Detection of In Situ Localization of Long Form Prolactin Receptor Messenger RNA in Lactating Rats by Biotin-Labeled Riboprobe.

Shirota, Mariko; Kurohmaru, Masamichi; Hayashi, Yoshihiro; Shirota, Kinji; Kelly, Paul A.

doi:10.1507/endocrj.42.69

Cited by 11 publications

(5 citation statements)

References 40 publications

(52 reference statements)

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“…Wild-type 129SV mammary epithelium adopted the less branched morphology of the endogenous Ragl ~'~ glands following transplant, confirming that systemic effects control this aspect of development, as recently demonstrated (Yant, 1998). Use of in situ hybridization analysis does not reveal expression of the PRLR in the mammary stromal cells of the mouse (Bera, 1994) or the rat (Meister, 1992;Ouhtit, 1993;Shirota, 1995). This suggests that prolactin is unlikely to act via the mammary stroma in rodents.…”

supporting

confidence: 65%

“…Similar defects in ductal branching and end-bud differentiation are also seen in mice lacking prolactin (Horseman, 1997) or Stat5a (Liu, 1998 (Yant, 1998). Use of in situ hybridization analysis does not reveal expression of the PRLR in the mammary stromal cells of the mouse (Bera, 1994) or the rat (Meister, 1992;Ouhtit, 1993;Shirota, 1995). This suggests that prolactin is unlikely to act via the mammary stroma in rodents.…”

Section: Discussionmentioning

confidence: 93%

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Control of the Mammary Cell Cycle Clock By Estrogen and Progesterone

Weinberg¹

1997

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Washington Headquarters Services, Directorate for Information Operations and Reports, 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302, and to the Office of Management and Budget,. Washington, DC 20503 AGENCY USE ONLY (Leave blank)2. REPORT DATE January 2 001 REPORT TYPE AND DATES COVEREDFinal (15 Jul 96 -31 Dec 00) TITLE AND SUBTITLE Control of the Mammary Cell Cycle Clock by Estrogen and Progesterone AUTHOR(S)Robert A. Weinberg, Ph.D. Both the growth and the development of the mammary gland are controlled by the female hormones estrogen, prolactin and progesterone, and by interactions between the epithelial and stromal compartments of the breast. Changes in the regulation of any of these processes may lead to breast cancer. We have investigated the role of progesterone in the process of sidebranching and alveologenesis in the mammary gland using mice lacking the progesterone receptor which are defective in these processes. By reconstituting murine mammary glands in vivo, we have shown that the progesterone receptor is required only in epithelial cells for proper sidebranching and alveologenesis to occur. Our studies indicate that progesterone acts in a paracrine manner and suggest that Wnt-4 is a mediator of the paracrine signals released from progesterone receptor-positive cells. In addition, we have characterized the role of the estrogen receptor (ER) in regulating the proliferation of breast cancer cells. We postulate that the ability of ER to control cyclin Dl expression and proliferation of breast cancer cells may be acquired during breast cancer progression. This is indicated by the fact that ectopic expression of the estrogen receptor in human epithelial cells does not, on its own, enable signaling between the ER and the cyclin Dl gene. Moreover, others have demonstrated that the ER-positive cells in the mammary epithelium are distinguishable from those that are actively mitotic. Finally, our work indicates that the effects of deletion of the prolactin receptor (PrlR) from mammary epithelial cells closely phenocopy the consequences of deleting cyclin Dl from these cells. We suggest that activation of the PrlR by its ligand results in the production of jnsuliJl-like growth factor-2 which in turn induces cyclin Dl synthesis in these cells^ ; - Conclusions 8 FUNDING NUMBERS DAMD17-96-1-6285 PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES)Whitehead SUBJECT TERMS Breast CancerReferences 9Appendices 10Final Report Laboratory of Robert A. Weinberg Ph.D.DAMD 17-96-1-6285Our research performed under the auspices of the Army Breast Cancer grant has focused on the ab...

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confidence: 65%

Section: Discussionmentioning

confidence: 93%

Control of the Mammary Cell Cycle Clock By Estrogen and Progesterone

Weinberg¹

1997

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“…This suggests that the failure of ductal side branching may be exerted by the mammary stroma. Although initial investigation failed to detect PRLR in the mammary stroma of the mouse or rat (Meister et al, 1992;Ouhtit et al, 1993a,b;Shirota et al, 1995), immunohistochemistry has found low levels in human breast cancer stroma using an antirat PRLR monoclonal (Reynolds et al, 1997) and through in situ hybridization (Mertani et al, 1998). Recently, the stroma of both rat (Camarillo et al, 2001) and mouse (Hovey et al, 2001) mammary gland has been shown to express PRLR.…”

Section: Ovarian Prlrs Are Required For Normal Pubertal Developmenmentioning

confidence: 99%

Investigation of the Transcriptional Changes Underlying Functional Defects in the Mammary Glands of Prolactin Receptor Knockout Mice

