Effect of gamma-radiation on healthy rat liver and gene expression of chemokines: In vivo and in vitro studies.

2010 ◽  
Vol 28 (15_suppl) ◽  
pp. e21107-e21107
Author(s):  
I. A. Malik ◽  
N. Naz ◽  
S. Khan ◽  
H. Christiansen ◽  
G. Ramadori
Keyword(s):  
Gene Expression ◽  
Gamma Radiation ◽  
Rat Liver ◽  
In Vitro Studies

Effect of X-irradiation on gene expression of rat liver chemokines: in vivo and in vitro studies

2008 ◽  
Vol 46 (01) ◽  
Author(s):  
F Moriconi ◽  
H Christiansen ◽  
H Christiansen ◽  
N Sheikh ◽  
J Dudas ◽  
...  
Keyword(s):  
Gene Expression ◽  
Rat Liver ◽  
In Vitro Studies ◽  
X Irradiation

197 Hepcidin and hemojuvelin gene expression in rat liver damage: In vivo and in vitro studies

2006 ◽  
Vol 44 ◽  
pp. S81-S82
Author(s):  
N. Sheikh ◽  
K. Tron ◽  
J. Dudas ◽  
B. Saile ◽  
D. Batusic ◽  
...  
Keyword(s):  
Gene Expression ◽  
Rat Liver ◽  
Liver Damage ◽  
In Vitro Studies

Development and regulation of glucose-6-phosphatase gene expression in rat liver, intestine, and kidney: in vivo and in vitro studies in cultured fetal hepatocytes

Diabetes ◽  
1998 ◽  
Vol 47 (6) ◽  
pp. 882-889 ◽  
Author(s):  
F. Chatelain ◽  
J. P. Pegorier ◽  
C. Minassian ◽  
N. Bruni ◽  
S. Tarpin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Rat Liver ◽  
In Vitro Studies ◽  
Fetal Hepatocytes

Tenascin gene expression in rat liver and in rat liver cells In vivo and in vitro studies

1991 ◽  
Vol 60 (1) ◽  
pp. 145-153 ◽  
Author(s):  
G. Ramadori ◽  
S. Schwogler ◽  
Th. Veit ◽  
H. Rieder ◽  
R. Chiquet-Ehrismann ◽  
...  
Keyword(s):  
Gene Expression ◽  
Rat Liver ◽  
Liver Cells ◽  
In Vitro Studies ◽  
Rat Liver Cells

Gene Expression Profiles in Rat Liver Slices Exposed to Hepatocarcinogenic Enzyme Inducers, Peroxisome Proliferators, and 17α-Ethinylestradiol

2006 ◽  
Vol 25 (5) ◽  
pp. 379-395 ◽  
Author(s):  
Gisela Werle-Schneider ◽  
Andreas Wölfelschneider ◽  
Marie Charlotte von Brevern ◽  
Julia Scheel ◽  
Thorsten Storck ◽  
...  
Keyword(s):  
Gene Expression ◽  
Rat Liver ◽  
Mode Of Action ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Peroxisome Proliferators ◽  
Liver Slices ◽  
Enzyme Inducers

Transcription profiling is used as an in vivo method for predicting the mode-of-action class of nongenotoxic carcinogens. To set up a reliable in vitro short-term test system DNA microarray technology was combined with rat liver slices. Seven compounds known to act as tumor promoters were selected, which included the enzyme inducers phenobarbital, α-hexachlorocyclohexane, and cyproterone acetate; the peroxisome proliferators WY-14,643, dehydroepiandrosterone, and ciprofibrate; and the hormone 17 α-ethinylestradiol. Rat liver slices were exposed to various concentrations of the compounds for 24 h. Toxicology-focused TOXaminer™ DNA microarrays containing approximately 1500 genes were used for generating gene expression profiles for each of the test compound. Hierarchical cluster analysis revealed that (i) gene expression profiles generated in rat liver slices in vitro were specific allowing classification of compounds with similar mode of action and (ii) expression profiles of rat liver slices exposed in vitro correlate with those induced after in vivo treatment (reported previously). Enzyme inducers and peroxisome proliferators formed two separate clusters, confirming that they act through different mechanisms. Expression profiles of the hormone 17 α-ethinylestradiol were not similar to any of the other compounds. In conclusion, gene expression profiles induced by compounds that act via similar mechanisms showed common effects on transcription upon treatment in vivo and in rat liver slices in vitro.

