scholarly journals Calnexin overexpression sensitizes recombinant CHO cells to apoptosis induced by sodium butyrate treatment

2008 ◽  
Vol 14 (1) ◽  
pp. 49-60 ◽  
Author(s):  
Chaya Mohan ◽  
Gyun Min Lee
Keyword(s):  
Sodium Butyrate ◽  
Cho Cells ◽  
Recombinant Cho Cells ◽  
Butyrate Treatment

scholarly journals Modulation of heparan sulfate biosynthesis by sodium butyrate in recombinant CHO cells

2014 ◽  
Vol 67 (2) ◽  
pp. 223-235
Author(s):  
Payel Datta ◽  
Bo Yang ◽  
Robert J. Linhardt ◽  
Susan T. Sharfstein
Keyword(s):  
Heparan Sulfate ◽  
Sodium Butyrate ◽  
Cho Cells ◽  
Recombinant Cho Cells

Expression of human Mn SOD in Chinese hamster ovary cells confers protection from oxidant injury

1993 ◽  
Vol 264 (6) ◽  
pp. L598-L605
Author(s):  
B. Warner ◽  
R. Papes ◽  
M. Heile ◽  
D. Spitz ◽  
J. Wispe
Keyword(s):  
Chinese Hamster Ovary ◽  
Cho Cells ◽  
Chinese Hamster Ovary Cells ◽  
Lethal Dose ◽  
Chinese Hamster ◽  
Eukaryotic Expression ◽  
Wild Type ◽  
Oxidant Injury ◽  
Sod Activity ◽  
Recombinant Cho Cells

Manganese superoxide dismutase (Mn SOD) is an important component of antioxidant defense in aerobic cells because of its location in the mitochondria, a significant source of oxygen radicals and an important target of oxidant injury. To test the hypothesis that increased mitochondrial Mn SOD protects from oxidant injury, Chinese hamster ovary (CHO) cells were transfected with a eukaryotic expression vector containing the human Mn SOD cDNA. In recombinant CHO cells, Mn SOD activity was increased threefold over wild-type controls. Acute survival during paraquat exposure (0–500 microM) was significantly improved in CHO cells expressing human Mn SOD, with 71% of recombinant CHO cells surviving at the 50% lethal dose (LD50) for wild-type CHO controls. Cell growth following exposure to paraquat (100 microM) was also significantly improved in recombinant CHO cells. CHO cells expressing human Mn SOD continued to grow and divide after paraquat exposure, whereas growth of wild-type CHO cells was negligible. Protection against oxidant-induced injury was directly related to increased Mn SOD, occurring in the absence of changes in other antioxidant enzymes including catalase, Cu,Zn SOD, and glutathione associated cellular antioxidant mechanisms. We conclude that increased expression of human Mn SOD in vitro directly confers protection against oxidant injury.

scholarly journals p300/CBP-associated factor (P/CAF) interacts with nuclear respiratory factor-1 to regulate the UDP-N-acetyl-alpha-d-galactosamine: polypeptide N-acetylgalactosaminyltransferase-3 gene

2003 ◽  
Vol 373 (3) ◽  
pp. 713-722 ◽  
Author(s):  
Hiroto IZUMI ◽  
Ryo OHTA ◽  
Gunji NAGATANI ◽  
Tomoko ISE ◽  
Yoshifumi NAKAYAMA ◽  
...  
Keyword(s):  
Sodium Butyrate ◽  
Nuclear Extract ◽  
Binding Motif ◽  
Induced Expression ◽  
Associated Factor ◽  
Nuclear Respiratory Factor ◽  
Nuclear Respiratory Factor 1 ◽  
Butyrate Treatment ◽  
Transcriptional Elements ◽  
Mcf 7

We demonstrated recently that expression of the UDP-N-acetyl-α-d-galactosamine: polypeptide N-acetylgalactosaminyltrans-ferase-3 (GalNAc-T3) gene is restricted to epithelial glands [Nomoto, Izumi, Ise, Kato, Takano, Nagatani, Shibao, Ohta, Imamura, Kuwano, Matsuo, Yamada, Itoh and Kohno (1999) Cancer Res. 59, 6214–6222]. In the present study, we show that sodium butyrate treatment of human breast cancer MCF-7 cells transcriptionally activates the GalNAc-T3 gene. Transient transfection of plasmids containing a reporter gene under the control of GalNAc-T3 indicated that several transcriptional elements are involved in response to sodium butyrate, with the nuclear respiratory factor-1 (NRF-1)-binding motif located between −88 and −77nt being the most important. Incubation of a labelled probe encompassing the NRF-1-binding motif with a nuclear extract of sodium butyrate-treated MCF-7 cells yielded a higher level of specific DNA–protein complex versus controls. Flag-tagged NRF-1 expressed in MCF-7 cells can bind to the NRF-1-binding motif of the GalNAc-T3 promoter. Nuclear content of NRF-1 remained constant in MCF-7 cells treated with or without sodium butyrate. Moreover, NRF-1 interacts with and is acetylated by p300/CBP-associated factor (P/CAF). Acetylation of NRF-1 enhances DNA binding. Co-transfection of the GalNAc-T3 reporter plasmid with either NRF-1 or P/CAF expression plasmid resulted in the activation of the GalNAc-T3 promoter. These results indicate a correlation between acetylation of NRF-1 by P/CAF and the butyrate-induced expression of the GalNAc-T3 gene. Additionally, induced expression of P/CAF may be a component of the adenocarcinoma differentiation process.

