Key Specifications Table
|Safety Information according to GHS|
|Material Size||40 assays|
|Reference overview||Application||Pub Med ID|
|In vivo efficacy of the histone deacetylase inhibitor suberoylanilide hydroxamic acid in combination with radiotherapy in a malignant rhabdoid tumor mouse model.|
Markus Thiemann,Susanne Oertel,Volker Ehemann,Wilko Weichert,Albrecht Stenzinger,Marc Bischof,Klaus-J Weber,Ramon Lopez Perez,Uwe Haberkorn,Andreas E Kulozik,Jürgen Debus,Peter E Huber,Claudia Battmann
Radiation oncology (London, England) 7 2012
Histone deacetylase inhibitors are promising new substances in cancer therapy and have also been shown to sensitize different tumor cells to irradiation (XRT). We explored the effect as well as the radiosensitizing properties of suberoylanilide hydroxamic acid (SAHA) in vivo in a malignant rhabdoid tumor (MRT) mouse model.
|Hepatic arterial reconstruction for orthotopic liver transplantation in the rat.|
Tomohide Hori,Lindsay B Gardner,Feng Chen,Ann-Marie T Baine,Toshiyuki Hata,Aimee R Herdt,Shinji Uemoto,Christopher B Eckman,Justin H Nguyen
The Journal of surgical research 178 2012
Orthotopic liver transplantation (OLT) models in rats have been investigated in many studies. The reconstruction of hepatic artery is required for reliable OLT and also requires advanced skills.
|Periostin is Down-regulated during Periodontal Inflammation.|
M Padial-Molina,S L Volk,A D Taut,W V Giannobile,H F Rios
Journal of dental research 91 2012
Periostin, a matricellular adapter protein highly expressed by periodontal ligament fibroblasts, is implicated in the maintenance of periodontal integrity, which is compromised during periodontal diseases. The aim of this study was to explore the influence of chronic periodontal inflammation on tissue periostin levels. Periodontal breakdown was induced in a pre-clinical ligature periodontal inflammatory disease model. Periodontal tissue specimens were harvested at baseline, 2 weeks, and 4 weeks and prepared for histologic, immunofluorescence, and micro-CT examination. Statistical analyses were conducted by Kruskal-Wallis, Mann-Whitney, and Spearman's tests. Periostin detection levels were reduced over time in response to the inflammatory process (1 ± 0.05; 0.67 ± 0.03; 0.31 ± 0.02; p < 0.001; baseline, 2, and 4 weeks, respectively). Simultaneously, alveolar bone loss increased from baseline to the 2- and 4-week time-points (0.40 ± 0.02 mm; 1.39 ± 0.08 mm; 1.33 ± 0.15 mm; p < 0.001), which was inversely correlated with the levels of periostin (ρ = -0.545; p < 0.001). In conclusion, periostin PDL tissue levels significantly decrease under chronic inflammatory response and correlate with the detrimental changes to the periodontium over time.
|Hepatitis B virus alters the antioxidant system in transgenic mice and sensitizes hepatocytes to Fas signaling.|
Wang, Q; Na, B; Ou, JH; Pulliam, L; Yen, TS
PloS one 7 e36818 2012
Hepatitis B virus (HBV) is a major etiological factor of hepatocellular carcinoma (HCC). However, the precise pathogenetic mechanisms linking HBV infection and HCC remain uncertain. It has been reported that decreased antioxidant enzyme activities are associated with severe liver injury and hepatocarcinogenesis in mouse models. It is unclear if HBV can interfere with the activities of antioxidant enzymes. We established a HBV transgenic mouse line, which spontaneously developed HCC at 2 years of age. We studied the activities of the antioxidant enzymes in the liver of the HBV transgenic mice. Our results showed that the antioxidant enzymes glutathione peroxidase and superoxide dismutase 2 were down-regulated in HBV transgenic mice and correlated with JNK activation. HBV enhanced the Fas-mediated activation of caspase 6, caspase 8 and JNK without enhancing the activation of caspase 3 and hepatocellular apoptosis. As a proper redox balance is important for maintaining cellular homeostasis, these effects of HBV on the host antioxidant system and Fas-signaling may play an important role in HBV-induced hepatocarcinogenesis.
