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1
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Expression of genes encoding mitochondrial proteins can distinguish nonalcoholic steatosis from steatohepatitis

100%
Bragoszewski P., Habior A., Walewska-Zielecka B., Ostrowski J.
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2007
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vol. 54
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issue 2
341-348
EN
In patients without substantial alcohol use, triglyceride accumulation in the liver can lead to nonalcoholic fatty liver disease (NAFLD) that may progress to nonalcoholic steatohepatitis (NASH). The differential diagnosis between NAFLD and NASH can be accomplished only by morphological examination. Although the relationship between mitochondrial dysfunction and the progression of liver pathologic changes has been described, the exact mechanisms initiating primary liver steatosis and its progression to NASH are unknown. We selected 16 genes encoding mitochondrial proteins which expression was compared by quantitative RT-PCR in liver tissue samples taken from patients with NAFLD and NASH. We found that 6 of the 16 examined genes were differentially expressed in NAFLD versus NASH patients. The expression of hepatic HK1, UCP2, ME2, and ME3 appeared to be higher in NASH than in NAFLD patients, whereas HMGCS2 and hnRNPK expression was lower in NASH patients. Although the severity of liver morphological injury in the spectrum of NAFLD-NASH may be defined at the molecular level, expression of these selected 6 genes cannot be used as a molecular marker aiding histological examination. Moreover, it is still unclear whether these differences in hepatic gene expression profiles truly reflect the progression of morphological abnormalities or rather indicate various metabolic and hormonal states in patients with different degrees of fatty liver disease.
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Increased expression of ribosomal protein S2 in liver tumors, posthepactomized livers, and proliferating hepatocytes in vitro.

100%
Kowalczyk P., Woszczyński M., Ostrowski J.
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2002
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vol. 49
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issue 3
615-624
EN
The ribosomal protein S2 (RPS2) is encoded by a gene from the highly conserved mammalian repetitive gene family LLRep3. It participates in aminoacyl-transfer RNA binding to ribosome, potentially affecting the fidelity of mRNA translation. These studies were designed to measure the expression of RPS2 during increased cell proliferation. Using Western and Northern blot analyses, we found that the levels of RPS2 protein and its corresponding mRNA were higher in mouse hepatocellular carcinoma, in mouse livers after one-third partial hepatectomy, and in serum-starved cultured hepatocytes following serum treatment. Our study shows that the increased expression of RPS2 correlates with increased cell proliferation. However, whether the altered expression of this protein reflects its involvement in cellular proliferation or represents an associated phenomena is still a key question that needs to be explored.
3
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Barrett's esophagus associates with a variant of IL23R gene

88%
Gaj P., Mikula M., Wyrwicz L., Regula J., Ostrowski J.
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2008
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vol. 55
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issue 2
365-369
EN
Gastroesophageal reflux disease is regarded as a spectrum of diseases: non-erosive reflux disease (NERD), erosive reflux disease (ERD), and the far end of the spectrum represented by patients with Barrett's esophagus. Among predisposing factors, both risk and protective polymorphic variants of several genes may influence the clinical outcomes of reflux disease. Consequently, different molecular mechanisms are likely to underlie the development of clinical variants of reflux disease. Ninety six patients with reflux disease were screened for polymorphisms of CARD15, SLC22A4 (OCTN1), SLC22A5 (OCTN2), DLG5, ATG16L1 and IL23R genes which had previously been found to associate with immune-mediated chronic inflammatory disorders. While none of the polymorphisms were associated with NERD or ERD, the 1142G/A variant of the IL23R gene was found to be a risk variant in Barrett's esophagus patients. The IL23/IL23R pathway may modulate STAT3 transcriptional activity which is an essential regulator not only of immune-mediated inflammation, but also of inflammatory-associated apoptosis resistance. Although the mechanisms of metaplastic transition of inflamed squamous epithelium are undetermined as yet, our findings suggest potential involvement of alternations in the IL23/IL23R pathway as a molecular background of Barrett's esophagus development.
4
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A common cis-element in promoters of protein synthesis and cell cycle genes

