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Vascular biologies

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A seed sequence variant in miR-145-5p causes multisystem smooth muscle dysfunction syndrome
Christian Lacks Lino Cardenas, … , Mark E. Lindsay, Patricia L. Musolino
Christian Lacks Lino Cardenas, … , Mark E. Lindsay, Patricia L. Musolino
Published January 17, 2023
Citation Information: J Clin Invest. 2023. https://doi.org/10.1172/JCI166497.
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A seed sequence variant in miR-145-5p causes multisystem smooth muscle dysfunction syndrome

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Abstract

Authors

Christian Lacks Lino Cardenas, Lauren C. Briere, David A. Sweetser, Mark E. Lindsay, Patricia L. Musolino

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Long non-coding RNA LEENE promotes angiogenesis and ischemic recovery in diabetes models
Xiaofang Tang, … , Sheng Zhong, Zhen Bouman Chen
Xiaofang Tang, … , Sheng Zhong, Zhen Bouman Chen
Published December 13, 2022
Citation Information: J Clin Invest. 2022. https://doi.org/10.1172/JCI161759.
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Long non-coding RNA LEENE promotes angiogenesis and ischemic recovery in diabetes models

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Abstract

Impaired angiogenesis in diabetes is a key process contributing to ischemic diseases such as peripheral arterial disease. Epigenetic mechanisms, including those mediated by long non-coding RNAs are crucial links connecting diabetes and the related chronic tissue ischemia. Here we identify the LncRNA that Enhances Endothelial Nitric oxide synthase Expression (LEENE) as a regulator of angiogenesis and ischemic response. LEENE expression is decreased in diabetic conditions in cultured endothelial cells (EC), mouse hindlimb muscles, and human arteries. Inhibition of LEENE in human microvascular ECs reduces their angiogenic capacity with a dysregulated angiogenic gene program. Diabetic mice deficient in leene demonstrate impaired angiogenesis and perfusion following hindlimb ischemia. Importantly, overexpression of human LEENE rescues the impaired ischemic response in leene knockout mice at tissue functional and single-cell transcriptomic levels. Mechanistically, LEENE RNA promotes transcription of pro-angiogenic genes in ECs, such as KDR and eNOS, potentially by interacting with LEO1, a key component of RNA Polymerase II-associated factor complex and MYC, a crucial transcription factor for angiogenesis. Taken together, our findings demonstrate an essential role for LEENE in the regulation of angiogenesis and tissue perfusion. Functional enhancement of LEENE to restore angiogenesis for tissue repair and regeneration may represent a potential strategy to tackle ischemic vascular diseases.

Authors

Xiaofang Tang, Yingjun Luo, Dongqiang Yuan, Riccardo Calandrelli, Naseeb Kaur Malhi, Kiran Sriram, Yifei Miao, Chih Hong Lou, Walter Tsark, Alonso Tapia, Aleysha T. Chen, Guangyu Zhang, Daniel Roeth, Markus Kalkum, Zhao V. Wang, Shu Chien, Rama Natarajan, John P. Cooke, Sheng Zhong, Zhen Bouman Chen

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A human TRPV1 genetic variant within the channel gating domain regulates pain sensitivity in rodents
Shufang He, … , Ye Zhang, Eric R. Gross
Shufang He, … , Ye Zhang, Eric R. Gross
Published December 6, 2022
Citation Information: J Clin Invest. 2022. https://doi.org/10.1172/JCI163735.
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A human TRPV1 genetic variant within the channel gating domain regulates pain sensitivity in rodents

