%0 Journal Article %J Int J Mol Sci %D 2018 %T Neuronal Dysfunction Associated with Cholesterol Deregulation. %A Marcuzzi, Annalisa %A Loganes, Claudia %A Valencic, Erica %A Piscianz, Elisa %A Monasta, Lorenzo %A Bilel, Sabrine %A Bortul, Roberta %A Celeghini, Claudio %A Zweyer, Marina %A Tommasini, Alberto %K Anticholesteremic Agents %K Cell Line, Tumor %K Cholesterol %K Electron Transport %K Humans %K Lovastatin %K Mitochondria %K Neurons %K Neuroprotective Agents %K Organophosphorus Compounds %K Ubiquinone %X

Cholesterol metabolism is crucial for cells and, in particular, its biosynthesis in the central nervous system occurs in situ, and its deregulation involves morphological changes that cause functional variations and trigger programmed cell death. The pathogenesis of rare diseases, such as Mevalonate Kinase Deficiency or Smith⁻Lemli⁻Opitz Syndrome, arises due to enzymatic defects in the cholesterol metabolic pathways, resulting in a shortage of downstream products. The most severe clinical manifestations of these diseases appear as neurological defects. Expanding the knowledge of this biological mechanism will be useful for identifying potential targets and preventing neuronal damage. Several studies have demonstrated that deregulation of the cholesterol pathway induces mitochondrial dysfunction as the result of respiratory chain damage. We set out to determine whether mitochondrial damage may be prevented by using protective mitochondria-targeted compounds, such as MitoQ, in a neuronal cell line treated with a statin to induce a biochemical block of the cholesterol pathway. Evidence from the literature suggests that mitochondria play a crucial role in the apoptotic mechanism secondary to blocking the cholesterol pathway. Our study shows that MitoQ, administered as a preventive agent, could counteract the cell damage induced by statins in the early stages, but its protective role fades over time.

%B Int J Mol Sci %V 19 %8 2018 May 19 %G eng %N 5 %1 http://www.ncbi.nlm.nih.gov/pubmed/29783748?dopt=Abstract %R 10.3390/ijms19051523 %0 Journal Article %J Taiwan J Obstet Gynecol %D 2014 %T Potential role of circulating microRNAs as early markers of preeclampsia. %A Ura, Blendi %A Feriotto, Giordana %A Monasta, Lorenzo %A Bilel, Sabrine %A Zweyer, Marina %A Celeghini, Claudio %K Adult %K Biomarkers %K Female %K Gestational Age %K Humans %K MicroRNAs %K Oligonucleotide Array Sequence Analysis %K Pilot Projects %K Pre-Eclampsia %K Pregnancy %K Retrospective Studies %X

OBJECTIVE: To identify microRNAs (miRNAs) differentially expressed at early stages of gestation (12-14 weeks) in the serum of pregnant women, who later developed severe preeclampsia (sPE) in the third trimester of pregnancy (n = 24) compared to women with normal pregnancy (n = 24).

MATERIALS AND METHODS: Sera from 12-14-week-gestation whole blood were subjected to microarray analysis with TaqMan Low Density Array chips (human microRNA panel V3.0), and to quantitative real-time polymerase chain reaction.

RESULTS: By using the TaqMan Low Density Array chip technology, 19 mature miRNAs appeared differentially expressed in the group of women who later developed sPE as compared to normal women. The expression of four miRNAs (miR-1233, miR-520, miR-210, miR-144) was validated by quantitative real-time polymerase chain reaction analysis. MiR-1233 was the most overexpressed in the serum of women who later developed sPE.

CONCLUSION: Circulating miRNAs deserve further investigation in order to explore their potential role in the pathogenesis of preeclampsia. In particular, miR-1233 might represent a potential marker of early sPE.

%B Taiwan J Obstet Gynecol %V 53 %P 232-4 %8 2014 Jun %G eng %N 2 %1 http://www.ncbi.nlm.nih.gov/pubmed/25017274?dopt=Abstract %R 10.1016/j.tjog.2014.03.001