Genomes and Genes
Affiliation: Ghent University
- Nitric oxide in shockA Cauwels
Department for Molecular Biomedical Research, VIB, Technologiepark 927, B 9052 Ghent, Belgium
Kidney Int 72:557-65. 2007..Amongst these, high hopes are set for selective iNOS inhibitors. But it might also be necessary to shift gears and focus on downstream cardiovascular targets of NO or on other vasodilating phenomena...
- Nitric oxide production by endotoxin preparations in TLR4-deficient miceAnje Cauwels
Department for Molecular Biomedical Research, VIB, B 9052 Ghent, Belgium Department of Biomedical Molecular Biology, Ghent University, B 9052 Ghent, Belgium Electronic address
Nitric Oxide 36:36-43. 2014..Surprisingly, the excessive iNOS-derived systemic NO production induced by impure LPS in TLR4⁻/⁻ is not accompanied by hypotension or morbidity...
- Nitrite protects against morbidity and mortality associated with TNF- or LPS-induced shock in a soluble guanylate cyclase-dependent mannerAnje Cauwels
Department for Molecular Biomedical Research, Flanders Institute for Biotechnology, 9052 Ghent, Belgium
J Exp Med 206:2915-24. 2009..In conclusion, we show that nitrite can protect against toxicity in shock via sGC-dependent signaling, which may include hypoxic vasodilation necessary to maintain microcirculation and organ function, and cardioprotection...
- Critical role for small and large conductance calcium-dependent potassium channels in endotoxemia and TNF toxicityAnje Cauwels
Department for Molecular Biomedical Research, Ghent University, Ghent, Belgium
Shock 29:577-82. 2008..Our results point to SK and BK channels as potential targets in septic shock treatment to be modulated preferentially together with sGC...
- Survival of TNF toxicity: dependence on caspases and NOAnje Cauwels
Department for Molecular Biomedical Research, VIB, B 9052 Ghent, Belgium
Arch Biochem Biophys 462:132-9. 2007..In addition, our results also indicate that caspases may exert an important endogenous negative feedback on oxidative stress as well...
- Anaphylactic shock depends on PI3K and eNOS-derived NOAnje Cauwels
Molecular Pathophysiology and Experimental Therapy Unit, Department for Molecular Biomedical Research, Ghent University, Belgium, and Cardiovascular Research Center, Massachusetts General Hospital, Charlestown, USA
J Clin Invest 116:2244-51. 2006....
- Dual role of endogenous nitric oxide in tumor necrosis factor shock: induced NO tempers oxidative stressA Cauwels
Molecular Pathophysiology and Experimental Therapy Unit, Department for Molecular Biomedical Research, Ghent University and Flanders Interuniversity Institute for Biotechnology VIB, Ghent, Zwijnaarde, Belgium
Cell Mol Life Sci 62:1632-40. 2005..Together, these in vivo results indicate that induced NO not only causes hemodynamic collapse, but is also essential for curbing TNF-induced oxidative stress, which appears to hinge on PLA2-dependent mechanisms...
- sGC(alpha)1(beta)1 attenuates cardiac dysfunction and mortality in murine inflammatory shock modelsEmmanuel S Buys
Department of Anesthesia and Critical Care, Cardiology Division, Anesthesia Center for Critical Care Research, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA
Am J Physiol Heart Circ Physiol 297:H654-63. 2009..Together, these findings suggest that cGMP generated by sGC(alpha)(1)beta(1) protects against cardiac dysfunction and mortality in murine inflammatory shock models...
- Caspase inhibition causes hyperacute tumor necrosis factor-induced shock via oxidative stress and phospholipase A2Anje Cauwels
Molecular Pathophysiology and Experimental Therapy Unit, Department for Molecular Biomedical Research, Ghent University and Flanders Interuniversity Institute for Biotechnology, Ghent, Belgium
Nat Immunol 4:387-93. 2003..In addition, survival of TNF toxicity seemed to require a caspase-dependent protective feedback on excessive reactive oxygen species (ROS) formation and phospholipase A2 activation...
- The soluble guanylate cyclase activator BAY 58-2667 protects against morbidity and mortality in endotoxic shock by recoupling organ systemsBenjamin Vandendriessche
Department for Molecular Biomedical Research, VIB, Ghent, Belgium Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium
PLoS ONE 8:e72155. 2013..We speculate that, considering the central role of sGC signaling in many pathways required for maintenance of (micro)circulatory homeostasis, BAY 58-2667 supports organ function by recoupling inter-organ communication pathways. ..
- TLR2 activation causes no morbidity or cardiovascular failure, despite excessive systemic nitric oxide productionAnje Cauwels
Department for Molecular Biomedical Research, VIB, Technologiepark 927, Ghent B 9052, Belgium
Cardiovasc Res 100:28-35. 2013..In addition, NOS produce superoxide in case of substrate or cofactor deficiency or oxidation. We hypothesized that excessive systemic iNOS-derived NO production is insufficient to trigger cardiovascular failure and shock...
