110-OR: Generation of a Novel Mouse Model to Study ß-Cell Proliferation

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 110-OR
Author(s):  
SHINSUKE TOKUMOTO ◽  
DAISUKE YABE ◽  
HISATO TATSUOKA ◽  
RYOTA USUI ◽  
MUHAMMAD FAUZI ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Mouse Model

scholarly journals Miquelianin Inhibits Allergic Responses in Mice by Suppressing CD4+ T Cell Proliferation

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1120
Author(s):  
Dae Woon Choi ◽  
Sun Young Jung ◽  
Gun-Dong Kim ◽  
So-Young Lee ◽  
Hee Soon Shin
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Mouse Model ◽  
Immune Responses ◽  
Reactive Oxygen Species Generation ◽  
Allergic Diseases ◽  
Cd4 T Cell ◽  
Th2 Cells ◽  
T Cell Proliferation ◽  
Heme Oxygenase 1

Allergic diseases, including atopic dermatitis (AD), induce type 2 helper T (Th2) cell-dominant immune responses. Miquelianin (quercetin 3-O-glucuronide, MQL) is an active compound in Rosae multiflorae fructus extract with anti-allergic properties. Here, we investigate the anti-allergic effects of MQL in an ovalbumin (OVA)-induced Th2-dominant mouse model and the associated mechanisms. Oral MQL suppressed cytokine and IL-2 production and proliferation of Th2 cells and upregulated heme oxygenase-1 (HO-1) in splenocytes. Ex vivo MQL suppressed Th1- and Th2-related immune responses by inhibiting CD4+ T cell proliferation, and upregulated HO-1 in CD4+ T cells by activating C-Raf–ERK1/2–Nrf2 pathway via induction of reactive oxygen species generation. In a trimellitic anhydride-induced AD-like mouse model, both topical and oral MQL ameliorated AD symptoms by suppressing Th2 immune responses. Our results suggest that MQL is a potential therapeutic agent for CD4+ T cell-mediated diseases, including allergic diseases.

scholarly journals Impaired CD4+T-cell proliferation and effector function correlates with repressive histone methylation events in a mouse model of severe sepsis

2010 ◽  
Vol 40 (4) ◽  
pp. 998-1010 ◽  
Author(s):  
William F. Carson ◽  
Karen A. Cavassani ◽  
Toshihiro Ito ◽  
Matthew Schaller ◽  
Makoto Ishii ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Severe Sepsis ◽  
T Cell ◽  
Mouse Model ◽  
Histone Methylation ◽  
Effector Function ◽  
Cd4 T Cell ◽  
T Cell Proliferation

scholarly journals Antrodia camphorataGrown on Germinated Brown Rice Suppresses Melanoma Cell Proliferation by Inducing Apoptosis and Cell Differentiation and Tumor Growth

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Minjung Song ◽  
Dong Ki Park ◽  
Hye-Jin Park
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Mouse Model ◽  
Melanoma Cell ◽  
Anticancer Agent ◽  
Brown Rice ◽  
B16f10 Melanoma ◽  
Germinated Brown Rice ◽  
Melanoma Cell Proliferation ◽  
Etoac Fraction

Antrodia camphoratagrown on germinated brown rice (CBR) was prepared to suppress melanoma development. CBR extracts were divided into hexane, EtOAc, BuOH, and water fractions. Among all the fractions, EtOAc fraction showed the best suppressive effect on B16F10 melanoma cell proliferation by CCK-8 assay. It also showed the increased cell death and the changed cellular morphology after CBR treatment. Annexin V-FITC/PI, flow cytometry, and western blotting were performed to elucidate anticancer activity of CBR. The results showed that CBR induced p53-mediated apoptotic cell death of B16F10. CBR EtOAc treatment increased melanin content and melanogenesis-related proteins of MITF and TRP-1 expressions, which supports its anticancer activity. Its potential as an anticancer agent was further investigated in tumor-xenografted mouse model. In melanoma-xenografted mouse model, melanoma tumor growth was significantly suppressed under CBR EtOAc fraction treatment. HPLC analysis of CBR extract showed peak of adenosine. In conclusion, CBR extracts notably inhibited B16F10 melanoma cell proliferation through the p53-mediated apoptosis induction and increased melanogenesis. These findings suggest that CBR EtOAc fraction can act as an effective anticancer agent to treat melanoma.

