Increase in Pit-1 mRNA Is Not Required for the Estrogen-Induced Expression of Prolactin Gene and Lactotroph Proliferation.

Tsukahara, Shin-Ichiro; Kambe, Fukushi; Suganuma, Nobuhiko; Tsutsumi, Yutaka; Seo, Hisao

doi:10.1507/endocrj.41.579

Cited by 5 publications

(5 citation statements)

References 28 publications

(41 reference statements)

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“…We used a retrovirus bearing the human Ret‐S cDNA (LPC‐Ret) or the empty construct (LPC). For retroviral expression, we needed actively dividing cells, and so we used estrogen‐induced lactotroph hyperplasia (Tsukahara et al , 1994). The LPC or LPC‐Ret retrovirus was delivered to estrogen‐injected female rats by stereotaxic injection.…”

Section: Resultsmentioning

confidence: 99%

“…However, there is no substantial in vivo evidence in rodents or humans to support this latter possibility: the Pit‐1 gene is not altered in adenomas, and Pit‐1 expression appears to be more closely related to GH secretion than to tumorigenesis (Delhase et al , 1993; Hoggard et al , 1993; Pellegrini et al , 1994). Moreover, Pit‐1 mutations have been found in human hypopituitarism without pituitary hypoplasia (Pfaffle et al , 1992), whereas no increase in Pit‐1 expression is required for in vivo estrogen‐induced lactotroph hyperplasia in rats (Tsukahara et al , 1994). Our data show that too much Pit‐1 is deleterious for the somatotroph; conversely, knocking down Pit‐1 prevents apoptosis.…”

Section: Discussionmentioning

confidence: 99%

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The dependence receptor Ret induces apoptosis in somatotrophs through a Pit-1/p53 pathway, preventing tumor growth

Cañibano

Rodriguez

Sáez

et al. 2007

EMBO J

110

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Somatotrophs are the only pituitary cells that express Ret, GFRα1 and GDNF. This study investigated the effects of Ret in a somatotroph cell line, in primary pituitary cultures and in Ret KO mice. Ret regulates somatotroph numbers by inducing Pit‐1 overexpression, leading to increased p53 expression and apoptosis, both of which can be prevented with Ret or Pit‐1 siRNA. The Pit‐1 overexpression is mediated by sustained activation of PKCδ, JNK, c/EBPα and CREB induced by a complex of Ret, caspase 3 and PKCδ. In the presence of GDNF, Akt is activated, and the Pit‐1 overexpression and resulting apoptosis are blocked. The adenopituitary of Ret KO mice is larger than normal, showing Pit‐1 and somatotroph hyperplasia. In normal animals, activation of the Ret/Pit‐1/p53 pathway by retroviral introduction of Ret blocked tumor growth in vivo. Thus, somatotrophs have an intrinsic mechanism for controlling Pit‐1/GH production through an apoptotic/survival pathway. Ret might be of value for treatment of pituitary adenomas.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The dependence receptor Ret induces apoptosis in somatotrophs through a Pit-1/p53 pathway, preventing tumor growth

Cañibano

Rodriguez

Sáez

et al. 2007

EMBO J

110

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“…Soybeans may also be estrogenic, resulting in their ability to stimulate the synthesis and secretion of PRL and GH. On the other hand, Tsukahara et al (1994) suggested that an increase in Pit-1 mRNA was not required for estrogen-induced lactotroph proliferation or PRL gene expression. In addition, Son et al (2001) suggested that isoflavones in soybeans may not be responsible for the synergistic goitrogenic effect of soybeans and iodine deficiency.…”

Section: Discussionmentioning

confidence: 99%

Dietary Soybean Enhances Pit-1 Dependent Pituitary Hormone Production in Iodine Deficient Rats

et al. 2005

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Reports have shown that soybeans are goitrogenic. In the present study, we investigated the effects of a high soybean diet in rats that were fed normal or iodine-deficient chow on the regulation of anterior pituitary hormone production. Iodine deficiency alone resulted in thyroid hyperplasia, reduced serum thyroxine levels, and a tendency towards an increase in serum thyroid stimulating hormone (TSH). The combination of a high soybean and low iodine diet (ID + DS) acted synergistically to induce thyroid hypertrophy, reduce serum thyroxine and tri-iodothyronine, and markedly increase serum TSH. Immunohistochemical analysis revealed that rats fed the ID + DS diet exhibited a marked increase in their number of pituitary TSH, prolactin (PRL), and growth hormone (GH) producing cells. Pituitary transcription factor-1 (Pit-1) which is involved in the expression of the TSH, PRL, and GH genes was also increased in ID + DS fed rats. These results suggest that a diet high in soybean products modulates anterior pituitary hormone production by regulating Pit-1 induction, in iodine-deficient animals.

