Androgenic induction of cystatin-related protein and the C3 component of prostatic binding protein in primary cultures from the rat lacrimal gland

Vanaken, Hilde; Claessens, Frank; Vercaeren, Inge; Heyns, Walter; Peeters, Benjamin; Rombauts, Wilfried

doi:10.1016/0303-7207(96)03866-x

Cited by 19 publications

(11 citation statements)

References 20 publications

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“…Studies in which up to 8 kb of the C3(1) 5'¯anking sequence were fused to the Cat reporter gene did not demonstrate any transcriptional response to androgen in co-transfection experiments Claessens et al, 1990;Tan et al, 1992). There is no evidence that estrogen is able to activate C3(1) transcription, although few studies have addressed this issue (Vanaken et al, 1996). The C3(1)/Tag transgenic construct which we developed contains 4.5 kb of the C3(1) 5'¯anking region without intronic sequences.…”

Section: Introductionmentioning

confidence: 99%

The C3(1)/SV40 T-antigen transgenic mouse model of mammary cancer: ductal epithelial cell targeting with multistage progression to carcinoma

et al. 2000

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The 5'¯anking region of the C3(1) component of the rat prostate steroid binding protein (PSBP) has been used to successfully target the expression of the SV40 large Tantigen (Tag) to the epithelium of both the mammary and prostate glands resulting in models of mammary and prostate cancers which histologically resemble the human diseases. Atypia of the mammary ductal epithelium develops at about 8 weeks of age, progressing to mammary intraepithelial neoplasia (resembling human ductal carcinoma in situ [DCIS]) at about 12 weeks of age with the development of invasive carcinomas at about 16 weeks of age in 100% of female mice. The carcinomas share features to what has been classi®ed in human breast cancer as in®ltrating ductal carcinomas. All FVB/N female mice carrying the transgene develop mammary cancer with about a 15% incidence of lung metastases. Approximately 10% of older male mice develop anaplastic mammary carcinomas. Unlike many other transgenic models in which hormones and pregnancy are used to induce a mammary phenotype, C3(1)/Tag mice develop mammary tumors in the mammary epithelium of virgin animals without hormone supplementation or pregnancy. Although mammary tumor development appears hormone-responsive at early stages, invasive carcinomas are hormone-independent, which corresponds to the loss of estrogen receptor-a expression during tumor progression. Molecular and biologic factors related to mammary tumor progression can be studied in this model since lesions evolve over a predictable time course. Genomic alterations have been identi®ed during tumor progression, including an ampli®cation of the distal portion of chromosome 6 containing ki-ras and loss of heterozygosity (LOH) in other chromosomal regions. We have demonstrated that stage speci®c alterations in the expression of genes which are critical regulators of the cell cycle and apoptosis are functionally important in vivo. C3(1)/Tag mice appear useful for testing particular therapies since growth of the mammary tumors can be reduced using chemopreventive agents, cytokines, and an anti-angiogenesis agent.

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Section: Introductionmentioning

confidence: 99%

The C3(1)/SV40 T-antigen transgenic mouse model of mammary cancer: ductal epithelial cell targeting with multistage progression to carcinoma

et al. 2000

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“…The function of CRP is still unknown, and no protease inhibitory activity has yet been demonstrated. CRP1 is expressed and androgen-regulated in organs that contain relatively higher levels of androgen receptors (64,65). Similarly, an early study by Roy and co-workers (66,67) has shown that the synthesis of A2U in the hepatic parenchymal cells is induced in vivo by androgen, glucocorticoid growth hormone, and insulin and inhibited by estrogen.…”

