Estrogen increases coagulation factor V mRNA levels via both estrogen receptor-alpha and -beta in murine bone marrow/bone

Movérare, Sofia; Skrtic, Stanko; Lindberg, Mattias F.; Dahlman-Wright, Karin; Ohlsson, Claes

doi:10.1530/eje.0.1510259

Cited by 14 publications

(18 citation statements)

References 23 publications

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“…The results of the present study are in conflict with those of the study performed by Movérare et al. [11], in which microarray analyses of liver samples from mice treated with 17β‐estradiol did not yield altered hepatic coagulation gene transcript levels as compared with vehicle‐treated mice. We have no explanation for this difference in findings, other than a difference in treatment protocol, that is, subcutaneous injection of 2.3 μg of 17β‐estradiol benzoate per mouse d −1 for 5 days per week for 3 weeks vs. our daily oral administration of 1 μg of EE for 10 days, or the fact that the cut‐off value of at least 1.6‐fold of the microarray data analyses might be too high to allow detection of the subtle changes in coagulation factor transcript levels.…”

Section: Discussioncontrasting

confidence: 99%

“…These genome‐wide results predict that estrogens potentially modulate transcription of a large number of coagulation genes expressed in the liver through the direct action of ERs. In this respect, it is surprising that coagulation‐dedicated cDNA microarray analyses of livers of mice treated with estrogen revealed that none of the liver‐specific coagulation genes was regulated by 17β‐estradiol [11].…”

Section: Introductionmentioning

confidence: 99%

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17α‐Ethinylestradiol rapidly alters transcript levels of murine coagulation genes via estrogen receptor α

Cleuren¹,

Linden²,

Visser

et al. 2010

Journal of Thrombosis and Haemostasis

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To cite this article: Cleuren ACA, van der Linden IK, de Visser YP, Wagenaar GTM, Reitsma PH, van Vlijmen BJM. 17a-Ethinylestradiol rapidly alters transcript levels of murine coagulation genes via estrogen receptor a. J Thromb Haemost 2010; 8: 1838-46.Summary. Background: Oral estrogen use is associated with changes in plasma levels of many coagulation proteins. Objective: To gain more insight into the underlying mechanism of estrogen-induced changes in coagulation. Methods: Ovariectomized female mice were used to study the impact of oral 17a-ethinylestradiol (EE) on plasma coagulation, hepatic coagulation gene transcript levels, and dependence on estrogen receptor (ER) a and ERb. Results: Ten days of oral EE treatment resulted in significantly reduced plasma activity levels of factor (F)VIII, FXII, combined FII/FVII/FX and antithrombin, whereas FIX activity significantly increased. Regarding hepatic transcript levels, oral EE caused significant decreases in fibrinogen-c, FII, FV, FVII, FX, FXII, antithrombin, protein C, protein Z, protein Z inhibitor and heparin cofactor II mRNA levels, whereas FXI levels significantly increased and transcript levels of FVIII, FIX, protein S and a 2 -antiplasmin remained unaffected. All EE-induced coagulation-related changes were neutralized by coadministration of the nonspecific ER antagonist ICI182780. In addition, ERa-deficient mice lacked the EE-induced changes in plasma coagulation and hepatic transcript profile, whereas ERb-deficient mice responded similarly to non-deficient littermate controls. A crucial role for the ER was further demonstrated by its rapid effects on transcription, within 2.5-5 h after EE administration, suggesting a short chain of events leading to its final effects. Conclusions: Oral EE administration has a broad impact on the mouse coagulation profile at the level of both plasma and hepatic mRNA levels. The effects on transcription are rapidly induced, mostly downregulatory, and principally mediated by ERa.