|Osteocyte network; a negative regulatory system for bone mass augmented by the induction of rankl in osteoblasts and sost in osteocytes at unloading.|
Takeshi Moriishi,Ryo Fukuyama,Masako Ito,Toshihiro Miyazaki,Takafumi Maeno,Yosuke Kawai,Hisato Komori,Toshihisa Komori
PloS one 7 2012
Reduced mechanical stress is a major cause of osteoporosis in the elderly, and the osteocyte network, which comprises a communication system through processes and canaliculi throughout bone, is thought to be a mechanosensor and mechanotransduction system; however, the functions of osteocytes are still controversial and remain to be clarified. Unexpectedly, we found that overexpression of BCL2 in osteoblasts eventually caused osteocyte apoptosis. Osteoblast and osteoclast differentiation were unaffected by BCL2 transgene in vitro. However, the cortical bone mass increased due to enhanced osteoblast function and suppressed osteoclastogenesis at 4 months of age, when the frequency of TUNEL-positive lacunae reached 75%. In the unloaded condition, the trabecular bone mass decreased in both wild-type and BCL2 transgenic mice at 6 weeks of age, while it decreased due to impaired osteoblast function and enhanced osteoclastogenesis in wild-type mice but not in BCL2 transgenic mice at 4 months of age. Rankl and Opg were highly expressed in osteocytes, but Rankl expression in osteoblasts but not in osteocytes was increased at unloading in wild-type mice but not in BCL2 transgenic mice at 4 months of age. Sost was locally induced at unloading in wild-type mice but not in BCL2 transgenic mice, and the dissemination of Sost was severely interrupted in BCL2 transgenic mice, showing the severely impaired osteocyte network. These findings indicate that the osteocyte network is required for the upregulation of Rankl in osteoblasts and Sost in osteocytes in the unloaded condition. These findings suggest that the osteocyte network negatively regulate bone mass by inhibiting osteoblast function and activating osteoclastogenesis, and these functions are augmented in the unloaded condition at least partly through the upregulation of Rankl expression in osteoblasts and that of Sost in osteocytes, although it cannot be excluded that low BCL2 transgene expression in osteoblasts contributed to the enhanced osteoblast function.
|Nanoporous peptide particles for encapsulating and releasing neurotrophic factors in an animal model of neurodegeneration.|
Justin Tan,Yajun Wang,Xiaopei Yip,Fergal Glynn,Robert K Shepherd,Frank Caruso
Advanced materials (Deerfield Beach, Fla.) 24 2012
Neurotrophin-BDNF can be effectively encapsulated in nanoporous poly(L-glutamic acid) particles prepared via mesoporous silica templating. The loaded BDNF can be released in a sustained manner with retained biological activity. Animal experiments demonstrate the released BDNF can efficiently rescue the auditory neurons (as indicated by the arrows) in the cochlea of guinea pigs with sensorineural hearing loss.
|Thrombin-sensitive dual fluorescence imaging and therapeutic agent for detection and treatment of synovial inflammation in murine rheumatoid arthritis.|
Doris Gabriel,Norbert Lange,Veronique Chobaz-Peclat,Maria Fernanda Zuluaga,Robert Gurny,Hubert van den Bergh,Nathalie Busso
Journal of controlled release : official journal of the Controlled Release Society 163 2012
We have developed a thrombin-sensitive polymeric photosensitizer prodrug (T-PS) to selectively image and eradicate inflammatory lesions in rheumatoid arthritis (RA). Thrombin is a serine protease up-regulated in synovial tissues of rheumatoid arthritis (RA) patients. T-PS consists of a polymeric backbone, to which multiple photosensitizer (PS) units are tethered via short thrombin-cleavable peptide linkers. Fluorescence emission and phototoxicity of the prodrug are efficiently quenched due to the interaction of neighboring photosensitizer units. The prodrug is passively delivered to the inflammation site via the enhanced permeability and retention (EPR) effect. Subsequent site-selective proteolytic cleavage of the peptide linkers restores its photoactivity by increasing the mutual distance between PS. Whole animal imaging in murine collagen-induced arthritis, an experimental model of RA revealed a dose-dependent fluorescence increase in arthritic paws after systemic prodrug injection. In addition, administration of T-PS resulted in much higher fluorescence selectivity for arthritic joints as compared to the free PS. Irradiation of the arthritic joints induced light dose dependent phototoxic effects such as apoptosis, vascular damage and local hemorrhage. Long-term observations showed complete regression of the latter. Irradiated non-arthritic tissues or non-irradiated arthritic tissues showed no histological effects after photodynamic therapy with T-PS. This illustrates that T-PS can localize inflammatory lesions with excellent selectivity and induce apoptosis and vascular shut down after irradiation.
