Society od University SurgeonsHypertonic saline solution induces prostacyclin production by increasing cyclooxygenase-2 expression*,**
Section snippets
Reagents
Escherichia coli 0111:B4 LPS (Sigma, St Louis, Mo) was dissolved in phosphate-buffered saline solution with 0.1% triethylamine at 1 mg/mL. PD 98059 (Calbiochem-Novabiochem, La Jolla, Calif) was dissolved in dimethyl sulfoxide to give a concentration of 50 mmol/L. SB202190 (Calbiochem) was dissolved in dimethyl sulfoxide to give a concentration of 10 mmol/L. Crystalline NaCl (J.T. Baker, Phillipsburg, NJ) was dissolved in sterile pyrogen-free water at a concentration of 2 mol. For HTS
Osmotic stress–activated p38 and ERK MAPK in HUVECs
We studied the osmotic stress activation of p38 and ERK by increasing the NaCl concentration in the culture media. The activation status of p38 and ERK was assessed by Western blot analyses, with their respective dual phospho-specific antibodies that recognize only the activated species of p38 or ERK. Equal protein loading was confirmed by Western blot analyses with an antibody to the total ERK MAPK. Osmotic stress activated both p38 and ERK with a similar pattern of activation (Fig 1). p38 and
Discussion
There is increasing evidence that some of the beneficial effects observed with hypertonic saline solution resuscitation may be due to a direct effect of increasing osmolarity on cell function, such as altering monocyte cytokine production and T-cell proliferation.14, 15 Previous and current observations from our laboratory support such a role; hypertonicity (specifically, an increase in NaCl concentration above 40 mmol/L) induced pronounced PGI2 production. Although the absolute fold increase
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ApoA-I mimetics favorably impact cyclooxygenase 2 and bioactive lipids that may contribute to cardiometabolic syndrome in chronic treated HIV
2021, Metabolism: Clinical and ExperimentalCitation Excerpt :We previously demonstrated that Tg6F reduced plasma LPS in BLT mouse models of chronic treated HIV [15]. ApoA-I mimetics reduce proinflammatory activity of LPS in vivo [11], an instigator of COX-2 and prostacyclin [20–22]. We also showed that HIV+/ART+ BLT mice had increased intestinal levels of COX-2 and 6kPGF1α in vivo.
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2017, Vascular PharmacologyCitation Excerpt :In renal medullary epithelial cells, hyperosmolar stress increases COX-2 promoter activity in a luciferase reporter assay [85,86]. In addition, hypertonic saline has been reported to induce COX-2 in rat macrophages [87] and human ECs [88]. The participation of NFAT transcription factors in COX-2 activation was also already shown in several additional cell types [89–94].
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2011, Bioorganic and Medicinal ChemistryCitation Excerpt :These results indicate that the protective effects of 1 might be due in part to inhibition of Cox-2 expression. It is known that members of the MAPK family play roles in chemical carcinogenesis by inducing Cox-2 gene expression,22,23 and that UVB irradiation significantly increases p38 and ERK activities in cultured human keratinocytes.24,25 An important role is played by p38 in signaling pathways associated with UVB-induced Cox-2 gene expression in human keratinocytes, whereas ERK may not be crucial in this process.19
Changes in estimating echocardiography pulmonary capillary wedge pressure after hypersaline plus furosemide versus furosemide alone in decompensated heart failure
2011, Journal of Cardiac FailureCitation Excerpt :The intact baroreflex-mediated response to the increase of cardiac and arterial filling leads to a reduction of systemic vascular resistance and suppressed neuroendocrine mediators, thereby promoting renal Na excretion. Moreover, HSS induces prostacyclin production and nitric oxide (NO)–dependent vasodilatation.45,46 These combined effects could explain the difference in echo-PCWP between the groups.
The role of p38 mitogen-activated kinase (MAPK) in the mechanism regulating cyclooxygenase gene expression in equine leukocytes
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Supported by National Institutes of Health Grants GM45873 and GM07037.
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Reprint requests: Saman Arbabi, MD, Harborview Medical Center, Department of Surgery, University of Washington, Box 359796, 325 Ninth Ave, Seattle, WA 98104.