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Systemic capillary leak syndrome secondary to decompression sickness.
BMJ Case Rep
July 2023
Division of Pulmonary, Critical Care and Sleep Medicine, University of Florida, Gainesville, Florida, USA.
Systemic capillary leak syndrome is a rare derangement of endothelial function characterised by extravasation of plasma and proteins into the interstitial space. Primary capillary leak syndrome is a rare, episodic medical illness of unknown molecular pathology while secondary capillary leak syndrome may be precipitated by any number of inflammatory and infectious syndromes. Decompression sickness, a disorder of depressurisation, has been identified as a very rare trigger.
View Article and Find Full Text PDFThe novel exchange protein activated by cyclic AMP 1 (EPAC1) agonist, I942, regulates inflammatory gene expression in human umbilical vascular endothelial cells (HUVECs).
Biochim Biophys Acta Mol Cell Res
February 2019
Institute of Biological Chemistry, Biophysics and Bioengineering, School of Engineering and Physical Sciences, Heriot-Watt University, Edinburgh Campus, Edinburgh EH14 4AS, UK. Electronic address:
Exchange protein activated by cyclic AMP (EPAC1) suppresses multiple inflammatory actions in vascular endothelial cells (VECs), partly due to its ability to induce expression of the suppressor of cytokine signalling 3 (SOCS3) gene, the protein product of which inhibits interleukin 6 (IL6) signalling through the JAK/STAT3 pathway. Here, for the first time, we use the non-cyclic nucleotide EPAC1 agonist, I942, to determine its actions on cellular EPAC1 activity and cyclic AMP-regulated gene expression in VECs. We demonstrate that I942 promotes EPAC1 and Rap1 activation in HEK293T cells and induces SOCS3 expression and suppresses IL6-stimulated JAK/STAT3 signalling in HUVECs.
View Article and Find Full Text PDFCyclic AMP-Elevating Capacity of Adenylate Cyclase Toxin-Hemolysin Is Sufficient for Lung Infection but Not for Full Virulence of Bordetella pertussis.
Infect Immun
June 2017
Institute of Microbiology of the CAS, v.v.i., Prague, Czech Republic
The adenylate cyclase toxin-hemolysin (CyaA, ACT, or AC-Hly) of targets phagocytic cells expressing the complement receptor 3 (CR3, Mac-1, αβ integrin, or CD11b/CD18). CyaA delivers into cells an N-terminal adenylyl cyclase (AC) enzyme domain that is activated by cytosolic calmodulin and catalyzes unregulated conversion of cellular ATP into cyclic AMP (cAMP), a key second messenger subverting bactericidal activities of phagocytes. In parallel, the hemolysin (Hly) moiety of CyaA forms cation-selective hemolytic pores that permeabilize target cell membranes.
View Article and Find Full Text PDFThe cyclic AMP phosphodiesterase 4D5 (PDE4D5)/receptor for activated C-kinase 1 (RACK1) signalling complex as a sensor of the extracellular nano-environment.
Cell Signal
July 2017
Department of Anatomy, Otago Medical School, University of Otago, Dunedin 9054, New Zealand.
The cyclic AMP and protein kinase C (PKC) signalling pathways regulate a wide range of cellular processes that require tight control, including cell proliferation and differentiation, metabolism and inflammation. The identification of a protein complex formed by receptor for activated C kinase 1 (RACK1), a scaffold protein for protein kinase C (PKC), and the cyclic AMP-specific phosphodiesterase, PDE4D5, demonstrates a potential mechanism for crosstalk between these two signalling routes. Indeed, RACK1-bound PDE4D5 is activated by PKCα, providing a route through which the PKC pathway can control cellular cyclic AMP levels.
View Article and Find Full Text PDFCyclic AMP-elevating Agents Promote Cumulus Cell Survival and Hyaluronan Matrix Stability, Thereby Prolonging the Time of Mouse Oocyte Fertilizability.
J Biol Chem
February 2016
From the Department of Biomedicine and Prevention, Section of Histology and Embryology, University of Rome Tor Vergata, Via Montpellier 1, 00133 Rome, Italy
Cumulus cells sustain the development and fertilization of the mammalian oocyte. These cells are retained around the oocyte by a hyaluronan-rich extracellular matrix synthesized before ovulation, a process called cumulus cell-oocyte complex (COC) expansion. Hyaluronan release and dispersion of the cumulus cells progressively occur after ovulation, paralleling the decline of oocyte fertilization.
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