PDGFR-Mediated Cytomegalovirus Infection of Megakaryocytes Induces Thrombocytopenia Via Demethylation of AML1 and IEX-1 in the TPO/c-Mpl Signaling Pathway Following Allo-HSCT

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 3937-3937
Author(s):  
Xiao-Hui Zhang ◽  
Feng Fei-er ◽  
Qian-ming Wang ◽  
Xiao-lu Zhu ◽  
Lan-ping Xu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Bone Marrow ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Hcmv Infection ◽  
Treated Group ◽  
In Vitro Studies ◽  
Significant Difference

Abstract Introduction: Human cytomegalovirus (HCMV) infection is a common complication of allogeneic hematopoietic stem cell transplantation (allo-HSCT), which is associated with high morbidity and mortality. Thrombocytopenia is one of the major hematological complications of HCMV infection. Possible causes include direct HCMV injury to hematopoietic progenitor cells and the microenvironment, as well as HCMV-related immune thrombocytopenia. Previous in vitro studies demonstrate that HCMV could directly infect megakaryocytes(MKs) and their progenitors, resulting in decreased CFU-MK and increased apoptosis, but the underlying mechanisms remain uncertain. It remains unknown whether HCMV can directly target MKs in vivo, how MK function changes after infection, why HCMV selectively infects certain patients and what inhibits MK maturation and results in apoptosis. It has been reported that patients with HCMV-related thrombocytopenia showed poor response to rhTPO, implying blockage of the TPO/c-Mpl signaling pathway. Our previous research indicated that PDGFR+CXCR4lowCCR5lowMKs are correlated with HCMV infection.We hypothesized that PDGFR+CXCR4lowCCR5lowMKs are more susceptible to HCMV infection. HCMV could directly target MKs both in vitro and in vivo, resulting in increased apoptosis and decreased MK ploidy. HCMV infection could possibly disturb the downstream TPO/c-Mpl signaling pathway, thereby inhibiting MK differentiation and maturation. Methods: We collected bone marrow from HCMV DNAemia patients post allo-HSCT for in vivo study. Transmission electron microscopy(TEM) was used to detect HCMV particles inside MKs. MKs were identified as CD41+vWF+cells by flow cytometry(FCM). To analyze the susceptibility of MKs to HCMV, expression levels of PDGFR, αvβ3, TLR2, CCR5 and CXCR4 in different groups were tested. Cell apoptosis was measured by Annexin V. MK ploidy was determined by FCM for propidium iodide (PI) staining. We also measured c-Mpl expression in MKs.In vitro study, we used plasma from HCMV-infected patients post allo-HSCT to infect MKs cultured from bone marrow CD34+ cells. We validated cell susceptibility with the same markers used in vivo. Next, inhibitors of the positive markers were co-cultured with MKs. We analyzed pp65 expression in the inhibitor-treated group and control group to explore potential prevention of HCMV infection. We investigated AML1 and IEX-1 in the downstream TPO/c-Mpl signaling pathway by PCR and Western Blot. We used bisulfite sequencing PCR (BSP) to study the methylation status in different gene expression profiles of AML1 and IEX-1. 5-ara-dC is a type of DNA methylation inhibitor. After incubation with MKs, we analyzed changes in gene expression and MKs function. Results: Using TEM, we managed to find HCMV particles in MKs from HCMV-infected patient bone marrow samples. The proportion of apoptosis markedly increased compared with HCMV-negative MKs, whereas the mean ploidy slightly decreased. C-Mpl expression showed no significant difference between the two groups. Pp65 positive cells showed elevated expression in PDGFR and reduced expression in CXCR4 and CCR5. In vitro studies revealed similar results. After treating with the PDGFR inhibitor IMC-3G3, the pp65 positive cell population was slightly decreased, but the Gleevec-treated group showed no difference. We found a decrease in both IEX-1 and AML1 on both the molecular and protein levels. Both gene promoters were hypermethylated in the HCMV-infected group. After demethylation with 5-ara-dC, IEX-1 and AML1expression levels were both up-regulated, and cell apoptosis was reduced. Conclusion: (1)HCMV inhibited megakaryocytic differentiation and maturation and reduced MKs polyploidy both in vivo and in vitro. (2)MKs positive for PDGFR and low in CXCR4 and CCR5 were more susceptible to HCMV infection. The PDGFR inhibitor IMC-3G3 protected MKs from HCMV infection. (3)The mechanism of HCMV-associated thrombocytopenia may be a disturbance of the TPO/c-Mpl signaling pathway in MKs through hypermethylation of the AML1 and IEX-1 promoters. Demethylation with 5-ara-dC could reverse cell apoptosis. Therefore, we illustrated the possible mechanism of HCMV-induced thrombocytopenia, highlighting new insights for future potential therapeutic approaches. Disclosures No relevant conflicts of interest to declare.

The development of phenylalanine hydroxylase in rat liver; in vivo, and in vitro studies utilizing fetal hepatocyte cultures

1988 ◽  
Vol 38 (1) ◽  
pp. 42-48 ◽  
Author(s):  
George C.T. Yeoh ◽  
Edward Edkins ◽  
Kirsten Mackenzie ◽  
Stephanie Fuller ◽  
Julian F.B. Mercer ◽  
...  
Keyword(s):  
Rat Liver ◽  
Phenylalanine Hydroxylase ◽  
In Vitro Studies ◽  
Hepatocyte Cultures ◽  
Fetal Hepatocyte

scholarly journals Cell Itinerary and Metabolic Fate of Proinsulin in Rat Liver: In Vivo and in Vitro Studies

Endocrinology ◽  
2003 ◽  
Vol 144 (12) ◽  
pp. 5308-5321 ◽  
Author(s):  
Bernard Desbuquois ◽  
Geneviève Chauvet ◽  
Mostafa Kouach ◽  
François Authier
Keyword(s):  
Rat Liver ◽  
In Vitro Studies ◽  
Metabolic Fate
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