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Quercetin, a flavonoid with multiple proven health benefits to both man and animals, displays a plethora of biological activities, collectively referred to as pleiotropic. The most studied of these are antioxidant and anti-inflammatory but modulation of signalling pathways is important as well. One of the lesser-known and recently discovered roles of quercetin, is modulation of microRNA (miRNA) expression. miRNAs are important posttranscriptional modulators that play a critical role in health and disease and many of these non-coding oligonucleotides are recognized as oncogenic or tumor suppressor miRNAs. This review is an evaluation of the recent relevant literature on the subject, with focus on the ability of quercetin to modulate miRNA expression. It includes a summary of recent knowledge on miRNAs deregulated by quercetin, an overview of quercetin pharmacokinetics and miRNA biogenesis, for the interested reader.

Aims: MicroRNAs of the miR-29 family members were one of the first microRNAs identified as possible therapeutic agents in malignant hematopoiesis. The aim of our review is to summarize the current state of knowledge on miR-29 family members., Methods: We performed literature searches involving miR-29 family members and their relationship to individual hematological malignancies, namely acute myeloid leukemia (AML), chronic lymphoblastic leukemia (CLL) and chronic myeloid leukemia (CML). We also searched for subgroups of hematological malignancies, e.g. multiple myeloma, that are regarded as members of the acute or chronic types of leukemias., Results: A number of genes appear to be regulated by miR-29 family members in various physiological and pathological situations. In our view regulation of Tcl-1, Mcl-1 and DNA methyltransferases is relevant in case of hematological malignancies, hence these are the focus of this review. miR-29 family members also function during normal T-cell and B-cell development., Conclusion: MiR-29 family members appear to govern some general features in commonly heterogenous hematological malignancies and therefore form a potential target for treatment.

Introduction: MicroRNAs (miRNAs) are small non-coding single-stranded RNA molecules that regulate gene expression at the post-transcriptional level. In the pathogenesis of chronic lymphocytic leukemia (CLL), miR-15a and miR-16-1 play an important role. These miRNAs are located on chromosome 13 in the 13q14.3 region, which is deleted in more than 55% of CLL patients. This aberration affects expression of miRNAs., Objectives: The study aimed at performing a molecular genetic analysis of miR-15a and miR-16-1 expression in a group of 39 patients diagnosed with CLL and determining the association between the expression of the two miRNAs and types of deletions in the 13q14 region., Methods: We used fluorescence in situ hybridiziation (FISH) for determination of mono- or biallelic deletion 13q and quantitative polymerase chain reaction (Q-RT-PCR) to revealed expression miR-15a and miR-16-1 in 39 patients suffering from CLL., Results: The analysis comprised 19 patients with monoallelic 13q14 deletion, 3 patients with biallelic deletion, 9 patients with both monoallelic and biallelic deletions, and 8 patients without 13q14 deletion serving as controls. The results showed different levels of miRNA expression in individual patients. Significantly higher normalized levels of miR-15a expression were found in the control group and patients with monoallelic 13q14 expression compared with patients with biallelic deletion. There was a significantly decreased expression of both miRNAs in patients with biallelic deletion of the 13q14 region but only when deletions were present in 77% or more of cells, as detected by fluorescent in situ hybridization (FISH).

Background: Discovery of uncoupling protein 2 (UCP2) in 1997 and demonstration of its wide tissue expression has triggered an important question about controlled oxidative phosphorylation uncoupling and the physiological function of this process. Uncoupling protein 2 (UcP2) is a mitochondrial protein that can influence the mitochondrial membrane potential and hence the production of reactive oxygen species by mitochondria. It is also thought to be involved in apoptotic signaling pathways and it has been suggested to be important in cardio- and neuroprotection., Methods and Results: We examined the recent literature (2003-2007) in the MedLine database for evidence linking p38, one of the stress-related protein kinases, with modulation of UCP2 expression in the heart. While two reports clearly demonstrate p38 as down-regulating UcP2 expression, only circumstantial evidence exists for cardiomyocytes. Conflicting results on p38-regulated cardiomyocyte survival after ischemia leave an open venue for hypotheses on the differential regulation of protein expression, including UCP2., Conclusions: Reviewing the evidence connecting UCP2 and its cytoprotective activities, we propose a tissue specific link that may explain the variable influence of p38 via modulation of UCP2 expression.