MP06-04 INDUCIBLE PROSTATE LUMINAL EPITHELIAL CELL-SPECIFIC DELETION OF CDH1 INDUCES MURINE PROSTATIC HYPERPLASIA, INFLAMMATION, AND STROMAL FIBROSIS

ABSTRACTInflammation and proinflammatory cytokines have been implicated in the progression of benign prostatic hyperplasia (BPH). Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine. Our previous study found that MIF is highly expressed in BPH epithelium. It has been reported that there is a correlation between MIF and clinical BPH progression. However, whether MIF has an effect on BPH epithelial cells is not clear. The aim of this study was to explore whether MIF has a role in BPH. Our results showed that immunohistochemistry (IHC) showed that MIF is highly expressed in the epithelium and that MIF and PCNA expression levels are higher in BPH samples than in control. CCK8 and flow cytometry assays showed that recombinant human MIF (rMIF) promoted the proliferation of BPH-1 and PWR-1E cells, while ISO-1 partially reversed this effect on proliferation. JC-1 assays showed that rMIF inhibited the apoptosis of BPH-1 and PWR-1E cells, and ISO-1 could partially reverse this inhibition. Moreover, western blotting indicated that rMIF downregulated P53 and upregulated COX-2. Furthermore, MIF-induced proliferation could be inhibited by celecoxib in the CCK8 and flow cytometry assay. MIF-inhibited apoptosis could be partially reversed by celecoxib in the JC-1 assay. Western blotting showed that celecoxib could partially reverse MIF-induced COX-2 upregulation and P53 downregulation. Together, MIF is highly expressed in BPH epithelium. In vitro, MIF promoted BPH epithelial cell growth by regulating COX-2 and P53 signaling. Targeting MIF may provide a new option for the improved treatment of BPH in the future.

Download Full-text

Corrigendum to “Thymic epithelial cell-specific deletion of Jmjd6 reduces aire protein expression and exacerbates disease development in a mouse model of autoimmune diabetes” [Biochemical and Biophysical Research Communications 489/1 (2017) 8–13]

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2017.08.003 ◽

2017 ◽

Vol 491 (4) ◽

pp. 1126

Author(s):

Toyoshi Yanagihara ◽

Takahiro Tomino ◽

Takehito Uruno ◽

Yoshinori Fukui

Keyword(s):

Epithelial Cell ◽

Mouse Model ◽

Protein Expression ◽

Autoimmune Diabetes ◽

Thymic Epithelial Cell ◽

Disease Development ◽

Specific Deletion

Download Full-text

Differential growth factor responses of epithelial cell cultures derived from normal human prostate, benign prostatic hyperplasia, and primary prostate carcinoma

Journal of Cellular Physiology ◽

10.1002/(sici)1097-4652(199611)169:2<269::aid-jcp6>3.0.co;2-m ◽

1996 ◽

Vol 169 (2) ◽

pp. 269-280 ◽

Cited By ~ 20

Author(s):

D.P. Chopra ◽

D.J. Grignon ◽

A. Joiakim ◽

P.A. Mathieu ◽

A. Mohamed ◽

...

Keyword(s):

Benign Prostatic Hyperplasia ◽

Growth Factor ◽

Epithelial Cell ◽

Cell Cultures ◽

Prostate Carcinoma ◽

Prostatic Hyperplasia ◽

Human Prostate ◽

Differential Growth ◽

Epithelial Cell Cultures ◽

Normal Human

Download Full-text

Miz1, a Novel Target of ING4, Can Drive Prostate Luminal Epithelial Cell Differentiation

The Prostate ◽

10.1002/pros.23249 ◽

2016 ◽

Vol 77 (1) ◽

pp. 49-59 ◽

Cited By ~ 3

Author(s):

Penny L. Berger ◽

Mary E. Winn ◽

Cindy K. Miranti

Keyword(s):

Cell Differentiation ◽

Epithelial Cell ◽

Luminal Epithelial Cell ◽

Epithelial Cell Differentiation ◽

Novel Target

Download Full-text

Effect of Nonionizing Radiation on Progesterone Treatment in Endometrial Hyperplasia: An Experimental Rat Study

Gynecologic and Obstetric Investigation ◽

10.1159/000519195 ◽

2021 ◽

pp. 1-7

Author(s):

Mehmet Unsal ◽

Erdem Fadiloglu ◽

Burcin Celik ◽

Fatih Kilic ◽

Omer Lutfi Tapisiz

Keyword(s):

Epithelial Cell ◽

Endometrial Hyperplasia ◽

Animal Experiments ◽

Cell Length ◽

Female Rats ◽

Luminal Epithelial Cell ◽

Progesterone Treatment ◽

Nonionizing Radiation ◽

Group B ◽

Rat Study

Objectives: The aim of the study was to evaluate the negative effect of nonionizing radiation on the treatment of endometrial hyperplasia (EH) with oral progesterone. Design: Forty oophorectomized Wistar Albino female rats were included in this experimental rat study. Materials and Methods: The 4 groups were planned as follows: Group A; sham group; Group B; group receiving oral estradiol hemihydrate 4 mg/kg/day; Group C; 4 mg/kg/day oral estradiol hemihydrate followed with 1 mg/day medroxy progesterone acetate (MPA) and Group D; 4 mg/kg/day oral estradiol hemihydrate followed with 1 mg/day MPA with exposure to nonionizing radiation at 1800 mHz/3 h/day. After the experimental model, uterine horns were sampled and the preparations were evaluated for pathological parameters (glandular density, epithelial cell length, and luminal epithelial cell length) via light microscopy. Nonionizing radiation was created by a signal generator and a compatible mobile phone. Results: Estrogen was found to increase all parameters related to EH (p < 0.05). Progesterone treatment was found to decrease parameters related to EH (Group B vs. C; luminal epithelial cell length, glandular density, and epithelial length; 11.2 vs. 13.2 μm p = 0.007; 32.5 vs. 35.5, p = 0.068; and 219.9 μm vs. 285 µm, p < 0.001, respectively). Final analyses revealed reduced effectiveness of progesterone treatment in the rats exposed to nonionizing radiation (Group C vs. D); luminal epithelial cell length, glandular density, and epithelial length (11.2 μm vs. 13.5 μm, p = 0.179; 32.5 vs. 52, p < 0.001; and 219.9 μm vs. 374.1 μm, p = 0.001, respectively). Limitations: The limitations of our study are that the results of animal experiments may not be appropriate for direct adaptation to humans and the relatively low number of rats included in the study. Conclusion: Nonionizing radiation reduces the effect of progesterone in patients receiving treatment for EH.

Download Full-text