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001-es BibID:BIBFORM076660
Első szerző:Biró Orsolya (molekuláris biológus)
Cím:Circulating exosomal and Argonaute-bound microRNAs in preeclampsia / Orsolya Biró, Ábel Fóthi, Bálint Alasztics, Bálint Nagy, Tamás I. Orbán, János Rigó
Dátum:2019
ISSN:0378-1119
Megjegyzések:Introduction: microRNAs (miRNAs) play important role in the regulation of placental development, and abnormal miRNA expression is associated with preeclampsia (PE). miRNAs are released from trophoblast cells to maternal blood flow, where they are highly stable, being encapsulated inside extracellular vesicles, like exosomes or bound to Argonaute proteins. In PE, placental dysfunction leads to aberrant extracellular miRNA secretion. hsamiR- 210 is a hypoxia-sensitive miRNA found to be upregulated in PE, however, it is unknown whether it is the cause or the consequence of the disease. Objective: Our aim was to analyze the expression of several miRNAs, including hsa-miR- 210 in placenta, exosome and Ago-bound fractions comparing normal (N) and PE pregnancies. We performed in vitro analyses of extracellular hsa-miR-210 secretion of trophoblast cell cultures (of villous and extravillous origin) under hypoxic condition. Methods: PE and N placenta samples were collected from C-sections, and blood samples were drawn from each pregnant woman in the third trimester. Htr-8 and Jar cell lines were cultured in exosome-free media and treated with hypoxia-mimetic agents. Exosome and Agobound fractions were isolated by membrane affinity spin column method from plasma and cell media. Short RNAs were extracted from exosomes and vesicle-free fractions, and total-RNA was isolated from the placenta samples. The RNA purity and concentration were measured by spectrophotometry. Expression analysis was carried out by qPCR with specific primers to target and reference miRNAs. Results: The level of hsa-miR-210 was significantly higher in PE placentas, which could cause a minor increase of exosomal and a high elevation of Ago-bound miR-210 in circulation. Hypoxia leads to intracellular hsa-miR-210 upregulation in trophoblast cell lines. In extravillous cell (HTR8) media, only the level of exosomal hsa-miR-210 was increased but no change in Ago-bound hsa-miR-210 level was observed. In contrast, in villous cell (JAR) media, the level of exosomal hsa-miR-210 was increased and enhanced release of Ago-bound hsa-miR-210 was also observed. Conclusion: Based on our data, we postulate that in PE, exosomal hsa-miR-210 are secreted actively from the trophoblast, and by intercellular communication, it may have a role in disease etiology. In addition, there is a passive release of Ago-bound hsa-miR-210 into the circulation, which may represent by-products of cell-death and is thereby a possible consequence of the disease.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
preeclampsia
exosomal
miRNA
Argonaute
Megjelenés:Gene. - 692 (2019), p. 138-144. -
További szerzők:Fóthi Ábel Alasztics Bálint Nagy Bálint (1956-) (molekuláris genetikus) Orbán Tamás I. Rigó János (1958-) (szülész-nőgyógyász)
Pályázati támogatás:K112112
OTKA
K113023
OTKA
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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2.

001-es BibID:BIBFORM074852
Első szerző:Myllykangas, Samuel
Cím:Helicobacter pylori infection activates FOS and stress-response genes and alters expression of genes in gastric cancer-specific loci / Samuel Myllykangas, Outi Monni, Bálint Nagy, Hilpi Rautelin, Sakari Knuutila
Dátum:2004
ISSN:1045-2257
Megjegyzések:We studied human gene expression changes caused by Helicobacter pylori infection by using an in vitro model and 13k cDNA microarrays. A gastric cancer cell line was infected with H. pylori strain NCTC 11637. H. pylori infection was found to induce differential expression of genes in chromosomal locations known to contain frequent chromosomal aberrations and gene mutations specific to gastric cancer. Based on the results of time series experiments, the primary transcription target of the infection seemed to be FOS, the expression of which significantly increased after H. pylori infection. H. pylori infection also activated transcription of several stress-response genes. H. pylori infection may predispose the host cell to DNA damage in the chromosomal locations specific to gastric cancer by activating transcription and promoting histone removal from these sites, thus exposing its target DNA to mutations.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Helicobacter pylori
FOS
gene expression
Megjelenés:Genes Chromosomes & Cancer. - 40 : 4 (2004), p. 334-341. -
További szerzők:Monni, Outi Nagy Bálint (1956-) (molekuláris genetikus) Rautelin, Hilpi Knuutila, Sakari
Internet cím:Szerző által megadott URL
DOI
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