|Knockdown of clusterin sensitizes pancreatic cancer cells to gemcitabine chemotherapy by ERK1/2 inactivation.|
Yong Tang,Fenghua Liu,Chunning Zheng,Shaochuan Sun,Yingsheng Jiang
Journal of experimental & clinical cancer research : CR 31 2012
|Uncoupling of PI3K from ErbB3 impairs mammary gland development but does not impact on ErbB2-induced mammary tumorigenesis.|
Hicham Lahlou,Thomas Müller,Virginie Sanguin-Gendreau,Carmen Birchmeier,William J Muller
Cancer research 72 2012
The formation of ErbB2/ErbB3 heterodimers plays a critical role in ErbB2-mediated signaling in both normal mammary development and mammary tumor progression. Through 7 phosphoinositide 3-kinase (PI3K) phosphotyrosine-binding sites, ErbB3 is able to recruit PI3K and initiate the PI3K/AKT signaling pathway. To directly explore the importance of the ErbB3/PI3K pathway in mammary development and tumorigenesis, we generated a mouse model that carries a mutant ErbB3 allele lacking the seven known PI3K-binding sites (ErbB3(Δ85)). Mice homozygous for the ErbB3(Δ85) allele exhibited an initial early growth defect and a dramatic impairment of mammary epithelial outgrowth. Although homozygous adult mice eventually recovered from the growth defect, their mammary glands continued to manifest the mammary outgrowth and lactation defects throughout their adult life. Interestingly, despite the presence of a profound mammary gland defect, all of the female ErbB3Δ85 mice developed metastatic ErbB2-induced mammary tumors secondary to mammary epithelial expression of an activated ErbB2 oncogene capable of compensatory PI3K signaling from both EGF receptor and ErbB2. Our findings therefore indicate that, although ErbB3-associated PI3K activity is critical for mammary development, it is dispensable for ErbB2-induced mammary tumor progression.
|Reduced intestinal tumorigenesis in APCmin mice lacking melanin-concentrating hormone.|
Jutta M Nagel,Brenda M Geiger,Apostolos K A Karagiannis,Beatriz Gras-Miralles,David Horst,Robert M Najarian,Dimitrios C Ziogas,Xinhua Chen,Efi Kokkotou
PloS one 7 2012
Melanin-concentrating hormone (MCH) is an evolutionary conserved hypothalamic neuropeptide that in mammals primarily regulates appetite and energy balance. We have recently identified a novel role for MCH in intestinal inflammation by demonstrating attenuated experimental colitis in MCH deficient mice or wild type mice treated with an anti-MCH antibody. Therefore, targeting MCH has been proposed for the treatment of inflammatory bowel disease. Given the link between chronic intestinal inflammation and colorectal cancer, in the present study we sought to investigate whether blocking MCH might have effects on intestinal tumorigenesis that are independent of inflammation.
|Advancing cancer research: From hallmarks & biomarkers to tumor microenvironment progression|
|Comprehensive solutions for studying cell health - Life, death, and everything in between.|
|A Comparative Analysis of Human Embryonic Stem Cells Cultured in a Variety of Media Conditions|
|ApopTag® Peroxidase In Situ Apoptosis Detection Kit|
|ApopTag® Peroxidase In Situ Apoptosis Detection Kit|