With temperature reduction of harvested cells allowed for constant cell production
With temperature reduction of harvested cells allowed for constant cell production in exponential phase. On the other hand, storage of intact cells was limited probably due to protease action. The 150 mL batch cultivation was scaled up to 5 L in a stirred bench-top bioreactor (Biostat B, Sartorius Stedim Biotech GmbH).Author details 1 Institute of Bioprocess and Biosystems Engineering, Hamburg University of Technology, Hamburg, D-21073, Germany. 2Cancer Center Hamburg, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, D-20246, Germany. Published: 22 November 2011 Reference 1. Balabanov S, et al: Hypusination of eukaryotic initiation factor 5A (eIF5A): a novel therapeutic target in BCR-ABL-positive leukemias identified by a proteomics approach. Blood 2007, 109(4).doi:10.1186/1753-6561-5-S8-P48 Cite this article as: Schaletzky et al.: Cultivation strategies of a BA/F3 cell line for fundamental cell research. BMC Proceedings 2011 5(Suppl 8):P48.Submit your next manuscript to BioMed Central and take full advantage of:?Convenient online submission ?Thorough peer review ?No space constraints or color figure charges ?Immediate publication on acceptance ?Inclusion in PubMed, CAS, Scopus and Google Scholar ?Research which is freely available for redistributionSubmit your manuscript at www.biomedcentral.com/submit
Nural-Guvener et al. Fibrogenesis Tissue Repair 2014, 7:10 http://www.fibrogenesis.com/content/7/1/RESEARCHOpen AccessHDAC class I inhibitor, Mocetinostat, (R)-K-13675MedChemExpress Pemafibrate reverses cardiac fibrosis in heart failure and diminishes CD90+ cardiac myofibroblast activationHikmet F Nural-Guvener1, Luidmila Zakharova1, James Nimlos1, Snjezana Popovic1, Diego Mastroeni2 and Mohamed A Gaballa1*AbstractBackground: Interstitial fibrosis and fibrotic scar formation contribute to cardiac remodeling and loss of cardiac function in myocardial infarction (MI) and heart failure. Recent studies PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/27107493 showed that histone deacetylase (HDAC) inhibitors retard fibrosis formation in acute MI settings. However, it is unknown whether HDAC inhibition can reverse cardiac fibrosis in ischemic heart failure. In addition, specific HDAC isoforms involved in cardiac fibrosis and myofibroblast activation are not well defined. Thus, the purpose of this study is to determine the effects of selective class I HDAC inhibition on cardiac fibroblasts activation and cardiac fibrosis in a congestive heart failure (CHF) model secondary to MI. Methods: MI was created by left anterior descending (LAD) coronary artery occlusion. Class I HDACs were selectively inhibited via Mocetinostat in CD90+ fibroblasts isolated from atrial and ventricular heart tissue in vitro. In vivo, Class I HDACs were inhibited in 3 weeks post MI rats by injecting Mocetinostat for the duration of 3 weeks. Cardiac function and heart tissue were analyzed at 6 weeks post MI. Results: In sham hearts, HDAC1 and HDAC2 displayed differential expression patterns where HDAC1 mainly expressed in cardiac fibroblast and HDAC2 in cardiomyocytes. On the other hand, we showed that HDAC1 and 2 were upregulated in CHF hearts, and were found to co-localize with CD90+ cardiac fibroblasts. In vivo treatment of CHF animals with Mocetinostat improved left ventricle end diastolic pressure and dp/dt max and decreased the total collagen amount. In vitro treatment of CD90+ cells with Mocetinostat reversed myofibroblast phenotype as indicated by a decrease in -Smooth muscle actin (-SMA), Collagen III, and Matrix metalloproteinase-2 (MMP2). Furt.
