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Archive - Nov 3, 2015

MicroRNA-146a in Epithelial-Cell-Derived Exosomes Can Induce Production of IL-10 in Monocytes and Inhibit Skewed Th2 Polarization in Nasal Mucosa; Results Suggest Possible Treatment for Allergic Disorders Such As Allergic Rhinitis

Researchers from the Shanghai Jiaotong University School of Medicine, the Shenzhen University School of Medicine, and the Guangzhou Medical University, all in China, have shown that microRNA-146a (miRNA-146a) from epithelial-cell-derived exosomes can induce the expression of interleukin-10 (IL-10) in monocytes. The IL-10-producing monocytes are then capable of suppressing effector T cell (Teff) activities and inhibiting the skewed T helper 2 (Th2) polarization in the nasal mucosa in a mouse model of allergic retinitis. The researchers noted that, while it is well known skewed Th2 polarization plays a critical role in the pathogenesis of allergic diseases, such a pathological condition has proven refractory to correction. In their new publication, however, the Chinese scientists conclude that their present data “indicate that miR-146a can induce IL-10-producing monocytes to suppress the skewed Th2 polarization, suggesting that miR-146a has potential in the treatment of allergic disorders, such as allergic rhinitis.” This work was published online on November 3, 2015 in an open-access article in Scientific Reports. The article is titled “Epithelial Cell-Derived Micro RNA-146a Generates Interleukin-10-Producing Monocytes to Inhibit Nasal Allergy.” In further detail, the authors write that their results suggest that human nasal epithelial cells produce miR-146a, which can be up-regulated by lipopolysaccharide (LPS) and suppressed by Th2 cytokines. The miR-146a can be released from nasal epithelial cells to the microenvironment, carried in exosomes.

[Scientific Reports article]

Jellyfish & Lampreys Swim with Unmatched Efficiency Using Low-Pressure Suction-Based Propulsion; Mechanism Had Previously Been Completely Misunderstood; Discovery May Revolutionize Ship Design

Millions of years ago, even before the continents had settled into place, jellyfish were already swimming the oceans with the same pulsing motions we observe today. Now, through clever experiments and insightful math, an interdisciplinary research team has revealed a startling truth about how jellyfish and lampreys, another ancient species that undulate like eels, move through the water with unmatched efficiency. "It confounds all our assumptions," said John Dabiri, Ph.D., a Professor of Civil and Environmental Engineering and of Mechanical Engineering at Stanford. "But our experiments show that jellyfish and lampreys actually suck water toward themselves to move forward, instead of pushing against the water behind them, as had been previously supposed." This new understanding of motion in fluids is published online on November 3, 2015 in an open-access article in Nature Communications article that Dr. Dabiri co-authored with Dr. Brad Gemmell of the University of South Florida, Dr. Sean Colin of Roger Williams University in Rhode Island, and Dr. John Costello of Providence College, also in Rhode Island. The Nature Communications article is titled “Suction-Based Propulsion As a Basis for Efficient Animal Swimming.” Dr. Dabiri, an engineer, and his collaborators, all biologists affiliated with the Marine Biological Laboratory at Woods Hole, Massachusetts, have spent years studying the propulsion systems of jellyfish and eel-like lampreys. Both animals long ago evolved into efficient swimmers. Each minimal pulsing or undulating movement helps them cover a significant distance. Studying nature for clues to improve human-made technologies is part of a field called biomimetics, and the collaborators originally set out to seek insights that might improve the design of submarines, ships, and the like. About three years ago, Dr.

Towering Coastal Redwoods & Japanese Cedars Store Water in Special Tissue in Leaves at Top of Tree; May Be Adaptation to Hydraulic Constaints of Transporting Root Water with Increased Height; Top Leaves May Absorb Water from Fog & Dew

A research team led by Associate Professor Ishii Roaki, Ph.D., and doctoral student Azuma Wakana from the Kobe University Graduate School of Agricultural Science has discovered that the water storage tissue that they recently found in the world's tallest tree, Sequoia sempervirens (coast redwood), which can reach heights up to 115 meters (379 feet), is also found in Japan's tallest trees, Cryptomeria japonica (Japanese cedar). The results of this research were published online on on 4 September 4, 2015 in the journal Trees. The article is titled “Function and Structure of Leaves Contributing to Increasing Water Storage with Height in the Tallest Cryptomeria japonica Trees of Japan.” How do tall trees supply water to pinnacle leaves? Until now, it was thought that the highest leaves of tall trees suffered from constant water deficit because the water absorbed by the roots had to be transported a long way. Even among tree physiologists, most research focused on identifying the constraints to water transport, which would define the limits of tree height. In 2012, Professor Ishii's research group climbed the world's tallest redwoods, and collected leaf samples from various heights. They discovered that, with increasing height in the tree, the proportion of "xylem tissue" which transports water from the roots decreased, whereas the proportion of "transfusion tissue," which stores water, increased. The team inferred that in these redwoods, the stored water came from moisture such as fog and dew absorbed through the leaf surface. On September 9, 2014, the group conducted field work in Japan’s Akita Prefecture to determine whether similar foliar water storage functions existed in Japan's tallest cedar trees, a close relative of the coast redwood, that can reach heights of over 50 meters (164 feet).