scholarly journals Improvement of the energy metabolism of recombinant CHO cells by cell sorting for reduced mitochondrial membrane potential

2007 ◽  
Vol 129 (4) ◽  
pp. 651-657 ◽  
Author(s):  
Georg Hinterkörner ◽  
Gudrun Brugger ◽  
Dethardt Müller ◽  
Friedemann Hesse ◽  
Renate Kunert ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Energy Metabolism ◽  
Mitochondrial Membrane Potential ◽  
Cell Sorting ◽  
Cho Cells ◽  
Mitochondrial Membrane ◽  
Recombinant Cho Cells

Genetic engineering of ?2,6-sialyltransferase in recombinant CHO cells and its effects on the sialylation of recombinant interferon-?

1996 ◽  
Vol 22 (1-3) ◽  
pp. 197-203 ◽  
Author(s):  
Lucia Monaco ◽  
Annie Marc ◽  
Alex Eon-Duval ◽  
Giulia Acerbis ◽  
Gianfranco Distefano ◽  
...  
Keyword(s):  
Genetic Engineering ◽  
Cho Cells ◽  
Recombinant Interferon ◽  
Recombinant Cho Cells

HIGH DENSITY AGGREGATE CULTURE OF RECOMBINANT CHO CELLS IN FLUIDIZED BED BIOREACTORS

1992 ◽  
pp. 421-423 ◽  
Author(s):  
M. Reiter ◽  
G. Blüml ◽  
T. Gaida ◽  
N. Zach ◽  
C. Schmatz ◽  
...  
Keyword(s):  
Fluidized Bed ◽  
Cho Cells ◽  
High Density ◽  
Recombinant Cho Cells ◽  
Aggregate Culture

Abstract P162: Butyrate, a Microbial Metabolite, Attenuates Angiotensin II-induced Hypertension and Gut Dysbiosis

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Seungbum Kim ◽  
Gilberto O Lobaton ◽  
Mohan K Raizada
Keyword(s):  
Angiotensin Ii ◽  
Sodium Butyrate ◽  
Ang Ii ◽  
Principal Coordinates Analysis ◽  
Gut Dysbiosis ◽  
Microbial Dysbiosis ◽  
Inflammatory Status ◽  
Principal Coordinates ◽  
Rdna Sequencing ◽  
Butyrate Treatment

Objectives: We have previously established that hypertension (HTN) is associated with gut dysbiosis in rat models and patients with high blood pressure. Gut dysbiosis was associated with an increase in Firmicutes/Bacteriodetes ratio and a decrease in butyrate-producing microbial populations. This led us to hypothesize that infusion of butyrate would overcome gut microbial dysbiosis induced butyrate deficiency and reverse angiotensin II (Ang II)-induced HTN. Design and Method: Four groups of C57BL6 mice were infused with either saline, Ang II (1000ng/kg/min), Ang II + sodium butyrate (1mg/kg), or sodium butyrate alone for 4 weeks. Fecal samples were analyzed by 16S bacterial rDNA sequencing for gut microbiome identification. Intestinal leukocytes were analyzed using FACS. Results: Ang II induced increase in MAP was significantly attenuated in mice co-administrated with butyrate (Control, 102.1±5.7 mmHg; Ang II, 148.3±8.1 mmHg; Ang II+Butyrate, 120.5±11.2 mmHg). Microbiota analysis demonstrated a significant increase of gut dysbiosis in Ang II-HTN that was normalized by butyrate treatment (F/B ratio: Control, 2.6; Ang II, 5.4; Ang II+Butyrate, 2.0). Principal Coordinates Analysis indicated each group in the input phylogenetic tree had significantly different microbial communities. LEfSe analysis showed that there were decreases of beneficial bacteria such as Lactobacillus and Bifidobacterium , and increases of Corynebacterium and Staphylococcus at the genus level of Ang II-HTN mice. Furthermore, inflammatory status of the gut as evidenced by the level of mucosal T cells in lamina propria from these groups showed that there was an increase of CCR2 + Th17 cells in Ang II-HTN mice, but not in butyrate co-treated mice (Control, 15.7%; Ang II, 28.4%; Ang II+Butyrate, 15%). Conclusions: These observations show that gut dysbiosis and the decrease of butyrate producing bacteria are associated with Ang II-HTN. Thus, supplementing butyrate in Ang II treated mice attenuated HTN and reversed gut dysbiosis, as well as normalizing the intestinal Th17. These data suggest butyrate producing bacteria could be considered as a novel probiotic therapy for hypertension.

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