Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 12

Liczba wyników na stronie
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników

Wyniki wyszukiwania

Wyszukiwano:
w słowach kluczowych:  HepG2 cell
help Sortuj według:

help Ogranicz wyniki do:
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
ABCC6 protein is an ATP-dependent transporter that is mainly found in the basolateral plasma membrane of hepatocytes. ABCC6 deficiency is the primary cause of several forms of ectopic mineralization syndrome. Mutations in the human ABCC6 gene cause pseudoxanthoma elasticum (PXE), an autosomal recessive disease characterized by ectopic calcification of the elastic fibers in dermal, ocular and vascular tissues. Mutations in the mouse ABCC6 gene were also associated with dystrophic cardiac calcification. Reduced levels of ABCC6 protein were found in a β-thalassemic mouse model. Moreover, some cases of generalized arterial calcification in infancy are due to ABCC6 mutations. In order to study the role of ABCC6 in the pathogenesis of ectopic mineralization, the expressions of genes involved in this process were evaluated in HepG2 cells upon stable knockdown of ABCC6 by small hairpin RNA (shRNA) technology. ABCC6 knockdown in HepG2 cells causes a significant upregulation of the genes promoting mineralization, such as TNAP, and a parallel downregulation of genes with anti-mineralization activity, such as NT5E, Fetuin A and Osteopontin. Although the absence of ABCC6 has been already associated with ectopic mineralization syndromes, this study is the first to show a direct relationship between reduced ABCC6 levels and the expression of pro-mineralization genes in hepatocytes.
Mercury poisoning is responsible for inducing serious adverse effects in living organisms. One of protection factors could be substances proven to possess high antioxidant and metal chelating activity - plant polyphenols. There are many sources of polyphenols in plant kingdom but the most interesting for food industry could be widely consumed herbs. Aim of the research was to evaluate antioxidative potential of selected plant extracts and its influence on HepG2 cells in different conditions. Ethanolic herbs extracts were characterised by total polyphenol content. Antioxidant activity was estimated with use of DPPH• and ABTS+• radicals scavenging methods and FRAP. Research included cells viability estimation by the MTT assay and cells exposition to HgCl2, chemical agent inducing cell death. Analysis of herbs extracts antioxidative activity showed best potential represented thyme and marjoram, highest FRAP was evaluated in samples with mint and marjoram extracts. On the basis of received results it was found that examined plant extracts showed weak protection against Hg presence in examined cells environment.
 Quantitative real-time RT-PCR study was conducted to reveal the effects of normal (5 mmol/l) and high (30 mmol/l) glucose without or with oleate (0.3 mmol/l) on mRNA levels of peroxisome proliferator-activated receptor- (PPAR-)α, -γ1, -γ2, and peroxisome proliferator-activated receptor-γ coactivator- (PGC-)1α and -1β in commercial human hepatoma-derived HepG2 cells maintained under low-serum condition. Significant decrease in PPAR-γ1 and PGC-1α mRNA levels to about 50 % was observed during the first 4 h incubation period. During the next 4 h period, both PPAR-γ1 and PGC-1α mRNAs were partly but significantly restored in high glucose batches. In this period, the presence of the transcriptional inhibitor actinomycin D revealed a significant protective effect of excess glucose on mature PPAR-γ1 and PGC-1α mRNAs. Furthermore, PPAR-γ1 and -γ2 mRNAs were differentially superinduced 1.2-2.5 fold in cells upon the administration of the translational inhibitor cycloheximide. When the cells were co-treated with the combination of cycloheximide and actinomycin D, superinduction was completely suppressed, however. Altogether, the experiments revealed, first, an unexpected protective effect of abundant glucose on PPAR-γ1 and PGC-1α mRNAs in HepG2 cells. Second, we demonstrated cycloheximide-induced, transcription-dependent upregulation of mature PPAR-γ1 and -γ2 mRNAs in HepG2 cells associated with preferential expression of the PPAR-γ2 mRNA variant. The results draw attention to as yet unexplored mechanisms involved in the control of PPAR and PGC genes.
ZBTB7A is a known proto-oncogene that is implicated in carcinogenesis and cell differentiation and development. Fully understanding the function of ZBTB7A in cellular processes could provide useful strategies for cancer treatment and development-associated disease therapy. Here, global mapping of ZBTB7A transcription factor binding sites was developed by utilizing microarray technology in HepG2 cells. The data obtained from the microarrays was further validated via chromatin immunoprecipitation-PCR (ChIP-PCR) and real time-PCR, and it was revealed that ZBTB7A may be one of the regulators of neural development. ZBTB7A target signal pathways were identified in signal pathway and GO (Gene Ontology) analyses. This is the first report on the global mapping of ZBTB7A downstream direct targets, and these findings will be useful in understanding the roles of ZBTB7A in cellular processes.
The systemic inflammatory reaction (acute phase response) is induced by many nox­ious stimuli but in all cases the inflammatory cytokines, such as interleukin-1-beta (IL-1/ß) and interleukin-6 (IL-6), are involved. Liver cell response to inflammation manifested by a characteristic change in the profile of synthesized plasma proteins (acute phase proteins) has been extensively studied. Here we describe a model system of cultured human hepatoma HepG2 cells stimulated with IL-1/ ß to evaluate the trans­criptome induced by this cytokine during 24 h of treatment. By using differential dis­play analysis we found IL-1/ß-induced upregulation of several genes coding for cellular trafficking/motor proteins, proteins participating in the translation machinery or in­volved in posttranscription/posttranslation modifications, proteases, proteins in­volved in cellular metabolism, activity modulators, proteins of the cell cycle machin­ery and also some new proteins so far functionally not classified.
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.