Songwei Wu

ORCID: 0000-0003-0592-2920
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About
Contact & Profiles
Research Areas
  • Ion channel regulation and function
  • Ion Channels and Receptors
  • Cardiac electrophysiology and arrhythmias
  • Pulmonary Hypertension Research and Treatments
  • Nitric Oxide and Endothelin Effects
  • Ion Transport and Channel Regulation
  • Receptor Mechanisms and Signaling
  • Neuroscience and Neuropharmacology Research
  • Cell Adhesion Molecules Research
  • Cancer-related gene regulation
  • Renin-Angiotensin System Studies
  • Erythrocyte Function and Pathophysiology
  • Kruppel-like factors research
  • Hemoglobinopathies and Related Disorders
  • Caveolin-1 and cellular processes
  • Neuroscience of respiration and sleep
  • Signaling Pathways in Disease
  • Wnt/β-catenin signaling in development and cancer
  • Blood Coagulation and Thrombosis Mechanisms
  • Myeloproliferative Neoplasms: Diagnosis and Treatment
  • S100 Proteins and Annexins
  • Platelet Disorders and Treatments
  • Magnesium in Health and Disease
  • Electrolyte and hormonal disorders
  • High Altitude and Hypoxia

Chongqing Medical University
2023

Army Medical University
2023

The Affiliated Yongchuan Hospital of Chongqing Medical University
2023

Beijing Children’s Hospital
2022

Capital Medical University
2022

University of Alabama at Birmingham
2019-2021

Augusta University
2014-2017

Georgia Regents Medical Center
2014-2016

University of South Alabama
2004-2013

Augusta University Health
2013

With unknown etiology and limited treatment options, neonatal hypoxic-ischemic brain damage (HIBD) remains a major cause of mortality in newborns. Ferroptosis, recently discovered type cell death triggered by lipid peroxidation, is closely associated with HIBD. High-mobility group box 1 (HMGB1), molecule inflammation damage, can induce neuronal However, it whether HMGB1 contributes to ferroptosis patients Herein, glycyrrhizin (GL), an inhibitor, was used investigate the relationship between...

10.1155/2022/8438528 article EN Oxidative Medicine and Cellular Longevity 2022-04-07

Although the formation of hydrostatic lung edema is generally attributed to imbalanced Starling forces, recent data show that endothelial cells respond increased vascular pressure and may thus regulate permeability formation. In combining real-time optical imaging Ca(2+) concentration ([Ca(2+)](i)) NO production with filtration coefficient (K(f)) measurements in isolated perfused lung, we identified a series responses constitute negative-feedback loop protect microvascular barrier. Elevation...

10.1161/circresaha.107.168724 article EN Circulation Research 2008-03-07

Hypoxic pulmonary vasoconstriction (HPV) is a physiological mechanism by which arteries constrict in hypoxic lung areas order to redirect blood flow with greater oxygen supply. Both sensing and the contractile response are thought be intrinsic arterial smooth muscle cells. Here we speculated that ideal site for might instead at alveolocapillary level, subsequent retrograde propagation upstream arterioles via connexin 40 (Cx40) endothelial gap junctions. HPV was largely attenuated...

10.1172/jci59176 article EN Journal of Clinical Investigation 2012-10-24

While Ca 2+ influx is essential for activation of the cell cycle machinery, processes that regulate in this context have not been fully elucidated. Electrophysiological and molecular studies identified multiple channel genes expressed mammalian cells. v 3.x gene family members, encoding low voltage-activated (LVA) or T-type channels, were first central nervous system subsequently non-neuronal tissue. Reports a potential role channels controlling proliferation conflict. The present study...

10.1161/01.res.0000163066.07472.ff article EN Circulation Research 2005-03-18

Platelet-activating factor (PAF) increases lung vascular permeability within minutes by activation of acid sphingomyelinase (ASM) and a subsequent nitric oxide (NO)-inhibitable Ca(2+)-dependent loss in barrier function.To elucidate the molecular mechanisms underlying this response.In isolated perfused rat mouse lungs, endothelial Ca(2+) concentration ([Ca(2+)](i)) was quantified real-time fluorescence imaging, caveolae cells were probed for entry channels. Regulation transient receptor...

10.1164/rccm.201104-0717oc article EN American Journal of Respiratory and Critical Care Medicine 2011-10-28

Store-operated calcium (SOC) entry represents the principal Ca 2+ pathway into nonexcitable cells. Despite intensive investigation, mechanisms underlying activation of SOC have remained elusive. The endothelial I channel is a -selective to which transient receptor potential (TRP) proteins TRPC1 and TRPC4 contribute subunits. Activation specifically regulated by spectrin–actin membrane skeleton; however, nature coupling between skeleton unknown. Here we demonstrate that protein 4.1 an...

10.1161/01.res.0000193597.65217.00 article EN Circulation Research 2005-10-28

Pulmonary vascular endothelial cells express a variety of ion channels that mediate Ca(2+) influx in response to diverse environmental stimuli. However, it is not clear whether from discrete functionally coupled specific outcomes. Thus we conducted systematic study mouse lung address the alpha(1G) T-type channel and transient receptor potential TRPV4 have functional roles pulmonary capillary endothelium. We used real-time fluorescence imaging for cytosolic Ca(2+), immunohistochemistry probe...