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Pain signals are relayed to the brain via a nociceptive system, and in rare situations, this nociceptive system contains genetic variants that can limit pain response. Here we questioned whether a human transient receptor potential vanilloid 1 (TRPV1) missense variant causes a resistance to noxious stimuli and further if we can target this region by a cell-permeable peptide as a pain therapeutic. Initially using a computational approach, we identified a human K710N TRPV1 missense variant in an otherwise highly conserved region of mammalian TRPV1. After generating a TRPV1K710N knock-in mouse using CRISPR/Cas9, we discovered the K710N variant reduced capsaicin-induced calcium influx in dorsal root ganglion neurons. The TRPV1K710N rodents also had less acute behavioral response to chemical noxious stimuli and less hypersensitivity to nerve injury-induced pain, while leaving the response to noxious heat intact. Furthermore, blocking this K710 region in wild-type rodents by a cell-penetrating peptide limited acute behavioral responses to noxious stimuli and rescued pain hypersensitivity induced by nerve injury back to baseline. These findings identify K710 TRPV1 as a discrete site crucial for the control of nociception and provides new insights into how to leverage rare genetic variants in humans to uncover fresh strategies for developing pain therapeutics.

Authors

Shufang He, Vanessa O. Zambelli, Pritam Sinharoy, Laura Brabenec, Yang Bian, Freeborn Rwere, Rafaela C.R. Hell, Beatriz Stein Neto, Barbara Hung, Xuan Yu, Meng Zhao, Zhaofei Luo, Chao Wu, Lijun Xu, Katrin J. Svensson, Stacy L. McAllister, Creed M. Stary, Nana-Maria Wagner, Ye Zhang, Eric R. Gross

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BAF60c prevents abdominal aortic aneurysm formation through epigenetic control of vascular smooth muscle cell homeostasis
Guizhen Zhao, … , Y. Eugene Chen, Jifeng Zhang
Guizhen Zhao, … , Y. Eugene Chen, Jifeng Zhang
Published September 6, 2022
Citation Information: J Clin Invest. 2022. https://doi.org/10.1172/JCI158309.
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BAF60c prevents abdominal aortic aneurysm formation through epigenetic control of vascular smooth muscle cell homeostasis

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Abdominal aortic aneurysm (AAA) is a life-threatening vascular disease. BAF60c, a unique subunit of the SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin remodeling complex, is critical for cardiac and skeletal myogenesis; yet, little is known about its function in the vasculature and, specifically, in AAA pathogenesis. Here, we found that BAF60c was downregulated in human and mouse AAA tissues, with primary staining to vascular smooth muscle cells (VSMC), confirmed by single-cell RNA-sequencing. In vivo studies revealed that VSMC-specific knockout of Baf60c significantly aggravated both AngII- and elastase-induced AAA formation in mice, with a significant increase in elastin degradation, inflammatory cell infiltration, VSMC phenotypic switch, and apoptosis. In vitro studies showed that BAF60c knockdown in VSMC resulted in the loss of contractile phenotype, increased VSMC inflammation, and apoptosis. Mechanistically, we demonstrated that BAF60c preserved VSMC contractile phenotype by strengthening serum response factor (SRF) association with its co-activator P300 and the SWI/SNF complex, suppressed VSMC inflammation by promoting a repressive chromatin state of the NFκB-target genes, as well as prevented VSMC apoptosis through transcriptional activation of KLF5-dependent BCL2 expression. Together, our identification of the essential role of BAF60c in preserving VSMC homeostasis expands its therapeutic potential in preventing and treating AAA.

Authors

Guizhen Zhao, Yang Zhao, Haocheng Lu, Ziyi Chang, Hongyu Liu, Huilun Wang, Wenying Liang, Yuhao Liu, Tianqing Zhu, Oren Rom, Yanhong Guo, Lin Chang, Bo Yang, Minerva T. Garcia-Barrio, Jiandie D. Lin, Y. Eugene Chen, Jifeng Zhang

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Lymphangiogenesis requires Ang2/Tie/PI3K signaling for VEGFR3 cell surface expression
Emilia A. Korhonen, … , Taija Mäkinen, Kari Alitalo
Emilia A. Korhonen, … , Taija Mäkinen, Kari Alitalo
Published June 28, 2022
Citation Information: J Clin Invest. 2022. https://doi.org/10.1172/JCI155478.
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Lymphangiogenesis requires Ang2/Tie/PI3K signaling for VEGFR3 cell surface expression

