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In Vitro Cell Dev Biol Anim. 2002 Mar;38(3):165-72.
EPN: a novel epithelial cell line derived from human prostate tissue.

Sinisi AA, Chieffi P, Pasquali D, Kisslinger A, Staibano S, Bellastella A, Tramontano D.

Dipartimento di Internistica Clinica e Sperimentale, Seconda Universita di Napoli, Italy. antonio.sinisnina2.it

This work reports the isolation and characterization of a line of human, nontransformed and differentiated prostate epithelial cells (EPN) in continuous culture. Primary cultures of epithelial prostate cells were set up using normal tissue isolated from a prostate sample collected after radical prostatectomy for cancer. After 70 passages, EPN cells did not undergo "Hayflike crisis" and were free of fibroblast contamination and were thus subcloned and characterized. EPN cells in culture, as prostate epithelial cells in vivo, express high-molecular weight cytokeratin and Pyk2, whereas they do not express desmin. EPN cells are nontransformed because they do not form colonies in semisolid medium and do not form tumors once injected into nude mice. EPN cells express the functional androgen receptor, which can mediate the mitogenic activity of testosterone. Finally, clonal production of the prostate-specific antigen could be detected in EPN cells. The availability of a line of epithelial nontransformed prostate cell in culture will be useful in investigating the complex process regulating normal prostate physiology as well as the development and progression of prostate tumors.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12026165&dopt=Abstract

Med Hypotheses. 2002 Apr;58(4):261-3.
Hormone-induced aberrations in electromagnetic adhesion signaling as a developmental factor of androgenetic alopecia.

Matilainen VA, Keinanen-Kiukaanniemi SM.

Department of Public Health Science and General Practice, University of Oulu, Finland.

In androgenetic alopecia, overactivation of the androgen hormone cascade in genetically predisposed persons leads to miniaturization of the dermal papilla of the hair follicle and to reduction in the number of papilla cells in the scalp, but the mechanisms explaining this miniaturization have remained unclear. According to our hypothesis, the increase of dihydrotestosterone (DHT) production in the overactive androgen state inhibits cell mitosis in the dermal papilla and contributes to the induction of programmed cell death (apoptosis). Normally, DNA molecules have a negative charge, which doubles in every cell mitosis. In the catagen and telogen phases, the sulphur-rich hair moves upwards, dehydrates and develops an increasing positive charge. In a normal hair-growth cycle, the epithelial column shortens and the secondary germ is formed and it invaginates the dermal papilla by electromagnetic attraction. In the mitotic inhibition state induced by DHT, the negative charge decreases, leading to a weakening of the electromagnetic adhesion forces and weaker electrical attraction between the undifferentiated germ cells and the dermal papilla. Insulin resistance has an additional pathogenic role in the excessive miniaturization of the hair follicle. The vasoactive substances associated with endothelial dysfunction in insulin resistance induce microcirculatory disturbance, perifollicular vasoconstriction and stimulation of smooth muscle cell proliferation in the vascular wall. This leads to microvascular insufficiency and local tissue hypoxia and progressive miniaturization of hair follicles. 2002 Elsevier Science Ltd. All rights reserved.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12027516&dopt=Abstract

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A differential display method was used to study genes the expression of which is altered during growth inhibition induced by medroxyprogesterone acetate (MPA). A transcript of G-protein-coupled receptor 30 (GPR30) was upregulated by MPA in estrogen-treated MCF-7 breast cancer cells. Northern-blot analysis showed a progestin-specific primary target gene, which was enhanced by progesterone and different progestins, but not by dihydrotestosterone or dexamethasone, and which was abrogated by antiprogestin RU486. The dose-dependent and time-dependent increase in GPR30 mRNA expression correlated with MPA-induced growth inhibition in MCF-7 cells. Additionally, GPR30 upregulation by progestin correlated with growth inhibition when a comparison was made between different breast cancer cell lines. The ERK1/ERK2 pathway is capable of inducing progesterone receptor-dependent and ligand-dependent transcription. Thus we sought to establish whether different MAPK pathway inhibitors affect progestin-induced GPR30 mRNA regulation. The regulation of GPR30 was independent of ERK pathway activation, but the p38 pathway inhibitor induced GPR30 expression, which suggested a potential gene regulation pathway. These data demonstrate a new progestin target gene, the expression of which correlates with growth inhibition.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12027886&dopt=Abstract

J Am Geriatr Soc. 2002 May;50(5):884-8.
Effects of resistance training on insulin-like growth factor and its binding proteins in men and women aged 60 to 85.

Borst SE, Vincent KR, Lowenthal DT, Braith RW.

Department of Exercise and Sport Sciences, University of Florida, Gainesville, Florida, USA. sborsharmacology.ufl.edu

OBJECTIVES: We have reported that resistance training (RT) elevates insulin-like growth factor (IGF-I) in healthy young adults. Our goals were to determine whether RT produces a similar effect in the healthy older persons and to determine the effects of low- versus high-intensity RT on hormonal status. SETTING: Center for Exercise Science, University of Florida, Gainesville. PARTICIPANTS: Sixty-two men and women (mean age = 68.1). INTERVENTION: A 6-month, 3-day/week program of low-intensity RT (LEX), high-intensity RT (HEX), or no exercise (CON). MEASUREMENTS: Before and after training, blood was drawn for hormone analysis. IGF-I, IGF binding protein-1 (IGFBP-1), and IGFBP-3 were measured at rest. Testosterone and cortisol were measured at rest and immediately after exercise. RESULTS: RT caused significant increases in 1-repetition maximum (1RM) strength and peak oxygen consumption (V02peak), which we have reported separately. Currently, we report that RT had no effect on the resting serum concentrations of IGF-I, IGFBP-1, IGFBP-3, testosterone, or cortisol. Acute resistance exercise caused no change in circulating testosterone in men or women but did cause a significant elevation of cortisol in the HEX group. This increase in cortisol was blunted as a result of training. CONCLUSIONS: We conclude that the increases in strength and endurance caused by RT were not mediated by increases in circulating IGF-I, IGFBPs, or testosterone.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12028176&dopt=Abstract

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