- Effect of Progesterone on COX-2 Expression and Proliferation of Prostate Stromal Cell.
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Soo Ryun Jung, Sung Han Kim, E Hwa Choi, Ji Eun Park, Eun Mi Jeon, Young Jin Kang, Kwang Youn Lee, Hyoung Chul Choi
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Yeungnam Univ J Med. 2006;23(1):62-70. Published online June 30, 2006
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DOI: https://doi.org/10.12701/yujm.2006.23.1.62
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 Abstract
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- BACKGROUND
Benign prostatic hyperplasia (BPH) is the most common benign tumor in older men; the etiology of this disease remains poorly understood. Testosterone and dihydrotestosterone (DHT) both act as androgen via a single androgen receptor. Testosterone is converted to DHT by 5alpha-reductase in prostatic stromal cells. Progesterone has been reported to inhibit DHT conversion; howevwe, its effect on prostatic stromal cells remains to be elucidated. MATERILAS AND METHODS: In this experiment, we investigated the effect of progesterone on androgen receptor expression induced by DHT. We also tested the effect of progesterone on cyclooxygenase-2 (COX-2) expression, as well as prostate stromal cell proliferation using the cell count kit-8. RESULTS: Progesterone did not cause an increase of prostate stromal cell proliferation. The mRNA expression of the androgen receptor and COX-2 were not changed by progesterone; the expressions of androgen receptor and COX-2 proteins were decreased by progesterone in prostate stromal cells. CONCLUSION: These results suggest that in prostate stromal cells, progesterone decreases androgen receptor protein expression, which results in decrement of COX-2 protein expression. This effect might be mediated by post-transcriptional regulation.
- Effects of Cyclooxygenase Inhibitors on Vascular Reactivity and Alterations of Cyclooxygenase Expression.
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Ki Young Lee, Jin Woo Park, Eun A Eum, Young Jin Kang, Kwang Youn Lee, Hyoung Chul Choi
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Yeungnam Univ J Med. 2006;23(1):36-44. Published online June 30, 2006
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DOI: https://doi.org/10.12701/yujm.2006.23.1.36
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Abstract
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- BACKGROUND
There is controversy regarding whether COX-2 specific inhibitors are associated with elevation of blood pressure. We compared the effects of aspirin, indomethacin, and celecoxib for vascular reactivity induced by phenylephrine. We also tested the effects of indomethacin and NO donor on COX-1 and COX-2 protein expression, as well as nitrite production in culture medium of vascular smooth muscle cells. MATERILAS AND METHODS: In this experiment, we used the isometric tension study for vascular reactivity. After 45 minutes of pretreatment with aspirin, indomethacin, celecoxib, and phenylephrine induced contractions were tested. COX-1 and COX-2 protein expressions were analyzed by Western blot and nitrite production by the Griess reaction. RESULTS: Although celecoxib pretreatment caused enhanced arterial contraction, aspirin pretreatment induced more potent arterial contraction than celecoxib in the isometric tension study of rabbit femoral artery. COX-1 protein expression was unchanged by indomethacin, SNP and NOR-3; COX-2 protein expression was increased by the addition of indomethacin, SNP, and NOR-3. Especially, NOR-3, a NO donor, significantly increased COX-2 protein expression with unstimulated conditions as well as LPS stimulation. Induction of nitrite production was higher with NOR-3 treatment than SNP treatment with LPS stimulation. CONCLUSION: These results suggest that aspirin caused more potent vascular contraction than celecoxib and indomethacin. COX-2 expression in VSMC depended on the types of NO donor and LPS stimulation.
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Yeungnam University College of Medicine