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Vascular endothelial growth factor C (VEGF-C) induces lymphangiogenesis via VEGF receptor-3 (VEGFR3), encoded by the most frequently mutated gene in human primary lymphedema. Angiopoietins (Angs) and their Tie receptors regulate lymphatic vessel development and mutations of the ANGPT2 gene were recently found in human primary lymphedema. However, the mechanistic basis of Ang2 activity in lymphangiogenesis is not fully understood. Here we used gene deletion, blocking antibodies, transgene induction and gene transfer to study how Ang2, its Tie2 receptor and Tie1 regulate lymphatic vessels. We discovered that VEGF-C-induced Ang2 secretion from lymphatic endothelial cells (LECs) is involved in full Akt activation downstream of phosphoinositide-3 kinase (PI3K). Neonatal deletion of genes encoding the Tie receptors or Ang2 in LECs, or administration of Ang2 blocking antibody decreased VEGFR3 presentation on LECs and inhibited lymphangiogenesis. A similar effect was observed in LECs upon deletion of PI3K catalytic p110α subunit or with small molecule inhibition of a constitutively active PI3K located downstream of Ang2. Deletion of Tie receptors or blockade of Ang2 decreased VEGF-C-induced lymphangiogenesis also in adult mice. Our results reveal important crosstalk between the VEGF-C and Ang signaling pathways and suggest new avenues for therapeutic manipulation of lymphangiogenesis by targeting Ang2-Tie-PI3K signaling.

Authors

Emilia A. Korhonen, Aino Murtomäki, Sawan Kumar Jha, Andrey Anisimov, Anne Pink, Yan Zhang, Simon Stritt, Inam Liaqat, Lukas Stanczuk, Laura Alderfer, Zhiliang Sun, Emmi Kapiainen, Abhishek Singh, Ibrahim Sultan, Anni Lantta, Veli-Matti Leppänen, Lauri Eklund, Yulong He, Hellmut G. Augustin, Kari Vaahtomeri, Pipsa Saharinen, Taija Mäkinen, Kari Alitalo

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Breast cancer chemotherapy induces vascular dysfunction and hypertension through NOX4 dependent mechanism
Piotr Szczepaniak, … , David G. Harrison, Tomasz J. Guzik
Piotr Szczepaniak, … , David G. Harrison, Tomasz J. Guzik
Published May 26, 2022
Citation Information: J Clin Invest. 2022. https://doi.org/10.1172/JCI149117.
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Breast cancer chemotherapy induces vascular dysfunction and hypertension through NOX4 dependent mechanism

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Cardiovascular disease is the major cause of morbidity and mortality in breast cancer survivors. Chemotherapy contributes to this risk. We aimed to define the mechanisms of long-term vascular dysfunction caused by neoadjuvant chemotherapy (NACT) and identify novel therapeutic targets. We studied arteries from postmenopausal women who had undergone breast cancer treatment using docetaxel, doxorubicin and cyclophosphamide (NACT), and women with no history of such treatment matched for key clinical parameters. Mechanisms were explored in wild-type and Nox4-/- mice and human microvascular endothelial cells. Endothelium-dependent vasodilatation is severely impaired in patients after NACT, while endothelium-independent responses remain normal. This was mimicked by 24-hour exposure of arteries to NACT agents ex-vivo. When applied individually, only docetaxel impaired endothelial function in human vessels. Mechanistic studies showed that NACT increased inhibitory eNOS phosphorylation of threonine 495 in a ROCK-dependent manner and augmented vascular superoxide and hydrogen peroxide production and NADPH oxidase activity. Docetaxel increased expression of NADPH oxidase NOX4 in endothelial and smooth muscle cells and NOX2 in the endothelium. NOX4 increase in human arteries may be mediated epigenetically by diminished DNA methylation of the NOX4 promoter. Docetaxel induced endothelial dysfunction and hypertension in mice. These were prevented in Nox4-/- and by pharmacological inhibition of Nox4 or Rock. Commonly used chemotherapeutic agents, and in particular, docetaxel, alter vascular function by promoting inhibitory phosphorylation of eNOS and enhancing ROS production by NADPH oxidases.