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“…One explanation for the finding of no difference of Pit-1 mRNA but greater pituitary PRL mRNA in OSe vs. ISe steers could be that although Pit-1 is indispensable for prolactin production, an increase in Pit-1 mRNA is not necessary to promote PRL gene expression. For example, in estrogen-treated rats, lactotroph proliferation and enhanced expression of PRL mRNA but not an increase in Pit-1 mRNA have been observed (Tsukahara et al, 1994).…”

Section: Ose Form Of Se Supplementation Had Greatermentioning

confidence: 99%

Forms of selenium in vitamin–mineral mixes differentially affect the expression of genes responsible for prolactin, ACTH, and α-MSH synthesis and mitochondrial dysfunction in pituitaries of steers grazing endophyte-infected tall fescue1

Yang

Burris

et al. 2018

Journal of Animal Science

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The goal of this study was to test the hypothesis that sodium selenite (inorganic Se, ISe), SEL-PLEX (organic forms of Se, OSe), vs. a 1:1 blend (MIX) of ISe and OSe in a basal vitamin-mineral (VM) mix would differentially alter pituitary transcriptome profiles in growing beef steers grazing an endophyte-infected tall fescue (E+) pasture. Predominately Angus steers (BW = 183 ± 34 kg) were randomly selected from fall-calving cows grazing E+ pasture and consuming VM mixes that contained 35 ppm Se as ISe, OSe, or MIX forms. Steers were weaned, depleted of Se for 98 d, and subjected to summer-long common grazing of a 10.1 ha E+ pasture containing 0.51 ppm ergot alkaloids. Steers were assigned (n = 8 per treatment) to the same Se-form treatments on which they were raised. Selenium treatments were administered by daily top-dressing 85 g of VM mix onto 0.23 kg soyhulls, using in-pasture Calan gates. As previously reported, serum prolactin was greater for MIX (52%) and OSe (59%) steers vs. ISe. Pituitaries were collected at slaughter and changes in global and selected mRNA expression patterns determined by microarray and real-time reverse transcription PCR analyses, respectively. The effects of Se treatment on relative gene expression were subjected to one-way ANOVA. The form of Se affected the expression of 542 annotated genes (P < 0.005). Integrated pathway analysis found a canonical pathway network between prolactin and pro-opiomelanocortin (POMC)/ACTH/α-melanocyte-stimulating hormone (α-MSH) synthesis-related proteins and that mitochondrial dysfunction was a top-affected canonical pathway. Targeted reverse transcription-PCR analysis found that the relative abundance of mRNA encoding prolactin and POMC/ACTH/α-MSH synthesis-related proteins was affected (P < 0.05) by the form of Se, as were (P ≤ 0.05) mitochondrial dysfunction-related proteins (CYB5A, FURIN, GPX4, and PSENEN). OSe steers appeared to have a greater prolactin synthesis capacity (more PRL mRNA) vs. ISe steers through decreased dopamine type two receptor signaling (more DRD2 mRNA), whereas MIX steers had a greater prolactin synthesis capacity (more PRL mRNA) and release potential by increasing thyrotropin-releasing hormone concentrations (less TRH receptor mRNA) than ISe steers. OSe steers also had a greater ACTH and α-MSH synthesis potential (more POMC, PCSK2, CPE, and PAM mRNA) than ISe steers. We conclude that form of Se in VM mixes altered expression of genes responsible for prolactin and POMC/ACTH/α-MSH synthesis, and mitochondrial function, in pituitaries of growing beef steers subjected to summer-long grazing an E+ pasture.

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Increase in Pit-1 mRNA Is Not Required for the Estrogen-Induced Expression of Prolactin Gene and Lactotroph Proliferation.

Cited by 5 publications

References 28 publications

The dependence receptor Ret induces apoptosis in somatotrophs through a Pit-1/p53 pathway, preventing tumor growth

The dependence receptor Ret induces apoptosis in somatotrophs through a Pit-1/p53 pathway, preventing tumor growth

Dietary Soybean Enhances Pit-1 Dependent Pituitary Hormone Production in Iodine Deficient Rats

Forms of selenium in vitamin–mineral mixes differentially affect the expression of genes responsible for prolactin, ACTH, and α-MSH synthesis and mitochondrial dysfunction in pituitaries of steers grazing endophyte-infected tall fescue1

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