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Low Anticoagulant Heparin Blocks Thrombin-Induced Endothelial Permeability in a PAR-Dependent Manner.
Abstract Acute lung injury and acute respiratory distress syndrome are accompanied by thrombin activation and fibrin deposition that enhances lung inflammation, activates endothelial cells and disrupts lung paracellular permeability. Heparin possesses anti-inflammatory properties but its clinical use is limited by hemorrhage and heparin induced thrombocytopenia. We studied the effects of heparin and low anticoagulant 2-O, 3-O desulfated heparin (ODSH) on thrombin-induced increases in paracellular permeability of cultured human pulmonary endothelial cells (EC). Pretreatment with heparin or ODSH blocked thrombin-ind...
Source: Vascular Pharmacology - January 24, 2014 Category: Drugs & Pharmacology Authors: Gonzales JN, Kim KM, Zemskova MA, Rafikov R, Heeke B, Varn MN, Black S, Kennedy TP, Verin AD, Zemskov EA Tags: Vascul Pharmacol Source Type: research

Angiotensin II upregulates KCa3.1 channels and stimulates cell proliferation in rat cardiac fibroblasts.
Abstract The proliferation of cardiac fibroblasts is implicated in the pathogenesis of myocardial remodeling and fibrosis. Intermediate-conductance calcium-activated K(+) channels (KCa3.1 channels) have important roles in cell proliferation. However, it is unknown whether angiotensin II (Ang II), a potent profibrotic molecule, would regulate KCa3.1 channels in cardiac fibroblasts and participate in cell proliferation. In the present study, we investigated whether KCa3.1 channels were regulated by Ang II, and how the channel activity mediated cell proliferation in cultured adult rat cardiac fibroblasts using electr...
Source: Biochemical Pharmacology - May 15, 2013 Category: Drugs & Pharmacology Authors: Wang LP, Wang Y, Zhao LM, Li GR, Deng XL Tags: Biochem Pharmacol Source Type: research

IL‐4 and IL‐13 inhibit IL‐1β and TNF‐α induced kinin B1 and B2 receptors through a STAT6‐dependent mechanism
Conclusions and ImplicationsThese data show, for the first time, that IL‐4 and IL‐13 decrease kinin receptors in a STAT6‐dependent mechanism, which can be one important mechanism by which these cytokines exert their anti‐inflammatory effects and impair bone resorption.
Source: British Journal of Pharmacology - April 25, 2013 Category: Drugs & Pharmacology Authors: PPC Souza, AB Brechter, RI Reis, CAS Costa, P Lundberg, UH Lerner Tags: Research Paper Source Type: research

Il‐4 and Il‐13 Inhibit Il‐1β and Tnf‐α Induced Kinin B1 and B2 Receptors Through a Stat6 Dependent Mechanism
Conclusions And ImplicationsThese data show, for the first time, that IL‐4 and IL‐13 decrease kinin receptors in a STAT6‐dependent mechanism, which can be one important mechanism by which these cytokines exert their anti‐inflammatory effects and impair bone resorption.
Source: British Journal of Pharmacology - January 28, 2013 Category: Drugs & Pharmacology Authors: P P C Souza, A B Brechter, R I Reis, C A S Costa, P Lundberg, U H Lerner Tags: Research Paper Source Type: research

Saxifragifolin D induces the interplay between apoptosis and autophagy in breast cancer cells through ROS-dependent endoplasmic reticulum stress.
In conclusion, SD inhibits breast cancer cell growth and induces interplay between apoptosis and autophagy through ROS-mediated endoplasmic reticulum stress. It will provide molecular bases for developing SD into a drug candidate for the treatment of breast cancer. PMID: 23348250 [PubMed - as supplied by publisher]
Source: Biochemical Pharmacology - January 21, 2013 Category: Drugs & Pharmacology Authors: Shi JM, Bai LL, Zhang DM, Yiu A, Yin ZQ, Han WL, Liu JS, Li Y, Fu DY, Ye WC Tags: Biochem Pharmacol Source Type: research

AMP-Activated Protein Kinase as Regulator of P2Y6 Receptor-Induced Insulin Secretion in Mouse Pancreatic β-Cells.
Abstract 5'-AMP-activated protein kinase (AMPK) and its pharmacological modulators have been targeted for treating type 2 diabetes. Extracellular uridine 5'-diphosphate (UDP) activates P2Y(6) receptors (P2Y(6)Rs) in pancreatic β-cells to release insulin and reduce apoptosis, which would benefit diabetes. Here, we studied the role of P2Y(6)R in activation of AMPK in MIN6 mouse pancreatic β-cells and insulin secretion. Treatment with a potent P2Y(6)R dinucleotide agonist MRS2957 (500nM) activated AMPK, which was blocked by P2Y(6)R-selective antagonist MRS2578. Also, MRS2957 induced phosphorylation of acetyl-coenzy...
Source: Biochemical Pharmacology - January 17, 2013 Category: Drugs & Pharmacology Authors: Balasubramanian R, Maruoka H, Jayasekara MP, Gao ZG, Jacobson KA Tags: Biochem Pharmacol Source Type: research

Inhibition of T-type calcium channels disrupts Akt signaling and promotes apoptosis in glioblastoma cells.
In this study, we found that inhibition of T-type Ca(2+) channels in GBM cells significantly reduced their survival and resistance to therapy. Moreover, either T-type selective antagonists, such as mibefradil, or siRNA-mediated knockdown of the T-type channel alpha subunits not only reduced cell viability and clonogenic potential, but also induced apoptosis. In response to channel blockade or ablation, we observed reduced phosphorylation of Akt and Rictor, suggesting inhibition of the mTORC2/Akt pathway. This was followed by reduction in phosphorylation of anti-apoptotic Bad and caspases activation. The apoptotic response ...
Source: Biochemical Pharmacology - December 31, 2012 Category: Drugs & Pharmacology Authors: Valerie NC, Dziegielewska B, Hosing AS, Augustin E, Gray LS, Brautigan DL, Larner JM, Dziegielewski J Tags: Biochem Pharmacol Source Type: research

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