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J A Rivero

Publications and source records attributed to J A Rivero.

6 recordsLinked to original sources
PubMed1998

Sodium butyrate stimulates PKC activation and induces differential expression of certain PKC isoforms during erythroid differentiation.

Sodium butyrate (NaB) is an differentiation inducer currently under clinical investigation as a potential therapy for the treatment of sickle cell disease and prostate cancer. Though the biologic effects of this agent is well documented, its mechanism of action remains largely known. The mechanisms by which it transduces its signal to the nucleus is the subject of intense investigation in our laboratory. In this report, we demonstrate that NaB stimulates PKC activation by 3-fold and induces differential expression of several PKC isoforms. Notably, it upregulates PKC epsilon and downregulates PKC beta during erythroid differentiation. These findings suggest that certain PKC isoforms may play important roles in the signal transduction mechanisms of this agent leading to regulation of erythroid proliferation and differentiation.

Butyrates↗
PubMed1996

Sodium butyrate induces tyrosine phosphorylation and activation of MAP kinase (ERK-1) in human K562 cells.

Butyrate is a naturally occurring 4-carbon fatty acid. Biologically, butyrate has been shown to affect the morphology and growth rate of mammalian cells, as well as induce gene expression. Moreover, butyrate has been proven to serve as an anticancer agent, which unlike others (methotrexate and hydroxyurea), is a nontoxic, safe alternative to cancer treatment. It also induces erythroid differentiation in K562 cells. However, its mechanism of action has yet to be determined. In this study we investigated the effects of sodium butyrate (NaB) on tyrosine phosphorylation in K562 erythroleukemic cells. We demonstrate that NaB induces both dose and time-dependent tyrosine phosphorylation of several proteins, the effects of which were blocked by the tyrosine kinase inhibitor genistein. Furthermore, NaB induces tyrosine phosphorylation and rapid activation of MAP kinase (ERK-1). These findings provide the first evidence that the signal transduction mechanism of NaB involves rapid tyrosine phosphorylation and activation of MAP kinase.

Butyrates↗
PubMed1996

Regulation of jun expression and activation of AP-1 activity by erythropoietin.

Erythropoietin (EPO) is a molecule which regulates hemoglobin gene expression during erythroid proliferation and differentiation. However, the mechanism by which it regulates gene expression is poorly understood. Secondly, unlike other hematopoietic factors which induce expression of early response genes, it is unknown whether EPO is capable of inducing the expression and activation of early response genes. In this study, evidence is presented that EPO induces the expression of early response genes c-jun, junD and c-fos mRNA, stimulates jun protein synthesis and induces activation of 5 x AP-1/CAT activity in hyman erythroleukemia K562 cells. Also, EPO appears to regulate jun expression at transcriptional, post transcriptional and translational levels. These observations suggest that jun and fos expression may be relevant in the mechanism of growth control by EPO.

Erythropoietin↗
PubMed1989

Different mechanisms contribute to simultaneous inhibition of urokinase and tissue-type plasminogen activators by glucocorticoids in human ovarian carcinoma cells.

Previous studies from our laboratory have demonstrated that OVCA 433 human ovarian carcinoma cells are glucocorticoid responsive by several criteria and contain high affinity, saturable, steroid-specific glucocorticoid receptors. These cells secrete both mammalian plasminogen activators (PAs), urokinase (uPA) and tissue-type PA (tPA). Treatment of OVCA 433 cells with 1 x 10(-7) M dexamethasone (Dex) for 4 days led to 77% and 83% reductions in the extracellular activities of uPA and tPA, respectively, released into serum-free conditioned medium during a 1-h period. Dex treatment led to a 71% decrease in the rate of extracellular uPA antigen accumulation, as determined by enzyme-linked immunosorbent assay, as well as a 73% reduction in steady state uPA mRNA levels. In contrast, Dex treatment led to only a 42% decrease in the rate of extracellular tPA antigen accumulation and a 48% decrease in tPA mRNA levels; such decreases were insufficient to account for the 83% reduction in tPA activity. Thus, while Dex-induced decreases in uPA antigen and mRNA levels accounted for all but 6% of the decrease in uPA activity, a large discrepancy existed between the magnitudes of decreased tPA activity and decreased tPA antigen and mRNA levels. OVCA 433 cells produce both PAI-1 and PAI-2, two specific PA inhibitors. Treatment of cells with 1 x 10(-7) M Dex for 4 days led to a 3.3-fold increase in the rate of extracellular PAI-1 accumulation, with little or no effect on PAI-2 accumulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Carcinoma↗
PubMed1969

[Not Available].

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Argentina↗