scholarly journals Halofuginone inhibition ofCOL1A2 promoter activity via a c-Jun-dependent mechanism

2002 ◽  
Vol 46 (10) ◽  
pp. 2748-2761 ◽  
Author(s):  
Tracy L. McGaha ◽  
Takao Kodera ◽  
Harry Spiera ◽  
Alexandru C. Stan ◽  
Mark Pines ◽  
...  
Keyword(s):  
Promoter Activity ◽  
Dependent Mechanism

scholarly journals Toxoplasma gondii excreted‐secreted antigens suppress Foxp3 promoter activity via a SP1‐dependent mechanism

2020 ◽  
Vol 24 (18) ◽  
pp. 10785-10791
Author(s):  
Jinling Chen ◽  
Jingjing Wang ◽  
Xuyang Gao ◽  
Dandan Zhu ◽  
Liuting Chen ◽  
...  
Keyword(s):  
Toxoplasma Gondii ◽  
Promoter Activity ◽  
Secreted Antigens ◽  
Dependent Mechanism

scholarly journals A novel U-STAT3-dependent mechanism mediates the deleterious effects of chronic nicotine exposure on renal injury

2012 ◽  
Vol 302 (6) ◽  
pp. F722-F729 ◽  
Author(s):  
Istvan Arany ◽  
Dustin K. Reed ◽  
Samira C. Grifoni ◽  
Kiran Chandrashekar ◽  
George W. Booz ◽  
...  
Keyword(s):  
Promoter Activity ◽  
Transforming Growth Factor ◽  
Smooth Muscle Actin ◽  
Transforming Growth Factor Β ◽  
Significant Loss ◽  
Fiber Formation ◽  
Chronic Nicotine ◽  
Structural Recovery ◽  
Tgf Β1 ◽  
Dependent Mechanism

Previous data from our group have demonstrated (Arany I, Grifoni S, Clark JS, Csongradi, Maric C, Juncos LA. Am J Physiol Renal Physiol 301: F125–F133, 2011) that chronic nicotine (NIC) exposure exacerbates acute renal ischemic injury (AKI) in mice that could increase the risk for development and progression of chronic kidney disease (CKD). It has been shown that proximal tubules of the kidney can acquire characteristics that may compromise structural recovery and favor development of inflammation and fibrosis following injury. Chronic NIC exposure can amplify this epithelial process although the mechanism is not identified. Recently, the unphosphorylated form of signal transducer and activator of transcription-3 (U-STAT3) has emerged as a noncanonical mediator of inflammation and fibrosis that may be responsible for the effects of chronic NIC. We found that levels of transforming growth factor β-1 (TGF-β1), α-smooth muscle actin (α-SMA), fibronectin, monocyte chemotactic protein-1 (MCP-1), and expression of U-STAT3 were increased in the ischemic kidneys of NIC-exposed mice. Chronic NIC exposure also increased TGF-β1-dependent F-actin reorganization, vimentin, fibronectin, and α-SMA expression as well as promoter activity of α-SMA and MCP-1 without significant loss of epithelial characteristics (E-cadherin) in cultured renal proximal tubule cells. Importantly, transduction of cells with a U-STAT3 mimetic (Y705F-STAT3) augmented stress fiber formation and also amplified NIC+TGF-β1-induced expression of α-SMA, vimentin, fibronectin, as well as promoter activity of α-SMA and MCP-1. Our results reveal a novel, chronic NIC-exposure-related and U-STAT3-dependent mechanism as mediator of a sustained transcription of genes that are linked to remodeling and inflammation in the kidney during injury. This process may facilitate progression of AKI to CKD. The obtained data may lead to devising therapeutic methods to specifically enhance the protective and/or inhibit adverse effects of STAT3 in the kidney.

Platelet Mobilization Induced by PAF and Its Role in the Thrombocytosis Triggered by Adrenaline in Rats

1989 ◽  
Vol 62 (04) ◽  
pp. 1107-1111 ◽  
Author(s):  
Hugo C Castro-Faria-Neto ◽  
Patricia T Bozza ◽  
Marco A Martins ◽  
Paulo M F L Dias ◽  
Patricia M R Silva ◽  
...  
Keyword(s):  
Receptor Antagonists ◽  
Blood Samples ◽  
Platelet Counts ◽  
Platelet Number ◽  
Edta Solution ◽  
Web 2086 ◽  
Dependent Mechanism

SummaryThe injection of PAP (6 μg/kg, i. v.) induced, in rats, haemoconcentration accompanied by an increase in the platelet number, as attested by the counts of platelets in blood samples diluted in formalin-free EDTA solution. This increase was significant at 15 min, peaked from 1 to 4 h and returned to basal levels 24 h after the lipid administration. The release of platelets induced by PAP was inhibited dose-dependently by specific PAP receptor antagonists such as WEB 2086 (0.5-2 mg/kg), BN 52021 and 48740 RP (5-25 mg/kg). Furthermore, platelet mobilization was clearly impaired in splenectomized animals stimulated by PAP, whereas thrombocytopenia and haemoconcentration by the same stimulus were intact. It was also noted that a second injection of PAP, 24 h after the initial stimulation with the lipid, failed to induce an increase in platelet counts, indicating autodesensitization. Desensitization to PAP or pretreatment with PAP antagonists clearly prevented the increase in the platelet counts after stimulation by adrenaline (15 μg/kg). These findings suggest that, in rats, PAP can induce release of platelets by a spleen-dependent mechanism and that this lipid may be relevant to the thrombocytosis triggered by adrenaline.

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