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

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

Regulation of Islet  -Cell Proliferation by Prolactin in Rat Islets

Diabetes ◽  
1994 ◽  
Vol 43 (2) ◽  
pp. 263-273 ◽  
Author(s):  
T. C. Brelje ◽  
J. A. Parsons ◽  
R. L. Sorenson
Keyword(s):  
Cell Proliferation ◽  
Islet Cell ◽  
Rat Islets

scholarly journals A New Anti-Estrogen Discovery Platform Identifies FDA-Approved Imidazole Anti-Fungal Drugs as Bioactive Compounds against ERα Expressing Breast Cancer Cells

2021 ◽  
Vol 22 (6) ◽  
pp. 2915
Author(s):  
Manuela Cipolletti ◽  
Stefania Bartoloni ◽  
Claudia Busonero ◽  
Martina Parente ◽  
Stefano Leone ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Bioactive Compounds ◽  
Estrogenic Activity ◽  
Estrogen Receptor Α ◽  
Breast Cancers ◽  
Cellular Models ◽  
Cancer Models ◽  
17Β Estradiol ◽  
Approved Drugs ◽  
Anti Fungal

17β-estradiol (E2) exerts its physiological effects through the estrogen receptor α (i.e., ERα). The E2:ERα signaling allows the regulation of cell proliferation. Indeed, E2 sustains the progression of ERα positive (ERα+) breast cancers (BCs). The presence of ERα at the BC diagnosis drives their therapeutic treatment with the endocrine therapy (ET), which restrains BC progression. Nonetheless, many patients develop metastatic BCs (MBC) for which a treatment is not available. Consequently, the actual challenge is to complement the drugs available to fight ERα+ primary and MBC. Here we exploited a novel anti-estrogen discovery platform to identify new Food and Drug Administration (FDA)-approved drugs inhibiting E2:ERα signaling to cell proliferation in cellular models of primary and MBC cells. We report that the anti-fungal drugs clotrimazole (Clo) and fenticonazole (Fenti) induce ERα degradation and prevent ERα transcriptional signaling and proliferation in cells modeling primary and metastatic BC. The anti-proliferative effects of Clo and Fenti occur also in 3D cancer models (i.e., tumor spheroids) and in a synergic manner with the CDK4/CDK6 inhibitors palbociclib and abemaciclib. Therefore, Clo and Fenti behave as “anti-estrogens”-like drugs. Remarkably, the present “anti-estrogen” discovery platform represents a valuable method to rapidly identify bioactive compounds with anti-estrogenic activity.

Combinatory effects of PBDEs and 17β-estradiol on MCF-7 cell proliferation and apoptosis

2011 ◽  
Vol 63 (1) ◽  
pp. 189-194 ◽  
Author(s):  
Kwiecińska Patrycja ◽  
Wróbel Anna ◽  
Ewa Ł. Gregoraszczuk
Keyword(s):  
Cell Proliferation ◽  
Proliferation And Apoptosis ◽  
17Β Estradiol ◽  
Mcf 7

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.

Hedgehog Inhibition With Cyclopamine Represses Tumor Growth and Prolongs Survival in a Transgenic Mouse Model of Islet Cell Tumors

2011 ◽  
Vol 253 (3) ◽  
pp. 546-552 ◽  
Author(s):  
Volker Fendrich ◽  
Johannes Rehm ◽  
Jens Waldmann ◽  
Malte Buchholz ◽  
Gerhard Christofori ◽  
...  
Keyword(s):  
Mouse Model ◽  
Tumor Growth ◽  
Transgenic Mouse ◽  
Islet Cell ◽  
Transgenic Mouse Model ◽  
Islet Cell Tumors
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