunodeficiency virus type 1 encoded viral protein Vpr is essential for infection of macrophages by HIV-1. Furthermore, these macrophages are resistant to cell death and are viral reservoir. However, the impact of Vpr on the macrophage proteome is yet to be comprehended. The goal of the present study was to use a stable-isotope labeling by amino acids in cell culture (SILAC) coupled with mass spectrometry-based proteomics approach to characterize the Vpr response in macrophages. Cultured human monocytic cells, U937, were differentiated into macrophages and transduced with adenovirus construct harboring the Vpr gene. More than 600 proteins were quantified in SILAC coupled with LC-MS/MS approach, among which 136 were significantly altered upon Vpr overexpression in macrophages. Quantified proteins were selected and clustered by biological functions, pathway and network analysis using Ingenuity computational pathway analysis. The proteomic data illustrating increase in abundance of enzymes in the glycolytic pathway (pentose phosphate and pyruvate metabolism) was further validated by western blot analysis. In addition, the proteomic data demonstrate down regulation of some key mitochondrial enzymes such as glutamate dehydrogenase 2 (GLUD2), adenylate kinase 2 (AK2) and transketolase (TKT). Based on these observations we postulate that HIV-1 hijacks the macrophage glucose metabolism pathway via the Vpr-hypoxia inducible factor 1 alpha (HIF-1 alpha) axis to induce expression of hexokinase (HK), glucose-6-phosphate dehyrogenase (G6PD) and pyruvate kinase muscle type 2 (PKM2) that facilitates viral replication and biogenesis, and long-term survival of macrophages. Furthermore, dysregulation of mitochondrial glutamate metabolism in macrophages can contribute to neurodegeneration via neuroexcitotoxic mechanisms in the context of NeuroAIDS.