Distribution of progesterone receptor in chicken: novel target organs for progesterone and estrogen action

Pasanen, Susanna; Ylikomi, Timo; Syvälä, Heimo; Tuohimaa, Pentti

doi:10.1016/s0303-7207(97)00192-5

Cited by 35 publications

(18 citation statements)

References 45 publications

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“…The fact that PR is expressed in pancreatic islets (17,18) suggests that the potential exists for a direct effect of progesterone signaling on insulin secretion in this tissue. To determine whether the lack of PR directly affects insulin secretion, we isolated pancreatic islets from female PRϩ͞ϩ and Ϫ͞Ϫ mice by collagenase digestion and measured insulin release in the medium after incubation with secretagogs for 30 min.…”

Section: Progesterone Modulates Glucose Homeostasis In Vivomentioning

confidence: 99%

Progesterone receptor knockout mice have an improved glucose homeostasis secondary to β-cell proliferation

Picard

Wanatabe

Schoonjans

et al. 2002

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

149

104

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Gestational diabetes coincides with elevated circulating progesterone levels. We show that progesterone accelerates the progression of diabetes in female db͞db mice. In contrast, RU486, an antagonist of the progesterone receptor (PR), reduces blood glucose levels in both female WT and db͞db mice. Furthermore, female, but not male, PR؊͞؊ mice had lower fasting glycemia than PR؉͞؉ mice and showed higher insulin levels on glucose injection. Pancreatic islets from female PR؊͞؊ mice were larger and secreted more insulin consequent to an increase in ␤-cell mass due to an increase in ␤-cell proliferation. These findings demonstrate an important role of progesterone signaling in insulin release and pancreatic function and suggest that it affects the susceptibility to diabetes.

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Section: Progesterone Modulates Glucose Homeostasis In Vivomentioning

confidence: 99%

Progesterone receptor knockout mice have an improved glucose homeostasis secondary to β-cell proliferation

Picard

Wanatabe

Schoonjans

et al. 2002

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

149

104

View full text Add to dashboard Cite

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“…Cytosol preparation and immunoblotting were performed as described previously (50). Cells were harvested and collected into Eppendorf tubes 48 h after transfection, and lysed with 150 ml cell lysis buffer (20 mM Hepes, pH 8.0, 20 mM NaCl, 0.5% Nodinet P-40, protease inhibitors (Complete Mini; Boehringer-Mannheim) and 1 mM dithiothreitol).…”

Section: Cytosol Preparation and Immunoblottingmentioning

confidence: 99%

Localization of glucocorticoid receptor interacting protein 1 in murine tissues using two novel polyclonal antibodies

Puustinen

Sarvilinna²,

Manninen³

et al. 2001

European Journal of Endocrinology

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Objective: Glucocorticoid receptor interacting protein 1 (GRIP1) is a coactivator that binds to the nuclear hormone receptors in a ligand-dependent manner and mediates transcriptional activation of the target genes. The aim of this study was to investigate GRIP1 expression in various murine tissues and whether the protein is nuclear, cytoplasmic, or both. Design: Two novel polyclonal antibodies against amino acids 34±47 and 468±481 of GRIP1 were raised and characterized in order to study the GRIP1 expression with immunohistochemistry. Results: Transient transfection studies with COS cells showed a clearly nuclear staining pattern and also immunohistochemical localization of GRIP1 was mainly nuclear, but cytoplasmic expression was seen as well. GRIP1 was expressed in epithelial cells of the submandibular gland, gastrointestinal tract, pancreas, kidney, uterus, mammary gland, testis, prostate, trachea, lungs and adrenal gland. GRIP1 was also detected in stromal cells of colon, rectum, urinary bladder, vagina, uterus, mammary gland and trachea, and to a lesser extent in esophagus, ureter, urethra, thymus and spleen. Smooth muscle cells of the gastrointestinal and urinary tract, uterus, epididymis, prostrate and bronchioles expressed GRIP1. Blood vessels of many organs, capsule of the kidney and prostate, mesovarium, adipocytes of the mammary gland, pericardium and cartilage of the trachea were also GRIP1-positive. Liver, thyroid gland and striated muscle did not express GRIP1. Conclusions: GRIP1 was expressed in a wide variety of murine organs, and expression varied between cell types and organs. In addition to mainly nuclear localization of endogenous GRIP1, cytoplasmic expression was seen as well.