88%
Wyrwicz L. S., Gaj P., Hoffmann M., Rychlewski L., Ostrowski J.
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EN
Gene promoters contain several classes of functional sequence elements (cis elements) recognized by protein agents, e.g. transcription factors and essential components of the transcription machinery. Here we describe a common DNA regulatory element (tandem TCTCGCGAGA motif) of human TATA-less promoters. A combination of bioinformatic and experimental methodology suggests that the element can be critical for expression of genes involved in enhanced protein synthesis and the G1/S transition in the cell cycle. The motif was identified in a substantial fraction of promoters of cell cycle genes, like cyclins (CCNC, CCNG1), as well as transcription regulators (TAF7, TAF13, KLF7, NCOA2), chromatin structure modulators (HDAC2, TAF6L), translation initiation factors (EIF5, EIF2S1, EIF4G2, EIF3S8, EIF4) and previously reported 18 ribosomal protein genes. Since the motif can define a subset of promoters with a distinct mechanism of activation involved in regulation of expression of about 5% of human genes, further investigation of this regulatory element is an emerging task.
5
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Mitochondria-associated satellite I RNA binds to hnRNP K protein

76%
Klimek-Tomczak K., Mikula M., Dzwonek A., Paziewska A., Wyrwicz L. S., Hennig E. E., Ostrowski J.
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2006
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vol. 53
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issue 1
169-178
EN
hnRNP K protein, which localizes to the nucleus, cytoplasm and mitochondria, is involved in the various cellular processes that compose gene expression. We used a SAGE-based assay to profile RNAs associated with hnRNP K protein in rat mitochondria. RNA was isolated from mitoplasts obtained from highly purified and RNase-treated mitochondria. Total RNA and RNA associated with hnRNP K protein were then used as input material for generating two SAGE libraries. Mitochondrion-derived tags isolated from the total mitoplast RNA library represented 86.3%, while those isolated from the library constructed from RNA associated with hnRNP K protein represented only 28.2% of selected tags. Thus, an unexpected number of nuclear-encoded RNAs were purified from mitochondria. Many of these transcripts were co-purified with hnRNP K protein, and high levels of nuclear-encoded RNAs co-immunoprecipitating with K protein corresponded to elevated hnRNP K protein levels of the organelle. The most abundant RNAs that were co-purified with hnRNP K protein represented transcripts originating from satellite I DNA. While satellite I RNA levels were higher in the nucleus and cytoplasm than in mitochondria, the most abundant binding of satellite I transcripts to hnRNP K protein was found in mitochondria. The role of satellite I RNA in mitochondria remains to be elucidated.
6
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Pre-analytical-related variability influencing serum peptide profiles demonstrated in a mass spectrometry-based search for colorectal and prostate cancer biomarkers

64%
Karczmarski J., Rubel T., Mikula M., Wolski J., Rutkowski A., Zagorowicz E., Dadlez M., Ostrowski J.
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2013
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vol. 60
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issue 3
417-425
EN
Although the degradome, which comprises proteolytic fragments of blood proteins, presents a potential source of diagnostic biomarkers, studies on cancer peptide biomarkers have provided inconsistent conclusions. In the present study, we reevaluated the usefulness of serum degradome analyses for searching peptide cancer biomarker candidates. Particular attention was paid to pre-analytical factors influencing the variability of determined peptide levels, including clotting time and control group selection. Studies were conducted on 44 and 86 serum samples collected from cancer patients and healthy individuals, respectively, using liquid chromatography electrospray ionization mass spectrometry (LC-ESI-MS)-based analyses. We identified 1373 unique peptides, nearly 40% of which originated from five blood proteins: fibrinogen alpha chain, apolipoprotein A-IV (APOA4), complement C3, apolipoprotein A-I, and alpha-1-antitrypsin. A set of 118 and 88 peptides exhibited highly significant differences (adjusted p-value ≤ 0.01 and fold change ≥ 2) in pair-wise comparisons of control vs. prostate cancer and control vs. colorectal cancer, respectively, with 37 peptides displaying a consistent direction of change for these pair-wise comparisons. The levels of 67 peptides differed significantly in serum samples collected from healthy individuals immediately prior to colonoscopy and those who underwent colonoscopic examination at least four weeks earlier. Of them, 49 peptides originated from APOA4. Whereas earlier studies, including ours, have utilized fragments of fibrinopeptide A (FPA) to distinguish cancer from healthy cases, here we show that their absolute abundance is a sensitive indicator of clotting time. These observations may have implications for future serum peptidome studies since these issues have not previously been recognized.
7
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Transcriptional changes between uninflamed ulcerative colitis and familial adenomatous polyposis pouch mucosa can be attributed to an altered immune response