Authors

Piotr Szczepaniak, Mateusz Siedlinski, Diana Hodorowicz-Zaniewska, Ryszard Nosalski, Tomasz P. Mikolajczyk, Aneta M. Dobosz, Anna Dikalova, Sergey Dikalov, Joanna Streb, Katarzyna Gara, Pawel Basta, Jaroslaw Krolczyk, Joanna Sulicka-Grodzicka, Ewelina Jozefczuk, Anna Dziewulska, Blessy Saju, Iwona Laksa, Wei Chen, John Dormer, Maciej Tomaszewski, Pasquale Maffia, Marta Czesnikiewicz-Guzik, Filippo Crea, Agnieszka Dobrzyn, Javid Moslehi, Tomasz Grodzicki, David G. Harrison, Tomasz J. Guzik

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Erythroid lineage Jak2V617F expression promotes atherosclerosis through erythrophagocytosis and macrophage ferroptosis
Wenli Liu, … , Alan R. Tall, Nan Wang
Wenli Liu, … , Alan R. Tall, Nan Wang
Published May 19, 2022
Citation Information: J Clin Invest. 2022. https://doi.org/10.1172/JCI155724.
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Erythroid lineage Jak2V617F expression promotes atherosclerosis through erythrophagocytosis and macrophage ferroptosis

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Elevated hematocrit is associated with cardiovascular risk; however, the causality and mechanisms are unclear. The JAK2V617F (Jak2VF) mutation increases cardiovascular risk in myeloproliferative disorders and in clonal hematopoiesis (CH). Jak2VF mice with elevated white blood cells, platelets and red blood cells (RBCs) display accelerated atherosclerosis and macrophage erythrophagocytosis. To investigate whether selective erythroid Jak2VF expression promotes atherosclerosis, we developed hyperlipidemic Erythropoietin Receptor Cre mice that express Jak2VF in the erythroid lineage (VFEpoR mice). VFEpoR mice without elevated blood cell counts showed increased atherosclerotic plaque necrosis, erythrophagocytosis and ferroptosis. Selective induction of erythrocytosis with low dose erythropoietin further exacerbated atherosclerosis with prominent ferroptosis, lipid peroxidation and endothelial damage. VFEpoR RBCs had reduced antioxidant defenses and increased lipid hydroperoxides. Phagocytosis of human or murine WT or JAK2VF RBCs by WT macrophages induced ferroptosis, which was prevented by the ferroptosis inhibitor Liproxstatin-1. Liproxstatin-1 reversed increased atherosclerosis, lipid peroxidation, ferroptosis and endothelial damage in VFEpoR mice and in Jak2VF chimeric mice simulating CH, but had no impact in controls. Erythroid lineage Jak2VF expression leads to qualitative and quantitative defects in RBCs that exacerbate atherosclerosis. Phagocytosis of RBCs by plaque macrophages promotes ferroptosis, suggesting a new therapeutic target to reduce RBC-mediated cardiovascular risk.

Authors

Wenli Liu, Nataliya K. Östberg, Mustafa Yalcinkaya, Huijuan Dou, Kaori Endo-Umeda, Yang Tang, Xintong Hou, Tong Xiao, Trevor Filder, Sandra Abramowicz, Yong-Guang Yang, Oliver Soehnlein, Alan R. Tall, Nan Wang

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Cardiac pericyte reprogramming by MEK inhibition promotes arteriologenesis and angiogenesis of the ischemic heart
Elisa Avolio, … , Massimo Caputo, Paolo Madeddu
Elisa Avolio, … , Massimo Caputo, Paolo Madeddu
Published March 29, 2022
Citation Information: J Clin Invest. 2022. https://doi.org/10.1172/JCI152308.
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Cardiac pericyte reprogramming by MEK inhibition promotes arteriologenesis and angiogenesis of the ischemic heart