Section: Discussionmentioning

confidence: 99%

Molecular Targets for Diabetes Mellitus-associated Erectile Dysfunction

Yohannes

Chang

Tar

et al. 2010

Molecular & Cellular Proteomics

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Protein expression profiles in rat corporal smooth muscle tissue were compared between animal models of streptozotocin-induced diabetes mellitus (STZ-DM) and agematched controls (AMCs) at 1 week and 2 months after induction of hyperglycemia with STZ treatment. At each time point, protein samples from four STZ-DM and four AMC rat corpora tissues were prepared independently and analyzed together across multiple quantitative twodimensional gels using a pooled internal standard sample to quantify expression changes with statistical confidence. A total of 170 spots were differential expressed among the four experimental groups. A subsequent mass spectrometry analysis of the 170 spots identified a total of 57 unique proteins. Network analysis of these proteins using MetaCore TM suggested altered activity of transcriptional factors that are of too low abundance to be detected by the two-dimensional gel method. The proteins that were down-regulated with diabetes include isoforms of collagen that are precursors to fibril-forming collagen type 1; Hsp47, which assists and mediates the proper folding of procollagen; and several proteins whose abundance is controlled by sex hormones (e.g. CRP1 and A2U). On the other hand, proteins seen or predicted to be up-regulated include proteins involved in cell apoptosis (e.g. p53, 14-3-3-␥, Serpinf1, Cct4, Cct5, and Sepina3n), proteins that neutralize the biological activity of nerve growth factor (e.g. anti-NGF 30), and proteins involved in lipid metabolism (e.g. apoA-I and apoA-IV). Subsequent Western blot validation analysis of p53, 14-3-3-␥, and Hsp47 confirmed increased p53 and 14-3-3-␥ and decreased Hsp47 levels in separate samples. According to the results from the Western blot analysis, Hsp47 protein showed a ϳ3-fold decrease at 1 week and was virtually undetectable at 2 months in diabetic versus control. Taken together, our results identify novel candidate proteins playing a role in erectile dysfunction in diabetes resulting from STZ treatment. Molecular & Cellular Proteomics 9:565-578, 2010. Erectile dysfunction (ED)1 is one of the many complications caused by diabetes mellitus. About 52% of men between the age of 40 and 70 years suffer from ED due to various causes, such as pathophysiological changes in nerves, blood vesicles, corporal smooth muscle tissue, and endothelial cells as well as psychological problems (such as stress) (1-3). As most of these risk factors for development of ED are inherent to diabetes mellitus, men with diabetes have a greater prevalence of ED and early onset of the disease compared with men without diabetes (4 -6). The current estimates suggest that as many as 75% of men with diabetes will develop some degree of ED at an earlier age (7). In addition, men with diabetes present with more severe dysfunction and are less responsive to current pharmacological therapies for ED (8 -10). Although ED is considered a disease impacting the "quality of life" of patients, it is often associated with depression, low self-esteem, and lower overall quality of ma...

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“…Because earlier studies by others Vanaken et al, 1996;Azzarolo et al, 1995Azzarolo et al, , 1997Azzarolo et al, , 1999 suggested positive effects of DHT on various lacrimal cell activities, we also investigated its effects on acinar cell proliferation. Our ®ndings presented here indicate that DHT, by itself, had a signi®cant but, relative to EGF, rather modest stimulatory effect on acinar cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

“…The selection of EGF and Matrigel was based upon a number of earlier reports citing their bene®cial roles (Oliver et al, 1987;Hann et al, 1989;Hann et al, 1991;Kelleher et al, 1991;Meneray et al, 1994;Millar et al, 1996;Chen et al, 1998;Vanaken et al, 1998). DHT was selected for evaluation based on the ®ndings that DHT enhanced production of the pIgR secretory component and other proteins (Vanaken et al, 1996) by acinar cells in vitro, that it increased lacrimal gland DNA content in hypophysectomized rats (Azzarolo et al, 1995) and ovariectomized rabbits (Azzarolo et al, 1997), and that it induced the appearance of mitotic ®gures in lacrimal glands of ovariectomized rabbits (Azzarolo et al, 1999). The use of HSM was encouraged by our earlier experience using this medium with another dif®cult-to-grow cell population, human hepatocytes.…”

Section: Discussionmentioning

confidence: 99%

“…Studies with rat lacrimal gland acinar cells in primary cultures have established that androgens support certain lacrimal functions, most notably secretion of the polymeric immunoglobulin receptor (pIgR) secretory component (Hann, Tatro and Sullivan, 1989;Hann, Kelleher and Sullivan, 1991;Kelleher et al, 1991), but also expression of cystatin-related protein and prostatic-binding protein (Vanaken et al, 1996). However, primary, non-transformed acinar cells have not been found to proliferate in vitro; so it has not been possible to study the molecular basis of the in¯uence of androgens on acinar cell division.…”

Section: Introductionmentioning

confidence: 97%

See 1 more Smart Citation

Proliferation of Lacrimal Gland Acinar Cells in Primary Culture. Stimulation by Extracellular Matrix, EGF, and DHT

Schönthal

Warren

Stevenson

et al. 2000

Experimental Eye Research

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Androgenic induction of cystatin-related protein and the C3 component of prostatic binding protein in primary cultures from the rat lacrimal gland

Cited by 19 publications

References 20 publications

The C3(1)/SV40 T-antigen transgenic mouse model of mammary cancer: ductal epithelial cell targeting with multistage progression to carcinoma

The C3(1)/SV40 T-antigen transgenic mouse model of mammary cancer: ductal epithelial cell targeting with multistage progression to carcinoma

Molecular Targets for Diabetes Mellitus-associated Erectile Dysfunction

Proliferation of Lacrimal Gland Acinar Cells in Primary Culture. Stimulation by Extracellular Matrix, EGF, and DHT

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