Potentiation of the Mitogenic Effect of Estrogen on the Pituitary-Gland by Alcohol-Consumption

De, Alok; Boyadjieva, Nadka; Pastorcic, Mg; Sarkar, DK

doi:10.3892/ijo.7.3.643

Cited by 22 publications

(41 citation statements)

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“…This interaction increases bFGF release maximally, thereby producing a maximal effect on cell proliferation. Previous studies have demonstrated that ethanol promotes estradiol cell proliferating action on lactotropes (De et al, 1995(De et al, , 2002. Estradiol is known to increase lactotropic cell production of TGF-␤3, which causes lactotropic cell proliferation by increasing bFGF release from FS cells (Hentges et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…Alcoholics also show elevated blood levels of estrogens (Vä limaki et al, 1990), which are believed to be due to peripheral conversion of weak androgens of estrogens. We have previously shown that, like estradiol, ethanol induces hyperprolactinemia by increasing prolactin release from lactotropes and by increasing the number of lactotropes in the anterior pituitary (De et al, 1995(De et al, , 2000(De et al, , 2002Hentges and Sarkar, 2001). We have also shown that ethanol and estradiol act similarly on the dopaminergic regulation of prolactin release (Oomizu et al, 2003).…”

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confidence: 87%

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Role of Protein Kinase C-Ras-MAPK p44/42 in Ethanol and Transforming Growth Factor-β3-Induced Basic Fibroblast Growth Factor Release from Folliculostellate Cells

Chaturvedi

Sarkar²

2005

J Pharmacol Exp Ther

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In the present study, we determined the interactive effects of ethanol and transforming growth factor ␤-3 (TGF-␤3) on basic fibroblast growth factor (bFGF) release from folliculostellate (FS) cells and the role of the mitogen-activated protein kinase (MAPK) pathway in this interaction. We found that TGF-␤3 and ethanol alone increased release of bFGF from FS cells, but together they showed markedly increased levels of bFGF compared with the individual effect. Ethanol and TGF-␤3 alone moderately increased activation of MAPK p44/42, but together they produced marked activation of MAPK p44/42. TGF-␤3 alone increased the activation of smad2. Ethanol did not activate smad2 or alter TGF-␤3 activation of smad2. Pretreatment of FS cells with a mitogen-activated protein kinase kinase 1/2 inhibitor or with a protein kinase C (PKC) inhibitor suppressed the TGF-␤3 and ethanol actions on MAPK p44/42 activation and bFGF release. Ethanol and TGF-␤3, either alone or in combination, increased the levels of active Ras. Furthermore, the MAPK p44/42 activation by TGF-␤3 and ethanol was blocked by overexpression of Ras N17, a dominant negative mutant of Ras p21. These data suggest that the PKC-activated Ras-dependent MAPK p44/42 pathway is involved in the cross talk between TGF-␤3 and ethanol to increase bFGF release from FS cells.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 87%

Role of Protein Kinase C-Ras-MAPK p44/42 in Ethanol and Transforming Growth Factor-β3-Induced Basic Fibroblast Growth Factor Release from Folliculostellate Cells

Chaturvedi

Sarkar²

2005

J Pharmacol Exp Ther

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“…The vector was linearized with EcoRI and used as a template to synthesize an antisense RNA probe with T7 RNA polymerase (Promega). The probe was purified by electrophoresis on a 6% polyacrylamide, 7 M urea gel as described previously (29).…”

Section: Methodsmentioning

confidence: 99%

An Upstream Element Containing an ETS Binding Site Is Crucial for Transcription of the Human Presenilin-1 Gene

Pastorcic¹,

Das²

1999

Journal of Biological Chemistry

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Deletion mapping of the human presenilin-1 (PS1) promoter delineated the most active fragment from ؊118 to ؉178 in relation to the transcription start site mapped in this study, in both human neuroblastoma SK-N-SH and hepatoma HepG2 cells. 5 deletions revealed that a crucial element controlling over 90% of the promoter activity in these cell lines is located between ؊22 and ؊6. A mutation altering only two nucleotides of the ETS consensus sequence present at ؊12 (GGAA to TTAA) has a similar effect. Electrophoretic mobility shift assays showed that a set of specific complexes between nuclear factors and the PS1 promoter are eliminated by this point mutation, as well as by competition with an ETS consensus oligonucleotide. Competition experiments in DNase I footprinting correlated with electrophoretic mobility shift assays and showed that only one of several footprints over the PS1 promoter is eliminated by competition with an ETS consensus oligonucleotide. It extends from ؊14 to ؊6 and surrounds the ETS motif present at ؊12. Thus, a crucial ETS element is present at ؊12 and binds a protein(s) recognizing specifically the ETS consensus motif. At least one such complex is eliminated by preincubating the nuclear extract with an antibody with broad cross-reactivity with Ets-1 and Ets-2 proteins, thus confirming that an ETS transcription factor(s) recognizes the ؊12 motif. Several Sp1 binding motifs at positions ؊70, ؊55, and ؉20 surround this ETS element. Competition DNase I footprinting showed that Sp1-like nuclear factors recognize specifically these sites in both cell lines. Furthermore, a combination of 5 and 3 deletions indicated the presence of positive promoter elements between ؊96 and ؊35 as well as between ؉6 and ؉42. Thus, transfection and footprinting assays correlate to suggest that Sp1 transcription factor(s) bind at several sites upstream and downstream from the initiation site and activate the transcription of the PS1 promoter. Sequences downstream from the transcription initiation site also contain major control elements. 3 deletions from ؉178 to ؉107 decreased promoter activity by 80%. However, further deletion to ؉42 increased promoter activity by 3-4-fold. Collectively, these data indicate that sequences upstream and downstream from the transcription start site each control over 80% of the promoter activity. Hence, this suggests that protein-protein interactions between factors recognizing downstream and upstream sequences are involved.