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Pericytes (PC) are abundant yet remain the most enigmatic and ill-defined cell population in the heart. Here, we investigated if PC can be reprogrammed to aid neovascularization. Primary PC from human and mouse hearts acquired cytoskeleton proteins typical of vascular smooth muscle cells (VSMC) upon exclusion of EGF/bFGF, which signal through ERK1/2, or exposure to the MEK-inhibitor PD0325901. Differentiated PC became more proangiogenic, more responsive to vasoactive agents, and insensitive to chemoattractants. RNA-Sequencing revealed transcripts marking the PD0325901-induced transition into proangiogenic, stationary VSMC-like cells, including the unique expression of two angiogenesis-related markers, aquaporin 1 (AQP1) and cellular retinoic acid-binding protein 2 (CRABP2), which were further verified at the protein level. This enabled us to trace PC during in vivo studies. In mice, implantation of Matrigel plugs containing human PC+PD0325901 promoted the formation of α-SMApos neovessels compared with PC only. Two-week oral administration of PD0325901 to mice increased the heart arteriolar density, total vascular area, arteriole coverage by PDGFRβposAQP1posCRABP2pos PC, and myocardial perfusion. Short-duration PD0325901 treatment of mice after myocardial infarction enhanced the peri-infarct vascularization, reduced the scar, and improved systolic function. In conclusion, myocardial PC have intrinsic plasticity that can be pharmacologically modulated to promote reparative vascularization of the ischemic heart.

Authors

Elisa Avolio, Rajesh Katare, Anita C. Thomas, Andrea Caporali, Daryl Schwenke, Michele Carrabba, Marco Meloni, Massimo Caputo, Paolo Madeddu

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Platelet olfactory receptor activation limits platelet reactivity and growth of aortic aneurysms
Craig N. Morrell, … , Ayman Elbadawi, Scott J. Cameron
Craig N. Morrell, … , Ayman Elbadawi, Scott J. Cameron
Published March 24, 2022
Citation Information: J Clin Invest. 2022. https://doi.org/10.1172/JCI152373.
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Platelet olfactory receptor activation limits platelet reactivity and growth of aortic aneurysms

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As blood transitions from steady laminar flow (S-flow) in healthy arteries to disturbed flow (D-flow) in aneurysmal arteries, platelets are subjected to external forces. Biomechanical platelet activation is incompletely understood and is a potential mechanism behind antiplatelet medication resistance. While it was demonstrated that anti-platelet drugs suppress growth of abdominal aortic aneurysms (AAA) in patients, we revealed a certain degree of platelet reactivity persisted in spite of aspirin therapy urging us to consider additional anti-platelet therapeutic targets. Transcriptomic profiling of platelets from patients with AAA revealed upregulation of a signal transduction pathway common to olfactory receptors (ORs), and this was explored as a mediator of AAA progression. Healthy platelets subjected to D-flow ex vivo, platelets from patients with AAA, and platelets in murine models of AAA demonstrated increased membrane olfactory receptor 2L13 (OR2L13) expression. A drug screen identified a molecule activating platelet OR2L13 which limited both biochemical and biomechanical platelet activation as well as AAA growth. This observation was further supported by selective deletion of the OR2L13 ortholog in a murine model of AAA that accelerated aortic aneurysm growth and rupture. These studies reveal that ORs regulate platelet activation in AAA and aneurysmal progression through platelet-derived mediators of aortic remodeling.

