Endothelial Cell News 4.06 February 25, 2019 | |
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TOP STORYStaphylococcus aureus Leukocidins Target Endothelial DARC to Cause Lethality in Mice Leukocidin ED and γ-hemolysin AB injured primary human endothelial cells in a Duffy antigen receptor for chemokines (DARC)-dependent manner, and mice with DARC-deficient endothelial cells were resistant to toxin-mediated lethality. During bloodstream infection in mice, DARC targeting by S. aureus caused increased tissue damage, organ dysfunction, and host death. [Cell Host Microbe] Abstract | Graphical Abstract | |
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PUBLICATIONS(Ranked by impact factor of the journal)Mechanistically, MST1 was activated by reactive oxygen species produced in the mitochondria in response to hypoxia, and activated MST1 promoted the nuclear import of FOXO1, thus augmenting its transcriptional regulation of polarity and migration-associated genes. [Nat Commun] Full Article tmem33 Is Essential for VEGF-Mediated Endothelial Calcium Oscillations and Angiogenesis Researchers found that transmembrane protein 33 (tmem33) localized to the endoplasmic reticulum in zebrafish endothelial cells (ECs) and was required for cytosolic calcium oscillations in response to Vegfa. tmem33-mediated endothelial calcium oscillations were critical for formation of endothelial tip cell filopodia and EC migration. [Nat Commun] Full Article Podocalyxin Is Required for Maintaining Blood-Brain Barrier Function during Acute Inflammation Using electrical cell substrate impedance sensing and live imaging, the authors found that, in the absence of podocalyxin, human umbilical vein endothelial cells fail to form an efficient barrier when plated on several extracellular matrix substrates. In addition, these monolayers lacked adherens junctions and focal adhesions and displayed a disorganized cortical actin cytoskeleton. [Proc Natl Acad Sci USA] Abstract | Press Release Inhibition of EZH2 Prevents Fibrosis and Restores Normal Angiogenesis in Scleroderma In endothelial cells, inhibition of enhancer of zeste homolog 2 (EZH2) restored normal angiogenesis in scleroderma via activating the Notch pathway, specifically by up-regulating the Notch ligand DLL4. [Proc Natl Acad Sci USA] Full Article In vitro data demonstrated that lymphotoxin-α promoted the proliferation, migration and tube formation of HUVECs by enhancing the PFKFB3-mediated glycolytic flux. Genetic and pharmacological inhibition of PFKFB3 suppressed the enhanced proliferation and migration of HUVECs. [Int J Cancer] Abstract Investigators determined that brain microvascular endothelial cells (BMECs) cultured in 3D under perfusion conditions were 10-100 times less permeable to sodium fluorescein, 3 kDa dextran, and albumin relative to human umbilical vein endothelial cell and human dermal microvascular endothelial cell controls, and the BMECs maintained barrier function for up to 21 days. [Stem Cell Reports] Full Article | Press Release Focal TLR4 Activation Mediates Disturbed Flow-Induced Endothelial Inflammation Researchers investigated whether toll-like receptor 4 (TLR4) could sense disturbed flow to mediate the subsequent endothelial inflammation. Disturbed flow in vitro increased TLR4 expression and activation in human endothelial cells and promoted monocyte-endothelial cell adhesion, which were inhibited in TLR4-knockdown endothelial cells. [Cardiovasc Res] Abstract The authors used recombinant human CXCL5 to stimulate HUVECs and found that their tube formation ability, proliferation, and migration were enhanced by the activation of the AKT/NF-κB/FOXD1/VEGF-A pathway in a CXCR2-dependent manner. [Cell Death Dis] Full Article Scientists investigated the effect of cholesterol [hypercholesterolemia and 7-ketocholesterol] on endoglin expression and regulation with respect to endothelial or vascular dysfunction in vivo and in vitro. [FASEB J] Abstract RHOG Activates RAC1 through CDC42 Leading to Tube Formation in Vascular Endothelial Cells Investigators found that siRNA-mediated depletion of RHOG strongly inhibited tube formation in vascular endothelial cells, an effect reversed by transfecting dominant active constructs of CDC42 or RAC1 in the RHOG-depleted cells. They also found CDC42 to be upstream from RAC1 in these cells. [Cells] Full Article Subscribe to one of our other 19 science newsletters such as Extracellular Matrix News & Cell Therapy News. | |