Darwin’s “Fecundity Selection” Theory Must Be Revised, New Report Suggests; Fewer Offspring May Be Advantage Due to Better Individual Care; Possible Effects of Male Involvement and Climate Change Must Also Be Considered

The "Fecundity Selection" theory, a key concept in Darwin’s theory of evolution that suggests that nature favors larger females that can produce greater numbers of off-spring must be redefined, according to scientists behind ground-breaking research published online on November 3, 2015 in Biological Reviews. The new article is titled “Fecundity Selection Theory: Concepts and Evidence.” The study concludes that the theory of fecundity selection, one of Charles Darwin’s three main evolutionary principles, also known as “fertility selection,” should be re-defined so that it no longer rests on the idea that more fertile females are more successful in evolutionary terms. The research highlights the observation that too many offspring can have severe negative implications for mothers and the success of their descendants, and that that males can also affect the evolutionary success of a brood. Darwin’s theory of fecundity selection was postulated in 1874 and, together with the principles of natural selection and sexual selection, remains a fundamental component of modern evolutionary theory. The fecundity selection theory describes the process of reproductive success among organisms as being defined by the number of successful offspring that reach breeding age. After years of research, however, an evolutionary biologist (Daniel Pincheira-Donoso, Ph.D.) from the Department of Life Sciences, University of Lincoln, UK, and his colleague John Hunt, Ph.D., also from the University of Lincoln, have now proposed a revised version of the theory of fecundity selection, which recommends an updated definition, adjusts its traditional predictions, and incorporates important new biological terms.

Exosomal MicroRNA-223 Contributes to Mesenchymal Stem Cell-Elicited Cardioprotection in Sepsis

Scientists at the University of Cincinnati College of Medicine, together with colleagues, have shown that the cardio-protective effects known to be associated with mesenchymal stem cells (MSCs) during sepsis are likely attributable, at least in part, to the high levels of microRNA-223 (miR-223) know to exist in MSC-derived exosomes that may reach the heart. According to the authors, their data indicates, for the first time, that exosomal miR-223 plays an essential role in MSC-induced cardio-protection in sepsis. The new work was published online on September 8, 2015 in an open-access article in Scientific Reports. The article is titled “Exosomal miR-223 Contributes to Mesenchymal Stem Cell-Elicited Cardioprotection in Polymicrobial Sepsis.” In a mouse model of sepsis, the scientists showed that injection of MSCs from which miR-223 had been eliminated (miR-223-KO MSCs), did not confer protection against the sepsis-triggered cardiac dysfunction, apoptosis, and inflammatory response in the model mice. However, wild-type MSCs (WT-MSCs) were able to provide protection that was associated with exosome release. Next, the scientists showed that treatment of sepsis-model mice with exosomes released from miR-223-KO MSCs significantly exaggerated sepsis-induced injury. On the other hand, treatment with WT-MSC-derived-exosomes displayed protective effects. The scientists then determined that miR-223-KO MSC-derived exosomes contained higher levels of Sema3A and Stat3, two known protein targets of miR-223 (5p & 3p), than were contained in WT-MSC-derived exosomes. Accordingly, these exosomal proteins from miR-223-KO MSC-derived exosomes were transferred to cardiomyocytes, leading to increased inflammation and cell death.

Mesenchymal Stem Cells Use Extracellular Vesicles (Microvesicles & Exosomes) to Transfer Depolarized Mitochondria & Shuttle TLR-Signaling Repressive miRNAs to Macrophages in Response to Oxidative Stress

A team led by scientists from the Florida campus of The Scripps Research Institute (TSRI) and the University of Pittsburgh has shown, for the first time, how one set of specialized cells survives under stress by manipulating the behavior of key immune system cells. The new study, published online on October 7, 2015 in an open-access article in Nature Communications, involved mesenchymal stem cells (which live in bone marrow and can differentiate into several different cell types used in bone and connective tissue) and macrophages (immune cells that usually respond to infectious agents or damaged cells by engulfing and consuming them). “This is the first time anyone has shown how mesenchymal stem cells provide for their own survival by recruiting and then suppressing normal macrophage activity,” said TSRI Professor Donald G. Phinney, who led the study, together with University of Pittsburgh Associate Professor Luis A. Ortiz, Ph.D. “This finally puts the crosstalk between these cells into the context of cell survival.” The team’s experiments showed that, like all other cells, mesenchymal stem cells (MSCs) experience stress due to tissue injury and inflammation. When this stress results in damage to the mitochondria (the power houses of the cell), the MSCs recruit the immune system’s macrophages—but in an unusual way. By re-engineering macrophage action with secreted microRNA (in MSC-derived exosomes), the stem cells protect themselves from being targeted and, instead, package their damaged mitochondria into microvesicles (MVs) and send them out to be engulfed by the macrophage. Once macrophages subsume the damaged mitochondria, the macrophages are able to re-purpose the mitochondria for their own use, replenishing their own energy supplies. Blocking the exchange of damaged mitochondrial to macrophages causes death of the MSCs.