64%
Paziewska A., Horbacka K., Goryca K., Mikula M., Jarosz D., Dabrowska M., Krokowicz P., Karon J., Ostrowski J.
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2015
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vol. 62
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issue 1
69-75
EN
A total proctocolectomy with ileal pouch-anal anastomosis (IPAA) is considered the surgery of choice for definitive management of familial adenomatous polyposis (FAP) and some patients with ulcerative colitis (UC). However, this surgical treatment is often associated with pouchitis, a long-term complication that occurs mostly in UC patients. The purpose of this study was to better define the molecular background of pouchitis. A microarray-based survey was performed using pouch mucosal samples collected from 28 and 8 patients undergoing surgery for UC and FAP, respectively. There were 4,770 genes that significantly differentiated uninflamed from inflamed mucosal samples, and their functional features were represented mostly by metabolic and cell proliferation pathways. In contrast, functional analyses of aberrantly expressed genes between UC and FAP samples, irrespective of mucosal inflammation status, revealed multiple pathways and terms that were linked to changes in immune response. Interestingly, the comparison of uninflamed UC and FAP samples identified a set of 29 altered probe sets, including an inflammation-related transcript encoding a Charcot-Leyden crystal (CLC) protein. The most distinct changes in gene expression profiles differentiating uninflamed UC and FAP pouch mucosal samples were attributed to the Gene Ontology category innate immune response. Our study confirmed that alterations in immune responses can be found between patients who underwent surgery for UC and FAP, independent of the pouch inflammation status. This observation may be important when managing IPAA patients.
8
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Up-regulation of human PNPase mRNA by β-interferon has no effect on protein level in melanoma cell lines

64%
Gewartowski K., Tomecki R., Muchowski L., Dmochow­ska A., Dzwonek A., Malecki M., Skurzak H., Ostrowski J., Stepien P. P.
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2006
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vol. 53
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issue 1
179-188
EN
Human mitochondrial polynucleotide phosphorylase (hPNPase) is an exoribonuclease localized in mitochondria. The exact physiological function of this enzyme is unknown. Recent studies have revealed the existence of a relationship between induction of hPNPase mRNA and both cellular senescence and growth arrest of melanoma cells following β-interferon treatment. The aim of this study was to verify whether the augmented hPNPase mRNA level results in increase of the protein level. In several cell lines established from five metastatic melanoma patients we did not find any such correlation. However, an elevated level of hPNPase protein was observed in interferon-induced HeLa and Jurkat cells. This increase was correlated with a slight shortening of poly(A) tails of mitochondrial ND3 transcript.
9
Content available remote

Gene expression alterations induced by low molecular weight heparin during bowel anastomosis healing in rats

52%
Krześniak N., Paziewska A., Rubel T., Skrzypczak M., Mikula M., Dzwonek A., Goryca K., Wyrwicz L. S., Jarosz D., Laubitz D., Woszczyński M., Bielecki K., Ostrowski J.
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2011
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vol. 58
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issue 1
79-87
EN
Colon anastomosis is therapeutically challenging because multiple, usually undetectable factors influence a spectrum of repair mechanisms. We hypothesized that low molecular weight heparins, routinely administered perioperatively, may differentially affect gene expression related to colon healing. Twenty pairs of untreated and enoxaparin-treated rats underwent left-side hemicolectomy with a primary end-to-end anastomosis. Normal colon and anastomotic bowel segments were resected on day 0 and on days 1, 3, 5, and 7 after surgery, respectively. Serial anastomosis transverse cross-sections were evaluated microscopically and by microarray (Rat Genome 230 2.0, Affymetrix). Differentially expressed probe sets were annotated with Gene Ontology. We also examined the influence of enoxaparin on fibroblast proliferation and viability in vitro. Among the 5476 probe sets, we identified differential expression at each healing time point, yielding 79 subcategories. Most indicated genes were involved in wound healing, including multicellular organismal development, locomotory behavior, immune response, cell adhesion, inflammatory response, cell-cell signaling, blood vessel development, and tissue remodeling. Although we found no intensity differences in histological features of healing between enoxaparin-treated and control rats, treatment did induce significant expression changes during early healing. Of these changes, 83 probe sets exhibited at least twofold changes and represented different functional annotations, including inflammatory response, regulation of transcription, regulation of apoptosis, and angiogenesis. Fibroblast culture confirmed an anti-viability effect of enoxaparin. Enoxaparin affects colon wound-related gene expression profiles, but further studies will resolve whether heparin treatment is a risk factor after intestinal surgery, at least in some patients.
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