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Section: Discussioncontrasting

confidence: 99%

Section: Introductionmentioning

confidence: 99%

17α‐Ethinylestradiol rapidly alters transcript levels of murine coagulation genes via estrogen receptor α

Cleuren¹,

Linden²,

Visser

et al. 2010

Journal of Thrombosis and Haemostasis

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“…(Lamote et al, 2007;Stygar et al, 2007) Bone (femur) 2 No fluorescence seen in osteocytes, bone marrow. (Moverare et al, 2004;Okazaki et al, 2002) Brain 11 Diffuse fluorescence throughout cerebrum and hypothalamus; none in optic chiasm, cerebellum, or hind brain. Marked increased fluorescence at several small points on the ventral surface.…”

Section: Esr2-icre Knock-in Mousementioning

confidence: 99%

“…Strong fluorescence seen in secretory cells. (Moverare et al, 2004) Colon 11 Diffuse to patchy fluorescence throughout mucosa, stronger and more widespread than in proximal GI tract. (Hasson et al, 2014;Levin, 2009) Ductus (vas) deferens 1 Limited, punctate fluorescence in some luminal epithelial cells; weaker than head and tail of epididymis.…”

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confidence: 99%

Generation of an estrogen receptor beta‐iCre knock‐in mouse

Cacioppo

Koo

Lin

et al. 2016

Genesis

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A novel knock-in mouse that expresses codon-improved Cre recombinase (iCre) under regulation of the estrogen receptor beta (Esr2) promoter was developed for conditional deletion of genes and for the spatial and/or temporal localization of Esr2 expression. ESR2 is one of two classical nuclear estrogen receptors and displays a spatio-temporal expression pattern and functions that are different from the other estrogen receptor, ESR1. A cassette was constructed that contained iCre, a polyadenylation sequence, and a neomycin selection marker. This construct was used to insert iCre in front of the endogenous start codon of the Esr2 gene of a C57BL/6J embryonic stem cell line via homologous recombination. Resulting Esr2-iCre mice were bred with ROSA26-lacZ and Ai9-RFP reporter mice to visualize cells of functional iCre expression. Strong expression was observed in the ovary, the pituitary, the interstitium of the testes, the head and tail but not body of the epididymis, skeletal muscle, the coagulation gland (anterior prostate), the lung, and the preputial gland. Additional diffuse or patchy expression was observed in the cerebrum, the hypothalamus, the heart, the adrenal gland, the colon, the bladder, and the pads of the paws. Overall, Esr2-iCre mice will serve as a novel line for conditionally ablating genes in Esr2-expressing tissues, identifying novel Esr2-expressing cells, and differentiating the functions of ESR2 and ESR1.

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“…Transcription factors over-represented in the promoter regions are hepatocyte nuclear factors (HNF4, HNF1) and estrogen receptor (ER). The connections between blood coagulation and ER (Farsetti et al, 1998;Moverare et al, 2004) / HNF-4 (Farsetti et al, 1998) have been reported. HNF-1 was reported to be involved in some stress response (Leu et al, 2001).…”

Section: Annotating Cgemsmentioning

confidence: 99%

Evolutionary-conserved Gene Expression Response Profiles Across Mammalian Tissues

Ji¹,

Blackwell²,

Fermin³

et al. 2007

OMICS: A Journal of Integrative Biology

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Gene expression responses are complex and frequently involve the actions of many genes to effect coordinated patterns. We hypothesized these coordinated responses are evolutionarily conserved and used a comparison of human and mouse gene expression profiles to identify the most prominent conserved features across a set of normal mammalian tissues. Based on data from multiple studies across multiple tissues in human and mouse, 13 gene expression modes across multiple tissues were identified in each of these species using principal component analysis. Strikingly, 1-to-1 pairing of human and mouse modes was observed in 12 out of 13 modes obtained from the two species independently. These paired modes define evolutionarily conserved gene expression response modes (CGEMs). Notably, in this study we were able to extract biological responses that are not overwhelmed by laboratory-to-laboratory or species-to-species variation. Of the variation in our gene expression dataset, 84% can be explained using these CGEMs. Functional annotation was performed using Gene Ontology, pathway, and transcription factor binding site over representation. Our conclusion is that we found an unbiased way of obtaining conserved gene response modes that accounts for a considerable portion of gene expression variation in a given dataset, as well as validates the conservation of major gene expression response modes across the mammals.

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Estrogen increases coagulation factor V mRNA levels via both estrogen receptor-alpha and -beta in murine bone marrow/bone

Cited by 14 publications

References 23 publications

17α‐Ethinylestradiol rapidly alters transcript levels of murine coagulation genes via estrogen receptor α

17α‐Ethinylestradiol rapidly alters transcript levels of murine coagulation genes via estrogen receptor α

Generation of an estrogen receptor beta‐iCre knock‐in mouse

Evolutionary-conserved Gene Expression Response Profiles Across Mammalian Tissues

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