Fluorescent proteins in animal cells for process development: Optimization of sodium butyrate treatment as an example

2002 ◽  
Vol 77 (5) ◽  
pp. 528-537 ◽  
Author(s):  
Lisa Hunt ◽  
Pascal Batard ◽  
Martin Jordan ◽  
Florian M. Wurm
Keyword(s):  
Sodium Butyrate ◽  
Process Development ◽  
Fluorescent Proteins ◽  
Animal Cells ◽  
Butyrate Treatment

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.

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.

scholarly journals In Vivo Changes in the Patterns of Chromatin Structure Associated with the Latent Herpes Simplex Virus Type 1 Genome in Mouse Trigeminal Ganglia Can Be Detected at Early Times after Butyrate Treatment

2007 ◽  
Vol 81 (23) ◽  
pp. 13248-13253 ◽  
Author(s):  
Donna M. Neumann ◽  
Partha S. Bhattacharjee ◽  
Nicole V. Giordani ◽  
David C. Bloom ◽  
James M. Hill
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Sodium Butyrate ◽  
Herpes Simplex Virus Type ◽  
Trigeminal Ganglia ◽  
Butyrate Treatment ◽  
Simplex Virus ◽  
Hsv 1

ABSTRACT During herpes simplex virus type 1 (HSV-1) latency in mouse dorsal root ganglia (DRG), chromatin associated with the latency-associated transcript (LAT) region of the viral genome is hyperacetylated at lysines 9 and 14 of histone 3 [H3(K9, K14)], while lytic genes are hypoacetylated. Explanted DRG exhibit a pattern of deacetylation of the LAT enhancer followed by acetylation of the ICP0 promoter at early times postexplant. Recently, we reported that sodium butyrate induced in vivo reactivation of HSV-1 in latent mice. In this study, we assessed the effect of sodium butyrate on the chromatin patterns of latent and butyrate-treated mouse trigeminal ganglia (TG) via chromatin immunoprecipitation (ChIP). We detected deacetylation of acetyl H3(K9, K14) of the LAT promoter and LAT enhancer regions as early as 0.5 h post-butyrate treatment, and this deacetylation corresponded to an increase in the acetylation of the lytic promoters ICP0 and ICP4 at 0.5 h and 1 h post-butyrate treatment, respectively. This is the first study to combine in vivo reactivation with the examination of the HSV-1 genome through ChIP assays at early times after the introduction of in vivo reactivation stimuli.

Apoptosis induced by sodium butyrate treatment increases immunogenicity of a rat colon tumor cell line

APOPTOSIS ◽  
1997 ◽  
Vol 2 (4) ◽  
pp. 403-412 ◽  
Author(s):  
O. Boisteau ◽  
F. Gautier ◽  
S. Cordel ◽  
F. Henry ◽  
J. Harb ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Line ◽  
Sodium Butyrate ◽  
Tumor Cell Line ◽  
Rat Colon ◽  
Colon Tumor ◽  
Butyrate Treatment ◽  
Colon Tumor Cell

scholarly journals Interleukin-2/sodium butyrate treatment cures rats bearing liver tumors after acquired 5-fluorouracil resistance

1998 ◽  
Vol 78 (6) ◽  
pp. 735-739 ◽  
Author(s):  
Sandrine Cordel ◽  
Benoît Dupas ◽  
Jean-Yves Douillard ◽  
Khaled Meflah
Keyword(s):  
Sodium Butyrate ◽  
Liver Tumors ◽  
Interleukin 2 ◽  
Butyrate Treatment

scholarly journals Reversible transcriptional activation of mdr1 by sodium butyrate treatment of human colon cancer cells.

1994 ◽  
Vol 269 (14) ◽  
pp. 10739-10746
Author(s):  
C.S. Morrow ◽  
M. Nakagawa ◽  
M.E. Goldsmith ◽  
M.J. Madden ◽  
K.H. Cowan
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Sodium Butyrate ◽  
Transcriptional Activation ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Butyrate Treatment ◽  
Human Colon Cancer Cells
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