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“…More specifically, our results strongly suggest that regulation of PRA protein expression is mediated by the actions of GR in response to glucocorticoids. The presence of PR in lungs of different species (Giannopoulos et al 1982, Moser & Daxenbichler 1982, Bullock et al 1987, Nielsen et al 1987, Camacho-Arroyo et al 1994, Pasanen et al 1997, Beyer et al 2003, is not surprising. However, our experiments do not provide evidence for the existence of PRB in mouse lung.…”

Section: Discussionmentioning

confidence: 97%

“…asthma and cancer) (Milne 1979, Haggerty et al 2003, Ishibashi et al 2005, the regulation and cellular distribution of PR protein isoforms in lung remain largely unknown. Previous studies have shown that PR mRNAs and proteins are found in rabbit (Giannopoulos et al 1982, Bullock et al 1987, Nielsen et al 1987, Camacho-Arroyo et al 1994, rodent (Moser & Daxenbichler 1982, Beyer et al 2003, and chicken (Pasanen et al 1997) lungs. In the present study, we sought to initially establish the presence of PR isoforms in mouse lung using reverse transcriptase (RT)-PCR and Western blotting analyses and on finding that PRA mRNA and protein were specifically expressed in mouse lung, we examined the possibility of regulation of PRA protein expression in mice during postnatal growth and development.…”

Section: Introductionmentioning

confidence: 95%

Developmental and hormonal regulation of progesterone receptor A-form expression in female mouse lung in vivo: interaction with glucocorticoid receptors

Shao¹,

Egecioglu²,

Weijdegård³

et al. 2006

Journal of Endocrinology

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Progesterone (P 4 ) regulates many aspects of physiological functions via two nuclear P 4 receptors (PR), PRA and PRB, which are members of a structurally related nuclear hormone receptor superfamily that includes glucocorticoid receptors (GR). The regulation and cellular distribution of PR protein isoforms have been extensively studied in reproductive tissues, but this is not the case in the lung. In the present study, reverse transcriptase (RT)-PCR, Western blotting, and immunolocalization supported the presence of PRA in the lung of female mice, with PRA protein levels significantly increased between postnatal day 7 and 12, declined at postnatal day 26, and minimal in adults when compared to postnatal day 2. The peak was temporally related to postnatal lung maturation in rodents. Immunoreactivity for PR was detected in the alveolar and bronchial epithelia. We then extended this study to examine, for the first time, the regulation of PRA protein expression in female mouse lung in vivo. Neither the increase in endogenous P 4 nor treatment with exogenous P 4 regulated PRA protein expression in female mouse lung. However, treatment of mice with the GR/PR antagonist RU 486, but not Org 31710 (a specific PR antagonist), significantly increased PRA protein expression in parallel to a decrease in GR protein expression. In addition, treatment with the synthetic glucocorticoid dexamethasone led to a decrease in PRA protein expression independent of endogenous P 4 levels. Furthermore, immunoprecipitation followed by Western blot analysis revealed that, under in vivo conditions, PRA physically interacted with GR in mouse lung. Confocal laser microscopy revealed that PRA and GR co-localized in the nuclei of alveolar epithelia cells, whereas nuclear PR and cytoplasmic GR were detected in bronchial epithelium. Taken together, our observations suggest that PRA may be an important physiological factor involved in postnatal lung development and that the regulation of PRA protein expression is not dependent on P 4 , but rather on functional glucocorticoid/GR signaling mediated by protein-protein interaction in the mouse lung.

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Distribution of progesterone receptor in chicken: novel target organs for progesterone and estrogen action

Cited by 35 publications

References 45 publications

Progesterone receptor knockout mice have an improved glucose homeostasis secondary to β-cell proliferation

Progesterone receptor knockout mice have an improved glucose homeostasis secondary to β-cell proliferation

Localization of glucocorticoid receptor interacting protein 1 in murine tissues using two novel polyclonal antibodies

Developmental and hormonal regulation of progesterone receptor A-form expression in female mouse lung in vivo: interaction with glucocorticoid receptors

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