Ormandy

Naylor²,

Harris³

et al. 2003

Recent Progress in Hormone Research

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Knockout (KO) mice have been created that carry null mutations of genes encoding molecules essential for prolactin (PRL) release, PRL, the receptor for prolactin (PRLR), and various members of the receptor's signaling pathway. This allowed an in vivo genetic analysis of the role of PRL in target organ function. In PRLKO and PRLRKO mice, mammary ductal side branching was absent, terminal end bud (TEB)-like structures persisted at the ductal termini well into maturity, and no alveolar buds formed along the ductal tree. Transplants of recombined mammary glands formed from stromal and epithelial elements with and without PRLR showed normal development, while supplementation of progesterone levels in PRLKO animals restored ductal side branching. During pregnancy, PRLR heterozygous animals initially showed normal ductal and alveolar development. However, alveolar development stalled during late pregnancy, preventing successful lactation. This defect could be rescued by the loss of a single allele of the suppressor of cytokine signaling (SOCS) 1 gene. Transplants of recombined glands containing PRLRKO epithelium and wild-type (WT) stroma formed alveolar buds during pregnancy but showed no lobuloalveolar development. Recombinations of WT epithelium and PRLRKO stroma showed normal development, demonstrating that a direct action of the lactogenic hormones is confined to the epithelium, to promote lobuloalveolar development. Transcript profiling of epithelial transplants expressing or not expressing PRLR was used during early pregnancy to investigate the transcriptional response to lactogens underlying this defect. Such profiling has identified a number of genes with well-characterized roles in mammary development, in addition to a number of novel transcripts.

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“…Ppp1r1b is a protein phosphatase involved in signal transduction pathways in human granulosa cells in response to dopamine and human chorionic gonadotropin stimulation [45]. Prlr encodes the prolactin receptor which is localized to granulosa cells as well as other cell types in the rat ovary [46]. Prolactin receptor expression in rat granulosa cells is increased by treatment of cultured cells with FSH, LH and hCG [47].…”

Section: Discussionmentioning

confidence: 99%

Microarray analysis of Foxl2 mediated gene regulation in the mouse ovary derived KK1 granulosa cell line: Over-expression of Foxl2 leads to activation of the gonadotropin releasing hormone receptor gene promoter

Escudero

Haller

Clay

et al. 2010

Journal of Ovarian Research

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BackgroundThe Foxl2 transcription factor is required for ovarian function during follicular development. The mechanism of Foxl2 regulation of this process has not been elucidated. Our approach to begin to understand Foxl2 function is through the identification of Foxl2 regulated genes in the ovary.MethodsTransiently transfected KK1 mouse granulosa cells were used to identify genes that are potentially regulated by Foxl2. KK1 cells were transfected in three groups (mock, activated, and repressed) and twenty-four hours later RNA was isolated and submitted for Affymetrix microarray analysis. Genesifter software was used to carry out analysis of microarray data. One identified target, the gonadotropin releasing hormone receptor (GnRHR) gene, was chosen for further study and validation of Foxl2 responsiveness. Transient transfection analyses were carried out to study the effect of Foxl2 over-expression on GnRHR gene promoter-luciferase fusion activity. Data generated was analyzed with GraphPad Prism software.ResultsMicroarray analysis identified 996 genes of known function that are potentially regulated by Foxl2 in mouse KK1 granulosa cells. The steroidogenic acute regulatory protein (StAR) gene that has been identified as Foxl2 responsive by others was identified in this study also, thereby supporting the effectiveness of our strategy. The GnRHR gene was chosen for further study because it is known to be expressed in the ovary and the results of previous work has indicated that Foxl2 may regulate GnRHR gene expression. Cellular levels of Foxl2 were increased via transient co-transfection of KK1 cells using a Foxl2 expression vector and a GnRHR promoter-luciferase fusion reporter vector. The results of these analyses indicate that over-expression of Foxl2 resulted in a significant increase in GnRHR promoter activity. Therefore, these transfection data validate the microarray data which suggest that Foxl2 regulates GnRHR and demonstrate that Foxl2 acts as an activator of the GnRHR gene.ConclusionsPotential Foxl2 regulated ovarian genes have been identified through microarray analysis and comparison of these data to other microarray studies. The Foxl2 responsiveness of the GnRHR gene has been validated and provided evidence of Foxl2 transcriptional activation of the GnRHR gene promoter in the mouse ovary derived KK1 granulosa cell line.

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Detection of In Situ Localization of Long Form Prolactin Receptor Messenger RNA in Lactating Rats by Biotin-Labeled Riboprobe.

Abstract: Abstract.Biotinylated riboprobe that specifically hybridized with messenger RNAs (mRNAs) encoding the long form of prolactin receptor (PRLRL) was transcribed from 269 by Hind III and Xho

Cited by 11 publications

References 40 publications

Control of the Mammary Cell Cycle Clock By Estrogen and Progesterone

Control of the Mammary Cell Cycle Clock By Estrogen and Progesterone

Investigation of the Transcriptional Changes Underlying Functional Defects in the Mammary Glands of Prolactin Receptor Knockout Mice

Microarray analysis of Foxl2 mediated gene regulation in the mouse ovary derived KK1 granulosa cell line: Over-expression of Foxl2 leads to activation of the gonadotropin releasing hormone receptor gene promoter

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