Authors

Craig N. Morrell, Doran Mix, Anu Aggarwal, Rohan Bhandari, Matthew Godwin, A. Phillip Owens III, Sean P. Lyden, Adam Doyle, Krystin Krauel, Matthew T. Rondina, Amy Mohan, Charles J. Lowenstein, Sharon Shim, Shaun Stauffer, Vara Prasad Josyula, Sara K. Ture, David I. Yule, Larry E. Wagner III, John M. Ashton, Ayman Elbadawi, Scott J. Cameron

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The Ca2+-gated channel TMEM16A amplifies capillary pericyte contraction and reduces cerebral blood flow after ischemia
Nils Korte, … , David Attwell, Paolo Tammaro
Nils Korte, … , David Attwell, Paolo Tammaro
Published March 22, 2022
Citation Information: J Clin Invest. 2022. https://doi.org/10.1172/JCI154118.
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The Ca2+-gated channel TMEM16A amplifies capillary pericyte contraction and reduces cerebral blood flow after ischemia

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Pericyte-mediated capillary constriction decreases cerebral blood flow in stroke after an occluded artery is unblocked. The determinants of pericyte tone are poorly understood. We show that a small rise in cytoplasmic Ca2+ concentration ([Ca2+]i) in pericytes activates chloride efflux through the Ca2+-gated anion channel TMEM16A, thus depolarizing the cell and opening voltage-gated calcium channels. This mechanism strongly amplifies the pericyte [Ca2+]i rise and capillary constriction evoked by contractile agonists and ischemia. In a rodent stroke model, TMEM16A inhibition slows the ischemia-evoked pericyte [Ca2+]i rise, capillary constriction and pericyte death, reduces neutrophil stalling and improves cerebrovascular reperfusion. Genetic analysis implicates altered TMEM16A expression in poor patient recovery from ischemic stroke. Thus, pericyte TMEM16A is a crucial regulator of cerebral capillary function, and a potential therapeutic target for stroke and possibly other disorders of impaired microvascular flow, such as Alzheimer’s disease and vascular dementia.

Authors

Nils Korte, Zeki Ilkan, Claire L. Pearson, Thomas Pfeiffer, Prabhav Singhal, Jason R. Rock, Huma Sethi, Dipender Gill, David Attwell, Paolo Tammaro

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MiR-33 fine-tunes atherosclerotic plaque inflammation
Mireille Ouimet, Hasini Ediriweera, and colleagues show that miR-33 controls the macrophage inflammatory program and promotes atherosclerotic plaque development…
Published October 26, 2015
Scientific Show StopperVascular biology

Contracting lacteals send lipids down the drain
Kibaek Choe, Jeon Yeob Jang, Intae Park and colleagues visualize lipid drainage through lacteals using intravital, video-rate microscopy…
Published October 5, 2015
Scientific Show StopperVascular biology

FOXC2 keeps lymphatic vessels leak-proof
Amélie Sabine and colleagues demonstrate that disturbed flow in lymphatic vasculature induces expression of the transcription factor FOXC2, which is essential for maintaining normal endothelial cell morphology and vessel integrity…
Published September 21, 2015
Scientific Show StopperVascular biology

Venous malformation model provides therapeutic insight
Elisa Boscolo and colleagues develop a murine model of venous malformation and demonstrate that rapamycin improves clinical symptoms of in this model and in patients…
Published August 10, 2015
Scientific Show StopperVascular biology

Lymphatic valves grow with the flow
Daniel Sweet and colleagues reveal that lymph flow is essential for lymphatic vessel maturation…
Published July 27, 2015
Scientific Show StopperVascular biology

GATA2 serves as a lymphatic rheostat
Jan Kazenwadel, Kelly Betterman, and colleagues reveal that the transcription factor GATA2 is essential for lymphatic valve development and maintenance…
Published July 27, 2015
Scientific Show StopperVascular biology

Factoring in factor XII in hereditary angioedema III
Jenny Björkqvist and colleagues elucidate the mechanism by which hereditary angioedema III-associated factor XII promotes vascular leakage…
Published July 20, 2015
Scientific Show StopperVascular biology

Regional regulation of atherosclerosis
Yogendra Kanthi, Matthew Hyman, and colleagues reveal that CD39 is regulated by blood flow and is protective against atherosclerosis…
Published June 29, 2015
Scientific Show StopperVascular biology
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