Myocardial infarction induces sympathetic hyperinnervation via a nuclear factor-κB-dependent pathway in rabbit hearts

2013 ◽  
Vol 535 ◽  
pp. 128-133 ◽  
Author(s):  
Ye Wang ◽  
Fei Suo ◽  
Ju Liu ◽  
Hesheng Hu ◽  
Mei Xue ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Dependent Pathway

scholarly journals Induction of cyclooxygenase-2 protein by lipoteichoic acid from Staphylococcus aureus in human pulmonary epithelial cells: involvement of a nuclear factor-κB-dependent pathway

2001 ◽  
Vol 134 (3) ◽  
pp. 543-552 ◽  
Author(s):  
Chien-Huang Lin ◽  
I-Hui Kuan ◽  
Horng-Mo Lee ◽  
Wen-Sen Lee ◽  
Joen-Rong Sheu ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Epithelial Cells ◽  
Lipoteichoic Acid ◽  
Nuclear Factor Κb ◽  
Cyclooxygenase 2 ◽  
Nuclear Factor ◽  
Pulmonary Epithelial Cells ◽  
Dependent Pathway

scholarly journals Integration of Rac-dependent Regulation of Cyclin D1 Transcription through a Nuclear Factor-κB-dependent Pathway

1999 ◽  
Vol 274 (36) ◽  
pp. 25245-25249 ◽  
Author(s):  
David Joyce ◽  
Boumediene Bouzahzah ◽  
Maofu Fu ◽  
Chris Albanese ◽  
Mark D’Amico ◽  
...  
Keyword(s):  
Cyclin D1 ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Dependent Pathway

scholarly journals Nuclear Factor-κB Protects the Adult Cardiac Myocyte Against Ischemia-Induced Apoptosis in a Murine Model of Acute Myocardial Infarction

Circulation ◽  
2003 ◽  
Vol 108 (25) ◽  
pp. 3075-3078 ◽  
Author(s):  
Arunima Misra ◽  
Sandra B. Haudek ◽  
Pascal Knuefermann ◽  
Jesus G. Vallejo ◽  
Zhijian J. Chen ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Murine Model ◽  
Cardiac Myocyte ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Induced Apoptosis

scholarly journals Targeted Deletion of Nuclear Factor κB p50 Enhances Cardiac Remodeling and Dysfunction Following Myocardial Infarction

2009 ◽  
Vol 104 (5) ◽  
pp. 699-706 ◽  
Author(s):  
Leo Timmers ◽  
J. Karlijn van Keulen ◽  
Imo E. Hoefer ◽  
Matthijs F.L. Meijs ◽  
Ben van Middelaar ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Remodeling ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Targeted Deletion

scholarly journals Gene Transfer of Inducible Nitric Oxide Synthase Affords Cardioprotection by Upregulating Heme Oxygenase-1 Via a Nuclear Factor-κB-Dependent Pathway

Circulation ◽  
2009 ◽  
Vol 120 (13) ◽  
pp. 1222-1230 ◽  
Author(s):  
Qianhong Li ◽  
Yiru Guo ◽  
Qinghui Ou ◽  
Chuanjue Cui ◽  
Wen-Jian Wu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Gene Transfer ◽  
Heme Oxygenase ◽  
Inducible Nitric Oxide Synthase ◽  
Nuclear Factor Κb ◽  
Heme Oxygenase 1 ◽  
Nuclear Factor ◽  
Oxide Synthase ◽  
Dependent Pathway ◽  
Inducible Nitric Oxide

scholarly journals Toll-Like Receptor 4 Activation Reduces Adrenal Chromaffin Cell Excitability Through a Nuclear Factor-κB-Dependent Pathway

Endocrinology ◽  
2013 ◽  
Vol 154 (1) ◽  
pp. 351-362 ◽  
Author(s):  
Mark K. Lukewich ◽  
Alan E. Lomax
Keyword(s):  
Neuropeptide Y ◽  
Adrenal Medulla ◽  
Action Potentials ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Neuropeptide Y Release ◽  
Adrenal Chromaffin ◽  
Dependent Pathway

The adrenal medulla contains fenestrated capillaries that allow catecholamines and neuropeptides secreted by adrenal chromaffin cells (ACCs) to readily access the circulation. These capillaries may also allow bacterial products to enter the adrenal medulla and interact with ACCs during infection. One potential mediator of this interaction is toll-like receptor 4 (TLR-4), a pattern-recognition receptor that detects lipopolysaccharide (LPS) from Gram-negative bacteria. Evidence suggests that excitable cells can express TLR-4 and that LPS can modulate important neuronal and endocrine functions. The present study was therefore performed to test the hypothesis that TLR-4 activation by LPS affects ACC excitability and secretory output. RT-PCR revealed that TLR-4, cluster of differentiation 14, myeloid differentiation protein-2, and myeloid-derived factor 88 are expressed within mouse adrenal medullae. TLR-4 immunoreactivity was observed within all tyrosine hydroxylase immunoreactive ACCs. Incubation of isolated ACCs in LPS dose dependently hyperpolarized the resting membrane potential and enhanced large conductance (BK) Ca2+-activated K+ currents. LPS (10 μg/ml) also increased rheobase, decreased the number of action potentials fired at rheobase, and reduced the percentage of ACCs exhibiting spontaneous and anodal break action potentials. Although catecholamine release was unaltered, LPS significantly reduced high-K+-stimulated neuropeptide Y release from isolated ACCs. LPS did not alter the excitability of ACCs from TLR-4−/− mice. Inhibition of nuclear factor-κB signaling with SC-514 (20 μm) abolished the effects of LPS on ACC excitability. Our findings suggest that LPS acts at TLR-4 to reduce ACC excitability and neuropeptide Y release through an nuclear factor-κB-dependent pathway.

scholarly journals Flavopiridol inhibits lipopolysaccharide-induced TNF-α production through inactivation of nuclear factor-κB and mitogen-activated protein kinases in the MyD88-dependent pathway

2011 ◽  
Vol 55 (3) ◽  
pp. 160-167 ◽  
Author(s):  
Abedul Haque ◽  
Naoki Koide ◽  
Imtiaz Iftakhar-E-Khuda ◽  
Abu Shadat Mohammod Noman ◽  
Erdenezaya Odkhuu ◽  
...  
Keyword(s):  
Protein Kinases ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Mitogen Activated Protein Kinases ◽  
Tnf Α ◽  
Mitogen Activated Protein ◽  
Dependent Pathway
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