Browsing by Subject "COX2"

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    Circ_DLEU2 knockdown represses cell proliferation, migration and invasion, and induces cell apoptosis through the miR-582-5p/COX2 pathway in acute myeloid leukemia
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2023) Dong, Shifang; Zhong, Haiying; Li, Lin
    Background. Acute myeloid leukemia (AML) is a malignant hematological neoplasm in adults. Researche indicates that circular RNAs (circRNAs) play paramount roles in the pathological process of AML. In this study, the role of circ_DLEU2 (circ_0000488) in AML is revealed. Methods. The expression of circ_DLEU2, microRNA-582-5p (miR-582-5p) and cyclooxygenase 2 (COX2) was determined by quantitative real-time PCR. Protein expression was detected by western blot. Cell proliferation was investigated by cell cycle, 5-Ethynyl29-deoxyuridine and 3-(4,5)-dimethylthiahiazo (-z-y1)- 3,5-di-phenytetrazoliumromide (MTT) assays. Cell apoptosis was elucidated by apoptosis analysis assay. The targeting relationship between miR-582-5p and circ_DLEU2 or COX2 was predicted by the starbase online database, and identified by a dual-luciferase reporter assay. Results. Circ_DLEU2 and COX2 expression were substantially up-regulated, while miR-582-5p was downregulated in AML marrow samples and cells compared with control groups. Circ_DLEU2 knockdown suppressed cell proliferation, whereas it induced cell arrest at G0/G1 phase and cell apoptosis in AML; however, these effects were attenuated by miR-582-5p inhibitor. Additionally, circ_DLEU2 was associated with miR-582-5p, and miR-582-5p bound to COX2 in AML cells. Also, we found that circ_DLEU2 regulated COX2 expression by interacting with miR-582-5p. Conclusion. Circ_DLEU2 silencing hindered AML malignant progression via downregulating COX2 through sponging miR-582-5p. Our finding provides a theoretical basis for studying circRNA-directed therapy of AML
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    COX2 inhibition during nephrogenic period induces ANG II hypertension and sex-dependent changes in renal function during aging
    (American Physiological Society, 2014-03-01) Reverte, Virginia; Tapia, Antonio; Loria, Analia; Salazar, Francisco; Llinas Más, María Teresa; Salazar, Francisco Javier; Fisiología
    This study was performed to test the hypothesis that ANG II contributes to the hypertension and renal functional alterations induced by a decrease of COX2 activity during the nephrogenic period. It was also examined whether renal functional reserve and renal response to volume overload and high sodium intake are reduced in 3–4- and 9–11-mo-old male and female rats treated with vehicle or a COX2 inhibitor during nephrogenic period (COX2np). Our data show that this COX2 inhibition induces an ANG II-dependent hypertension that is similar in male and female rats. Renal functional reserve is reduced in COX2np-treated rats since their renal response to an increase in plasma amino acids levels is abolished, and their renal ability to eliminate a sodium load is impaired (P < 0.05). This reduction in renal excretory ability is similar in both sexes during aging but does not induce the development of a sodium-sensitive hypertension. However, the prolonged high-sodium intake at 9–11 mo of age leads to a greater proteinuria in male than in female (114 ± 12 μg/min vs. 72 ± 8 μg/min; P < 0.05) COX2np-treated rats. Renal hemodynamic sensitivity to acute increments in ANG II is unaltered in both sexes and at both ages in COX2np-treated rats. In summary, these results indicate that the reduction of COX2 activity during nephrogenic period programs for the development of an ANG II-dependent hypertension, reduces renal functional reserve to a similar extent in both sexes, and increases proteinuria in males but not in females when there is a prolonged increment in sodium intake.