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REVIEWSRecent in vivo and in vitro studies have revealed that the gap junctions of endothelial cells participate in the promotion of angiogenesis. The authors review the implication for endothelial gap junctions and cellular mechanics in vascular angiogenesis. [Cancers] Full Article Visit our reviews page to see a complete list of reviews in the endothelial cell research field. | |
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INDUSTRY NEWSPfizer Receives European Approval for ZIRABEV™ (Bevacizumab), a Biosimilar to Avastin® Pfizer Inc. announced the European Commission has approved ZIRABEV™ for the treatment of metastatic carcinoma of the colon or rectum, metastatic breast cancer, unresectable advanced, metastatic or recurrent non-small cell lung cancer, advanced and/or metastatic renal cell cancer and persistent, recurrent or metastatic carcinoma of the cervix. [Pfizer Inc.] Press Release Exelixis, Inc. announced it is initiating Phase I clinical development for XL092, the first internally-discovered Exelixis compound to enter the clinic following the company’s reinitiation of drug discovery activities. XL092 is a next-generation oral tyrosine kinase inhibitor that targets VEGF receptors, MET, and other kinases implicated in cancer’s growth and spread. [Exelixis, Inc.] Press Release Hemostemix Announces UC Davis Health Added as a Trial Site for Phase II Clinical Trial Hemostemix Inc. announced that it has received all approvals for the UC Davis Health located in Sacramento, California to be the clinical trial site for the company’s Phase II clinical trial for critical limb ischemia. [Hemostemix Inc.] Press Release | |
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POLICY NEWSMoldovan Mathematician among Academics Running in General Election Several researchers, including one mathematician, are running for seats in Moldova’s parliament this month. They hope to depoliticize science, improve education and address high levels of brain drain in the small country of 3.5 million people. [Nature News] Editorial Open-Access Pioneer Randy Schekman on Plan S and Disrupting Scientific Publishing Nobel laureate Randy Schekman shook up the publishing industry when he launched the open-access journal eLife in 2012. Armed with millions in funding from three of the world’s largest private biomedical charities — the Wellcome Trust, the Max Planck Society and the Howard Hughes Medical Institute — Schekman designed the journal to compete with publishing powerhouses such as Nature, Science and Cell. [Nature News] Editorial Foreign Governments Want to Boost Their Biotech Industries — So They’re Setting Up Shop in Boston Cities and states around the corner and around the country have angled for years to set themselves up as the next Kendall Square, hoping to import some of the magic of Boston’s biotech hub and its job-creating economic engine. Increasingly, foreign governments are pushing for the same. [STAT News] Editorial
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EVENTSNEW DASCS2019 Stem Cell conference Visit our events page to see a complete list of events in the community.
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JOB OPPORTUNITIESNEW Postdoctoral Position – Angiogenesis/Vascular Biology (Johns Hopkins University) NEW Vascular Biologist – RNA Therapeutics (Guide Therapeutics) NEW Postdoctoral Fellow – Vascular Biology (Stanford School of Medicine) NEW Postdoctoral Fellow – Vascular Biology (University of Nevada, Reno) Tier 2 Canada Research Chair – Cardiovascular/Vascular Health (University of Ottawa) Faculty Position – Clinical & Experimental Therapeutics (Augusta University) Postdoctoral Position – Cardiovascular Research (University of Hawaii) Postdoctoral Fellows – Vascular Immunology & Immunotherapy (Uppsala University) Postdoctoral Fellowship – Vascular & Valvular Biology (Yale University School of Medicine) Assistant/Associate Adjunct Professor – Cardiovascular Medicine (UC Davis) Recruit Top Talent: Reach potential candidates by posting your organization’s career opportunities on the Connexon Creative Job Board at no cost.
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