Prostatitis in the Rat

Müntzing, Jonas; Sufrin, Gerald; Murphy, Gerald P.

doi:10.3109/00365597909179995

Cited by 39 publications

(20 citation statements)

References 11 publications

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“…Models evaluating spontaneous, age-and genetically dependent prostatitis [7,8], and bacterial prostatitis [5] were followed by models demonstrating the autoimmune characteristics of the inflammation [9,10]. The model described in this paper examined the pathogenesis of inflammation from a mucosal surface perspective.…”

Section: Discussionmentioning

confidence: 99%

Rat model of experimentally induced abacterial prostatitis

et al. 2000

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Section: Discussionmentioning

confidence: 99%

Rat model of experimentally induced abacterial prostatitis

et al. 2000

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“…65 By the age of 20 weeks, 88% of Copenhagen rats develop spontaneous lateral prostatic lobe inflammation; in contrast, prostatitis develops in only 6% of (Copenhagen Â Fischer) 344 males. 66 Naslund et al 67 reported that 12-week-old Lewis, Wistar, and Sprague-Dawley males had a 30, 0 and 0% incidence of spontaneous lateral prostate inflammation, respectively; the incidence of this lobe specific nonbacterial prostate inflammation was increased considerably in older (40-to 52-week-old) Lewis (72%) and Wistar (27%) males, but not in Sprague-Dawley rats (0%).…”

Section: Rat Models Of Prostatitismentioning

confidence: 99%

Experimental rodent models of prostatitis: limitations and potential

Vykhovanets

Resnick

MacLennan

et al. 2007

Prostate Cancer Prostatic Dis

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Prostatitis is a polyetiological inflammation of the prostate gland in men characterized by pelvic pain, irritative voiding symptoms, and sexual dysfunction. Histologically prostatitis is characterized by poly-and mononuclear cell infiltrates (neutrophils, lymphocytes, macrophages and plasma cells) in the stromal connective tissue around the acini or ducts. Prostatitis is an important worldwide health problem in men. The pathogenesis and diagnostic criteria for the condition are obscure, with the result that the development of management programs for this condition has been hindered. Animal model(s) might be useful in elucidating mechanisms involved in the molecular pathogenesis of chronic nonbacterial prostatitis and chronic pelvic pain syndrome. Given that prostatitis might have a multifactorial etiology, several animal models with unique features may prove helpful. This review examines a number of experimental rodent models of prostatitis and evaluates their advantages and limitations.

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“…By employing tissuerecombination techniques, it has been demonstrated that the growth and differentiation of normal epithelium is regulated either inductively or permissively by neighboring mesenchymal components (5,6). Studies of stromal-epithelial interaction in the prostate gland revealed that mesenchyme isolated from the fetal urogenital sinus (7,8) but not from the prostate of newborns (9) or adults (10) can stimulate proliferation of well-differentiated adult epithelium. Mesenchymal mediation of sex steroid action on glandular epithelium has also been demonstrated.…”

mentioning

confidence: 99%

Fibroblast-mediated acceleration of human epithelial tumor growth in vivo.

Camps

Chang

Hsu

et al. 1990

Proc. Natl. Acad. Sci. U.S.A.

363

230

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Transformed fibroblasts coinoculated with epithelial cells accelerated the growth and shortened the latency period of human epithelial tumors in athymic mice. Addition of NbF-1 fibroblasts caused epithelial tumors to grow from five marginally tumorigenic or "nontumorigenic" (nontumorforming) human tumor cell lines or strains: PC-i (prostate), WH (bladder), , and cells derived from the ascites fluids of patients with metastatic renal pelvic or prostate cancers. Evidence for the human and epithelial nature of these experimental tumors was provided by histologic, immunohistochemical, Southern and dot-blot hybridization, and cytogenetic analyses. Transformed fibroblasts induced predominantly carcinosarcomas, whereas nontumorigenic fibroblasts (NIH 3T3) and lethally irradiated transformed fibroblasts induced exclusively carcinomas. The fibroblast-epithelial interaction appears to occur bidirectionally and does not result from cell fusion. Because coculture experiments in vitro did not demonstrate an increased cell proliferation, it appears that undefined host factors can influence tumor growth. This tumor model may be useful in drug-screening programs and in mechanistic studies of factors regulating human tumor growth and progression.Interactions between epithelium and mesenchyme mediate crucial aspects of normal development and are also believed to be important in neoplasia (1)(2)(3)(4). By employing tissuerecombination techniques, it has been demonstrated that the growth and differentiation of normal epithelium is regulated either inductively or permissively by neighboring mesenchymal components (5, 6). Studies of stromal-epithelial interaction in the prostate gland revealed that mesenchyme isolated from the fetal urogenital sinus (7, 8) but not from the prostate of newborns (9) or adults (10) can stimulate proliferation of well-differentiated adult epithelium. Mesenchymal mediation of sex steroid action on glandular epithelium has also been demonstrated. The growth of the prostate (7, 8), the regression of the mammary gland by androgen stimulation (11,12), and the growth (13) and the expression of progesterone receptors (14) by the mammary epithelium in response to estrogen have been shown to be mediated by the indirect action of sex steroids on the fibromuscular stroma.Stromal influences on epithelial neoplasia have also been documented in the salivary gland (15), the mammary gland (16), the urinary bladder (17), and the skin (18 Tumorigenicity Determinations. The athymic nude BALB/c mouse strain (20-25 g, Charles River Breeding Laboratories) was used in all experiments. Tumor volumes were calculated by the formula weight x length x height x 0.5236 (24). With the exception of the PC-3 cell line (25), our definition of "tumorigenicity" conformed to the published data. Dot Blot and Southern Hybridization. DNA was prepared from tissues and tumors according to the method described by Davis et al. (26), with slight modification to include treatment steps with proteinase K (0.2 mg/ml, Sigma) and RNase A (20 ,g/...

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Prostatitis in the Rat

Cited by 39 publications

References 11 publications

Rat model of experimentally induced abacterial prostatitis

Rat model of experimentally induced abacterial prostatitis

Experimental rodent models of prostatitis: limitations and potential

Fibroblast-mediated acceleration of human epithelial tumor growth in vivo.

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