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Unlike other types of blood components, refrigeration of platelets leads to their rapid clearance from the circulation after transfusion. Platelets must therefore be stored at room temperature, a serious limitation to their use for transfusions. Viktoria Rumjantseva et al. now dissect two platelet clearance pathways by which exposed carbohydrate residues on platelets are recognized by receptors on liver macrophages and hepatocytes, which differentially control the clearance of short-term– and long-term–refrigerated platelets.
Torsten Roepke et al. show that the potassium channel subunit KCNE2—which previously has been most recognized for its role in controlling electrical activity in the heart—is important for normal thyroid function. KCNE2, together with its partner KCNQ1, is expressed in both mouse and human thyroid epithelial cells, and Kcne2 deficiency in mice leads to a constellation of defects resulting from decreased thyroid hormone biosynthesis. These results suggest new genetic links between thyroid and heart function.
Insulin action in the brain is known to inhibit food intake. Now Leona Plum and her colleagues show that in hypothalamic neurons insulin inhibits FoxO1-mediated transcriptional repression of Cpe, a gene that encodes a carboxypeptidase that is required for proper processing of key anorexigenic neuropeptides. The team also found that this pathway is disturbed in states of diet-induced obesity, suggesting that obesity-induced insulin resistance may affect obesity even further.
Dying tumor cells release ATP, which activates the NLRP3 inflammasome in dendritic cells, enabling the secretion of interleukin-1β and the subsequent priming of tumor-specific interferon-γ-producing T lymphocytes.
Lissencephaly is a developmental brain disorder caused by mutations in LIS1 and characterized by impaired neuronal migration. Inhibiting calpain prevents LIS1 degradation in heterozygous mice and rescues the defective neuronal migration in utero.
Canonical Wnt signaling is known to be crucial in embryonic organ development. Joseph Gleeson and his colleagues now report that it is also important in the adult homeostasis of the kidney, especially after injury, and that disruption of this signaling pathway results in cystic kidney disease.
Ischemia causes pericytes on brain microvessels to contract, obstructing erythrocyte transit even after blood flow is restored. This contraction, which depends on the production of oxygen and nitrogen radicals, represents a novel pathophysiological mechanism in stroke.
Enterotoxigenic Bacteroides fragilis, a bacterium from the intestinal flora, may promote colon tumor formation through a pathway that involves Stat3 expression and T helper type 17 immune responses.
Although endogenous inhibitors of blood vessel growth have been studied extensively, specific inhibitors of lymphatic vessel growth have not been identified. Albuquerque et al. now identify truncated, secreted versions of mouse and human VEGFR-2 receptors generated by alternative splicing. The mouse protein acts as an endogenous inhibitor of lymphatic vessel growth in the cornea and skin, and its administration had therapeutic effects in mouse models of corneal injury and transplantation.
Suppression of the immune system could block autoimmune disease pathogenesis. Here Jacques Galipeau and his colleagues report that a fusion protein of two cytokines can induce immunosuppressive regulatory B cells. Transferring these cells into a mouse model of multiple sclerosis reduces disease in the mice.
Contrary to the belief that basal-like breast cancers develop from mammary stem cells in BRCA1 mutation carriers, an aberrant luminal progenitor population might be the target for transformation in basal tumors in these individuals (pages 842–844).
Infection with HSV-2 increases the likelihood of HIV acquisition, but suppression of HSV-2 reactivation with antiviral drugs does not seem to reduce the acquisition of HIV. Laurence Corey and colleagues provide a potential mechanism underlying this observation, showing that even after acyclovir treatment for the HSV-2 infection, many inflammatory and immune cells possessing the receptors required for HIV infection persist in the mucosa, making the initial 'spark' of infection more likely.
In these new reports, three different research groups independently find that various T cell populations are crucial mediators of obesity-induced metabolic dysfunction. They also show that pharmacological approaches that target these T cells are beneficial, thus opening the door to possible new therapeutic approaches to treating obesity-related diseases such as diabetes (pages 846–847, 921–929 and 930–939).
In these new reports, three different research groups independently find that various T cell populations are crucial mediators of obesity-induced metabolic dysfunction. They also show that pharmacological approaches that target these T cells are beneficial, thus opening the door to possible new therapeutic approaches to treating obesity-related diseases such as diabetes (pages 846–847, 914–920 and 921–929).
In these new reports, three different research groups independently find that various T cell populations are crucial mediators of obesity-induced metabolic dysfunction. They also show that pharmacological approaches that target these T cells are beneficial, thus opening the door to possible new therapeutic approaches to treating obesity-related diseases such as diabetes (pages 846–847, 914–920 and 930–939).
Bone is a dynamic tissue and requires the precise coordination of formation with loss. Here, Xu Cao and his colleagues show that the bone-chewing activity of osteoclasts results in the local release of active TGF-β1 from the surface of the bone, inducing the migration of nearby bone-forming osteoblastic progenitor cells to this resorbed region. In this manner, proper matching of the localized rates of bone loss and bone creation is ensured (pages 729–731).
Ewing's sarcoma family tumors are dependent on an oncogenic fusion protein, most commonly EWS-FLI1, which interacts with RNA helicase A (RHA) in transcriptional complexes. Erkizan et al. have identified a small molecule that inhibits the interaction of RHA with EWS-FLI1 and impairs the growth of Ewing's sarcoma xenografts in mice. The findings provide evidence that targeting tumor-specific transcription factors may be a feasible approach to treating cancer.
B cell–depleting antibodies have therapeutic efficacy against arthritis. Here Jane Grogan and her colleagues report a new approach to depleting pathogenic T cells. They show that lymphotoxin-α is upregulated on the surface of activated TH1 and TH17 CD4+ cells, which have a pathogenic role in several autoimmune diseases, and a monoclonal antibody targeted to lymphotoxin-a can inhibit collagen-induced arthritis and EAE in mice (pages 732–733).