In Vivo Fluorescence Microendoscopic Monitoring of Stent-Induced Fibroblast Cell Proliferation in an Esophageal Mouse Model

2018 ◽  
Vol 29 (12) ◽  
pp. 1756-1763
Author(s):  
Eun Jung Jun ◽  
Ho-Young Song ◽  
Jung-Hoon Park ◽  
Yoon Sung Bae ◽  
Bjorn Paulson ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Mouse Model ◽  
Fibroblast Cell ◽  
In Vivo Fluorescence

scholarly journals MicroRNAs 106b and 222 Improve Hyperglycemia in a Mouse Model of Insulin-Deficient Diabetes via Pancreatic β-Cell Proliferation

EBioMedicine ◽  
2017 ◽  
Vol 15 ◽  
pp. 163-172 ◽  
Author(s):  
Sohei Tsukita ◽  
Tetsuya Yamada ◽  
Kei Takahashi ◽  
Yuichiro Munakata ◽  
Shinichiro Hosaka ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Mouse Model ◽  
Pancreatic Β Cell ◽  
Β Cell

scholarly journals 17β-Estradiol Promotes Islet Cell Proliferation in a Partial Pancreatectomy Mouse Model

2017 ◽  
Vol 1 (7) ◽  
pp. 965-979 ◽  
Author(s):  
Tingting Wu ◽  
Jinyong Xu ◽  
Shengchun Xu ◽  
Lianzhong Wu ◽  
Youyu Zhu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Mouse Model ◽  
Islet Cell ◽  
Partial Pancreatectomy ◽  
17Β Estradiol

Small molecule tolfenamic acid inhibits PC-3 cell proliferation and invasion in vitro, and tumor growth in orthotopic mouse model for prostate cancer

The Prostate ◽  
2012 ◽  
Vol 72 (15) ◽  
pp. 1648-1658 ◽  
Author(s):  
Umesh T. Sankpal ◽  
Maen Abdelrahim ◽  
Sarah F. Connelly ◽  
Chris M. Lee ◽  
Rafael Madero-Visbal ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Mouse Model ◽  
Tumor Growth ◽  
Small Molecule ◽  
Tolfenamic Acid ◽  
Orthotopic Mouse Model ◽  
Proliferation And Invasion

Overcoming resistance to antiandrogens with a TGF-β RI inhibitor in preclinical mouse model of PCa.

2018 ◽  
Vol 36 (6_suppl) ◽  
pp. 288-288
Author(s):  
Channing Judith Paller ◽  
Hong Pu ◽  
Diane Begemann ◽  
Mary Nakazawa ◽  
Natasha Kyprianou
Keyword(s):  
Cell Proliferation ◽  
Mouse Model ◽  
Western Blot ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Epithelial Mesenchymal Transition ◽  
Combined Treatment ◽  
Prostate Tumor ◽  
Metastatic Progression ◽  
Mesenchymal Transition

288 Background: Epithelial-mesenchymal transition (EMT) is a significant contributor to PCa metastatic progression and therapeutic resistance in patients treated with the androgen receptor (AR) directed therapies. We previously demonstrated that aberrant TGF-β signaling accelerates prostate tumor progression in the TRAMP mouse model of tumorigenesis via selective effects on EMT. Methods: We hypothesize that the combination of the TGF-β receptor inhibitor, galunisertib (G), and enzalutamide (E) will perturb the interactive signaling between TGF-β and AR signaling affecting the phenotypic landscape of EMT. This perturbation may be exploited in our mouse model, towards enhanced anti-tumor efficacy in advanced castration-resistant PCa (CRPC). We treated 2-week old mice for two weeks with the G (75mg/kg) and/or E (30mg/kg) in combination and as single agents. Results: Treatment with G alone or in combination with E resulted in a significant reduction in prostate tumor weight without affecting total body weight. Immunohistochemical (IHC) and Western blot analysis showed that, while treatment with the G alone led to increased apoptosis and decreased cell proliferation, combination of G and E had significantly higher efficacy in inducing apoptosis and inhibiting cell proliferation than either E or G alone. As expected treatment with the G decreased the levels of nuclear Smad4 protein; the combination of G and E further decreased nuclear Smad4 expression. Furthermore the combination of G and E reversed phenotypic EMT to MET (mesenchymal-epithelial-transition), as assessed by the increase in E-cadherin among the prostate tumor cell populations. IHC and Western blot analysis also revealed that the combined treatment of G and E led to a significant decrease in nuclear AR levels compared to E-only-treated or vehicle-control tumors. Conclusions: These results provide significant insights as to the therapeutic impact of G to effectively impair the TGF-β signaling and overcome resistance of PCa patients to E by reversing EMT to potentially sensitize tumors to the antiandrogen effect. This study has major translational relevance; the combination of G and E may lead to synergistic anti-tumor impact in patients with CRPC.

scholarly journals Mathematical Modeling of Tumor Cell Proliferation Kinetics and Label Retention in a Mouse Model of Lung Cancer

2013 ◽  
Vol 73 (12) ◽  
pp. 3525-3533 ◽  
Author(s):  
Yanyan Zheng ◽  
Helen Moore ◽  
Alexandra Piryatinska ◽  
Trinidad Solis ◽  
E. Alejandro Sweet-Cordero
Keyword(s):  
Mathematical Modeling ◽  
Lung Cancer ◽  
Cell Proliferation ◽  
Mouse Model ◽  
Tumor Cell ◽  
Tumor Cell Proliferation ◽  
Proliferation Kinetics
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