Characterization of protein kinase C in rat and human prostates

Garcia-Paramio, Pilar; Carmena, Marı́a J.; Román, F.; Colás, Begoña; Prieto, Juan Carlos

doi:10.1007/bf01150476

Cited by 5 publications

(3 citation statements)

References 33 publications

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“…Hence, E 2 may activate PKC activity in these cells by enhancing intracellular Ca 2ϩ . It should be noted that human BPH tissue reportedly contains TPA-but not Ca 2ϩ -activated PKC isoforms (25). Hence, in prostate epithelial cells, the effect of E 2 on melatonin receptors may be predominantly mediated by a PKC isoform(s) that is not directly regulated by Ca 2ϩ .…”

Section: Discussionmentioning

confidence: 99%

“…Activation of PKC by androgens has also been reported in some studies (22), but not in others (23,24). Human BPH tissue has been reported to contain phospholipid-dependent, phorbol 12-myristate 13-acetate (TPA)-activated, PKC isoforms (25). Hence, in the present study we investigated the possibility that the effects of E 2 on melatonin receptors and responses in prostate epithelial cells were mediated by PKC.…”

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confidence: 93%

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Interplay between Sex Steroids and Melatonin in Regulation of Human Benign Prostate Epithelial Cell Growth

Gilad¹,

Matzkin

Zisapel³

1997

The Journal of Clinical Endocrinology & Metabolism

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Human benign prostatic epithelial cells contain functional melatonin receptors that can suppress cell growth and viability. The development of benign prostatic hyperplasia in men is assumed to result from androgen-estrogen imbalance. These data indicate that 1) DHT and E 2 enhance prostate epithelial cells growth, but reduce cell growth when combined; 2) DHT extenuates the inhibitory effects of melatonin on epithelial cell growth; and 3) E 2 acts to inactivate melatonin receptors and consequently responses in human epithelial benign prostatic hyperplasia cells. This process is probably mediated by protein kinase C.Together, these results show an interplay between melatonin and sex steroids in the regulation of benign prostatic epithelial cell growth. (J Clin Endocrinol Metab 82: 2535-2541, 1997) B ENIGN PROSTATE hyperplasia (BPH) is a disease of men characterized by symptoms of urinary obstruction caused by abnormal, nonmalignant, prostate growth. The prevalence of BPH increases sharply in men over 50 yr of age (1). Age-related changes in circulating concentrations of testosterone and estrogen, their balance, or their receptors in the prostate have been postulated to play a role in the development of BPH in man (2-4). In dogs, induction of BPH required administration of both dihydrotestosterone (DHT) and 17␤-estradiol (E 2 ) (5). The presence of DHT and E 2 receptors was confirmed in BPH tissues (6), although most of the E 2 receptors were located in stromal cells (7,8).Melatonin, produced nocturnally by the pineal gland, plays a major role in the coordination of seasonal reproduction and pubertal development in mammals (9). The production of melatonin declines with age (9). We recently found by in vitro autoradiography, specific binding sites for In a number of studies, melatonin-binding sites in the brain as well as melatonin responses have been shown to depend on the presence of sex steroids. In the female rat hypothalamus and medulla-pons, ovariectomy produced a large estradiol-reversible decrease in low affinity [125 I]melatonin-binding sites (12). In parallel, the inhibitory effects of melatonin on dopamine release from the hypothalamus diminished in ovariectomized female rats and was reinstated by estradiol supplementation (13). In male hamsters maintained in a long day environment, castration produced a large testosterone-reversible decrease in low affinity

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 93%

Interplay between Sex Steroids and Melatonin in Regulation of Human Benign Prostate Epithelial Cell Growth

Gilad¹,

Matzkin

Zisapel³

1997

The Journal of Clinical Endocrinology & Metabolism

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“…Regarding isoforms being involved in PKCmediated contractions, previous publications using cultured stromal cells provided controversial findings. Thus, it has not only been reported that PKC activity in human tissues was calcium-independent (i.e., not imparted by PKCα, -β, or -γ) 41 but also that contractions by PKC-activating phorbol esters were susceptible to calcium channel blockers. 15 As our detection by RT-PCR was semiquantitative and based on isoform-specific primers, conclusive comparisons of expression levels cannot be performed between the different isoforms.…”

Section: Effects Of Gf109203x and Go6983 In The Presence Of L-name And Diclofenacmentioning

confidence: 99%

Inhibition of human prostate smooth muscle contraction by the inhibitors of protein kinase C, GF109203X, and Go6983

Huang

Liu

et al. 2021

The Prostate

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Introduction: Prostate smooth muscle contraction is promoted by receptor-induced activation of intracellular signaling pathways. The presumed involvement in etiology and medical treatment of lower urinary tract symptoms (LUTS) suggestive of benign prostatic hyperplasia (BPH) imparts a high clinical relevance to prostate smooth muscle contraction, which is contrasted by incomplete understanding at the molecular level. Involvement of protein kinase C (PKC) has been commonly assumed, but available studies were limited to nonhuman prostate smooth muscle or cell cultures.Here, we examined the effects of the PKC inhibitors Go6983 and GF109203x on contractions of human prostate tissues.Methods: Prostate tissues were obtained from radical prostatectomy. Contractions were induced by electric field stimulation (EFS), α 1 -adrenergic agonists (noradrenaline, phenylephrine, methoxamine), thromboxane A 2 analog U46619, endothelin-1, or calcium chloride in an organ bath.Results: GF109203X (500 nM) and Go6983 (300 nM) reduced EFS-, noradrenaline-, phenylephrine-, methoxamine-, and U46619-induced contractions of human prostate tissues, with maximum inhibitions approaching up to 55%. Using concentrations of 3 µM, GF109203X and Go6983 inhibited EFS-and noradrenaline-induced contractions, with similar effect sizes as 500 and 300 nM, respectively. Endothelin-1induced contractions were not inhibited by GF109203X, and to neglectable extent by Go6983. After depolarization in calcium-free solution, calcium chloride-induced concentration-dependent contractions, which were inhibited by GF109203X and Go6983.Conclusions: GF109203X and Go6983 inhibit neurogenic, α 1 -adrenergic, and thromboxane A 2 -induced smooth muscle contractions in the human prostate, suggesting a role of PKC for human prostate smooth muscle contraction. The inhibition may by be imparted by inhibition of calcium sensitivity.

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Regulation of the expression of protein kinase C isoenzymes in rat ventral prostate: effects of age, castration and flutamide treatment

et al. 2002

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Characterization of protein kinase C in rat and human prostates

Cited by 5 publications

References 33 publications

Interplay between Sex Steroids and Melatonin in Regulation of Human Benign Prostate Epithelial Cell Growth

Interplay between Sex Steroids and Melatonin in Regulation of Human Benign Prostate Epithelial Cell Growth

Inhibition of human prostate smooth muscle contraction by the inhibitors of protein kinase C, GF109203X, and Go6983

Regulation of the expression of protein kinase C isoenzymes in rat ventral prostate: effects of age, castration and flutamide treatment

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