10.1152/ajplung.00015.2009 article EN AJP Lung Cellular and Molecular Physiology 2009-07-18

Canonical transient receptor potential 4 (TRPC4) contributes to the molecular composition of a channel encoding for calcium selective store-operated current, I(SOC), whereas Orai1 critically comprises highly release activated I(CRAC). However, may interact with TRPC proteins and influence their activation permeation characteristics. Endothelium expresses both TRPC4 Orai1, it remains unclear as whether interacts through TPRC4 channel.We tested hypothesis that channel's important endothelial...

10.1161/circresaha.112.269506 article EN Circulation Research 2012-04-26

In the present study, we demonstrate that lung microvascular endothelial cells express a Cav3.1 (alpha1G) T-type voltage-gated Ca2+ channel, whereas macrovascular do not channels. Voltage-dependent activation indicates current is shifted to positive potential, at which maximum -10 mV; voltage-dependent conductance and inactivation properties suggest "window current" in range of -60 -30 mV. Thrombin-induced transitions membrane potential activate resulting physiologically relevant rise...

10.1161/01.res.0000087148.75363.8f article EN Circulation Research 2003-07-22

Store-operated calcium (SOC) entry is sufficient to disrupt the extra-alveolar, but not alveolar, endothelial cell barrier. Mechanism(s) underlying such insensitivity transitions in cytosolic ([Ca 2+ ] i ) microvascular cells are unknown. Depletion of stored Ca activates a larger SOC response extra-alveolar (pulmonary artery; PAECs) than alveolar microvascular; PMVECs) cells. In vivo permeation studies revealed that store depletion similar nonselective cationic conductances PAECs and PMVECs,...

10.1161/01.res.0000163632.67282.1f article EN Circulation Research 2005-03-25

10.1016/j.bbamcr.2012.06.027 article EN Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 2012-07-02

Mechanism(s) underlying activation of store-operated Ca2+ entry currents, ISOC, remain incompletely understood. F-actin configuration is an important determinant channel function, although the nature interaction between cytoskeleton and ISOC channels unknown. We examined whether spectrin membrane skeleton couples store depletion to entry. Thapsigargin activated endothelial cell (-45 pA at -80 mV) that reversed +40 mV, was inwardly rectifying when charge carrier, inhibited by La3+ (50...

10.1083/jcb.200106156 article EN The Journal of Cell Biology 2001-09-17

Calcium agonists induce membrane depolarization in endothelial cells through an unknown mechanism. Present studies tested the hypothesis that pulmonary artery express a cyclic nucleotide-gated (CNG) cation channel activated by store-operated calcium entry to produce depolarization. In whole-cell configuration, voltage-clamped revealed large non-inactivating, outwardly rectifying cationic current absence of extra- or intracellular Ca2+ was reduced upon replenishment Ca2+. The inward...

10.1074/jbc.m002795200 article EN cc-by Journal of Biological Chemistry 2000-06-01

Several metabolic, cardiovascular and neurological disorders are characterized by mitochondrial dysfunction followed dysregulation of cellular energetics. Mitochondria play an important role in ATP production cell death regulation. NLRX1, a mitochondria-targeted protein, is known to negatively regulate innate immunity responses. However, the this protein homeostasis following injury not well understood. To understand mechanisms underlying effect acute regulating NLRX1 signaling pathways, we...

10.3389/fimmu.2019.02431 article EN cc-by Frontiers in Immunology 2019-10-24

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel that currently causing pandemic and has been termed disease (COVID-19). The elderly or those with preexisting conditions like diabetes, hypertension, coronary heart disease, chronic obstructive pulmonary cerebrovascular kidney dysfunction are more likely to develop severe cases when infected. Patients COVID-19 admitted the ICU have higher mortality than non-ICU patients. Critical illness consistently posed challenge not...

10.1165/rcmb.2021-0374ps article EN cc-by-nc-nd American Journal of Respiratory Cell and Molecular Biology 2022-03-29

Pulmonary endothelium displays considerable heterogeneity along the vascular axis, from arteries to capillaries veins. Griffonia simplicifolia is a lectin that recognizes pulmonary microvascular with preference over extra-alveolar in both and veins, yet precise location where this phenotypic shift occurs poorly resolved. We gelatin-filled circulation agarose-loaded airways then labeled lung enable visualization of endothelial transition zone. Endothelium vessels internal diameters less than...

10.1086/674879 article EN Pulmonary Circulation 2014-03-01

Regulated P-selectin surface expression provides a rapid measure for endothelial transition to proinflammatory phenotype. In general, results from Weibel-Palade body (WPb) exocytosis. Yet, it is unclear whether pulmonary capillary endothelium possesses WPbs or regulated and, if so, how inflammatory stimuli initiate We used immunohistochemistry, immunofluorescence labeling, ultrastructural assessment, and an isolated perfused lung model demonstrate that lacks but P-selectin. Thrombin...

10.1152/ajplung.00331.2009 article EN AJP Lung Cellular and Molecular Physiology 2010-05-01
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