- The in vivo contribution of hematopoietic cells to systemic TNF and IL-6 production during endotoxemiaJennyfer Bultinck
Molecular Pathophysiology and Experimental Therapy Unit, Department of Molecular Biomedical Research, Ghent University and Flanders Interuniversity Institute of Biotechnology VIB, Ghent Zwijnaarde, Belgium
Cytokine 36:160-6. 2006..Moreover, LPS-induced IL-6 production in parenchymal cells may be partially mediated by the TNF/TNF-R1 pathway as evidenced by the systemic IL-6 levels in LPS-treated wild type (WT), TNF-R1-deficient and chimeric mice...
- Systemic NO production during (septic) shock depends on parenchymal and not on hematopoietic cells: in vivo iNOS expression pattern in (septic) shockJennyfer Bultinck
Department for Molecular Biomedical Research, Ghent University VIB, Technologiepark 927, Ghent 9052, Belgium
FASEB J 20:2363-5. 2006....
- Reactive oxygen species and small-conductance calcium-dependent potassium channels are key mediators of inflammation-induced hypotension and shockAnje Cauwels
Department for Molecular Biomedical Research, VIB, Technologiepark 927, 9052 Ghent, Belgium
J Mol Med (Berl) 88:921-30. 2010..Moreover, they may also explain why antioxidants other than tempol fail to provide survival benefit during shock...
- Cardiovascular and pharmacological implications of haem-deficient NO-unresponsive soluble guanylate cyclase knock-in miceRobrecht Thoonen
Laboratory for Molecular Pathology and Experimental Therapy, Inflammation Research Center, VIB, B 9052 Ghent, Belgium
Nat Commun 6:8482. 2015..Apo-sGC mice represent a unique experimental platform to study the in vivo consequences of sGC oxidation and the therapeutic potential of sGC activators. ..
- Simultaneous targeting of IL-1 and IL-18 is required for protection against inflammatory and septic shockTom Vanden Berghe
1 Inflammation Research Center, VIB, Ghent, Belgium
Am J Respir Crit Care Med 189:282-91. 2014..Sepsis is one of the leading causes of death around the world. The failure of clinical trials to treat sepsis demonstrates that the molecular mechanisms are multiple and are still insufficiently understood...
- Nitrite regulation of shockAnje Cauwels
Department for Molecular Biomedical Research, VIB, Technologiepark 927, B 9052, Ghent, Belgium
Cardiovasc Res 89:553-9. 2011....
- A multiscale entropy-based tool for scoring severity of systemic inflammationBenjamin Vandendriessche
1Inflammation Research Center, VIB, Ghent, Belgium 2Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium 3Department of Intensive Care Medicine, Ghent University Hospital, Ghent, Belgium 4Department of Management, Technology and Economics, ETH Zurich, Zurich, Switzerland 5Center for Neurogenomics and Cognitive Research, VU University Amsterdam, Amsterdam, The Netherlands
Crit Care Med 42:e560-9. 2014..Early detection and start of appropriate treatment are highly correlated with survival of sepsis and septic shock, but the currently available predictive tools are not sensitive enough to identify patients at risk...
- Severity of sepsis-induced acute kidney injury in a novel mouse model is age dependentBert Maddens
Department of Pharmacology, Toxicology and Biochemistry, Ghent University, Ghent, Belgium
Crit Care Med 40:2638-46. 2012..In addition, the age dependency of the severity of sepsis and sepsis-induced AKI was studied by validating this model in three different age categories...
- Protection against TNF-induced lethal shock by soluble guanylate cyclase inhibition requires functional inducible nitric oxide synthaseA Cauwels
MPET, Department of Molecular Biology, Flanders Interuniversity Institute for Biotechnology, Ghent University, Belgium
Immunity 13:223-31. 2000..These data imply that iNOS- (and not eNOS-) derived NO is an endogenous protective molecule indispensable to survive a TNF challenge and exerting this beneficial effect via sGC-independent mechanisms...
- MAPK-activated protein kinase 2-deficiency causes hyperacute tumor necrosis factor-induced inflammatory shockBenjamin Vandendriessche
Inflammation Research Center, VIB, Ghent, 9052, Belgium
BMC Physiol 14:5. 2014..Additionally, research in various disease models has indicated the kinase as an interesting inhibitory drug target for various acute or chronic inflammatory diseases...
- RIP kinase-dependent necrosis drives lethal systemic inflammatory response syndromeLinde Duprez
Department for Molecular Biomedical Research, the Flanders Institute for Biotechnology VIB, 9052 Ghent, Belgium
Immunity 35:908-18. 2011....
- IL-17 produced by Paneth cells drives TNF-induced shockNozomi Takahashi
Rheumatology Research and Advanced Therapeutics, Radboud University Nijmegen Medical Centre, 6500 HB Nijmegen, Netherlands
J Exp Med 205:1755-61. 2008..These data indicate that innate immune cytokine responses in the local mucosa may participate in rapidly amplifying responses to systemic inflammatory challenges...