Heterogeneity and ontogenesis of progestin receptors in rabbit lung

Giannopoulos, George; Phelps, David S.; Munowitz, P

doi:10.1016/0022-4731(82)90008-5

Cited by 5 publications

(2 citation statements)

References 28 publications

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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: 99%

“…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: 99%

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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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