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“…Interestingly, in one of these monkeys, immunocytochemical examination of the pituitary gland showed apparent pituitary hyperplasia. In laboratory rats, chronic ethanol administration increases plasma PRL levels and pituitary weight in cyclic female rats and ovariectomized rats as well as potentiating estrogen mitogenic effects in ovariectomized female rats [42,43]. Therefore, clinical as well as animal data suggest that ethanol consumption is a positive risk factor for prolactinomas and hyperprolactinemia, possibly due to ethanol's ability to increase endogenous estrogenic activity.…”

Section: Cell Cycle Genomic Instability and Tumorigenesis In Lactotmentioning

confidence: 99%

Genesis of Prolactinomas: Studies Using Estrogen-Treated Animals

Sarkar

2006

Frontiers of Hormone Research

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Prolactin-secreting adenomas (prolactinomas) are the most prevalent form of pituitary tumors in humans. Our knowledge of the formation of these tumors is limited. Experimental work in animal has uncovered that estradiol exposure leads to prolactinoma formation via orchestrated events involving dopamine D2 receptors, transforming growth factor-β (TGF-β) isoforms and their receptors, as well as factors secondary to TGF-β action. Additionally, these studies determined that TGF-β and b-FGF interact to facilitate the communication between lactotropes and folliculo-stellate cells that is necessary for the mitogenic action of estradiol. The downstream signaling that governs lactotropic cell proliferation involves activation of the MAP kinase p44/42-dependent pathway.Pituitary tumors are primarily adenomas; they account for approximately 10-15% of intracranial tumors. They cause significant morbidity due to local invasion, hypopituitarism or hormone hypersecretion [1,2]. Pituitary tumors are classified as either functioning and secreting excessive amounts of active hormones, or as endocrinologically inactive and secreting no hormones or inactive hormones. Pituitary tumors are also classified by virtue of their size into the arbitrary division of those less than 1 cm as microadenomas and those more than 1 cm as macroadenomas. Pituitary tumors secreting excess prolactin are characterized as prolactinomas. Prolactinomas are the most frequently occurring neoplasm in the human pituitary [3,4]. In the general population, 1:2,800 men and 1:1,050 women are considered to have prolactinomas [5]. In human subjects, prolactinomas occur as both macroadenomas and microadenomas. In addition, mixed growth hormone and prolactin-secreting adenomas are documented to exist in a substantial number of acromegaly patients.Hyperprolactinoma is a condition in which plasma prolactin (PRL) levels are elevated above normal levels. Hyperprolactinemia, with elevation of serum prolactin of more than 200 ng/ml, is characteristically associated with prolactinomas [6]. Hyperprolactinemia causes reproductive dysfunction such as amenorrhea, galactorrhea, and infertility in women [7]. Amenorrhea and galactorrhea may occur alone or together [8]. Up to 25% of patients with secondary amenorrhea have been diagnosed with hyperprolactinemia. Many of these patients showed micro-prolactin adenomas or macro-prolactin adenomas in the pituitary. Although treatments that alter central dopaminergic neuronal functions cause an elevated serum PRL level, in most cases hyperprolactinemia is due to a pituitary tumor. In women, prolactinomas are mainly microadenomas. These microadenomas are rarely associated with hypopituitarism or central nervous system dysfunction. Idiopathic hyperprolactinemia, without demonstrable pituitary or hypothalamic disease, has also been identified. In men, prolactinomas are mainly

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Potentiation of the Mitogenic Effect of Estrogen on the Pituitary-Gland by Alcohol-Consumption

Cited by 22 publications

References 0 publications

Role of Protein Kinase C-Ras-MAPK p44/42 in Ethanol and Transforming Growth Factor-β3-Induced Basic Fibroblast Growth Factor Release from Folliculostellate Cells

Role of Protein Kinase C-Ras-MAPK p44/42 in Ethanol and Transforming Growth Factor-β3-Induced Basic Fibroblast Growth Factor Release from Folliculostellate Cells

An Upstream Element Containing an ETS Binding Site Is Crucial for Transcription of the Human Presenilin-1 Gene

Genesis of Prolactinomas: Studies Using Estrogen-Treated Animals

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