The effect of progesterone on estrogen-induced uterine blood flow

Resnik, Robert; Brink, G.; Plumer, Michael H.

doi:10.1016/0002-9378(77)90617-2

Cited by 63 publications

(15 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus, our finding that progesterone does not inhibit uterine artery caveolin 1 expression seems to have provided a reasonable, direct explanation as to why progesterone does not increase uterine blood flow in various animal models. Additionally, concomitant progesterone treatment partially attenuates the estrogen-induced acute (120-min) increase in uterine blood flow in OVX sheep [40,42,43]. These previous data may have implied that progesterone might be able to inhibit the observed stimulatory effects of estrogen on NOS3 dissociation from caveolin 1 [20], thereby antagonizing the stimulatory effects of estrogen on NOS3 activation, although this theory needs to be tested.…”

Section: Reciprocal Regulation Of Uterine Artery Caveolinmentioning

confidence: 77%

“…The scenario of the effects of progesterone on uterine vasodilatation is much less distinct. It has been previously reported that progesterone treatment alone does not stimulate uterine blood flow [40] and that during prolonged estrogen infusion, progesterone treatment does not have any major effects on estrogen-induced uterine vasodilatation [41], even though both treatments are capable of stimulating uterine artery endothelial NOS3 expression [13, present study]. Thus, our finding that progesterone does not inhibit uterine artery caveolin 1 expression seems to have provided a reasonable, direct explanation as to why progesterone does not increase uterine blood flow in various animal models.…”

Section: Reciprocal Regulation Of Uterine Artery Caveolinmentioning

confidence: 99%

See 1 more Smart Citation

Global Protein Expression Profiling Underlines Reciprocal Regulation of Caveolin 1 and Endothelial Nitric Oxide Synthase Expression in Ovariectomized Sheep Uterine Artery by Estrogen/Progesterone Replacement Therapy1

Chen

Jia²,

Barker

et al. 2006

Biology of Reproduction

View full text Add to dashboard Cite

Ovariectomized (OVX) ewes were assigned to receive vehicle, progesterone (P4, 0.9-g controlled internal drug release vaginal implants), estradiol-17beta (E2, 5 microg/kg bolus + 6 microg kg(-1) day(-1)), or P4 + E2 for 10 days (n = 3/group). Uterine artery endothelial proteins were mechanically isolated on Day 10. The samples were used for protein expression profiling by the Ciphergen Proteinchip system and immunoblotting analysis of endothelial nitric oxide synthase (NOS3, also termed eNOS) and caveolin 1. Uterine artery rings were cut and analyzed by immunohistochemistry to localize NOS3 and caveolin 1 expression. With the use of the IMAC3 protein chip with loading as little as 2 microg protein/sample, many protein peaks could be detected. Compared to vehicle controls, a approximately 133.1-kDa protein was identified to be upregulated by 2- to 4-fold in OVX ewes receiving E2, P4, and their combination, whereas a approximately 22.6-kDa protein was downregulated by 2- to 4-fold in OVX ewes receiving E2 and E2/P4, but not P4 treatments. Western blot analysis revealed that E2, P4, and their combination all increased NOS3 protein, whereas E2 and its combination with P4, but not P4 alone, downregulated caveolin 1 expression. Immunohistochemical analysis revealed that NOS3 was mainly localized in the endothelium and upregulated by E2, whereas caveolin 1 was localized in both endothelium and smooth muscle and downregulated by E2. Thus, our data demonstrate that uterine artery endothelial NOS3 and caveolin 1 are regulated reciprocally by estrogen replacement therapy. In keeping with the facts that E2, but not P4, causes uterine vasodilatation and that E2 and P4 increase NOS3 expression, but only E2 decrease caveolin 1 expression, our current study suggests that both increased NOS3 expression and decreased caveolin 1 expression are needed to facilitate estrogen-induced uterine vasodilatation.

show abstract

Section: Reciprocal Regulation Of Uterine Artery Caveolinmentioning

confidence: 77%

Section: Reciprocal Regulation Of Uterine Artery Caveolinmentioning

confidence: 99%

Global Protein Expression Profiling Underlines Reciprocal Regulation of Caveolin 1 and Endothelial Nitric Oxide Synthase Expression in Ovariectomized Sheep Uterine Artery by Estrogen/Progesterone Replacement Therapy1

Chen

Jia²,

Barker

et al. 2006

Biology of Reproduction

View full text Add to dashboard Cite

show abstract

“…PGIS, but no other prostaglandin isomerases, was examined because PGI 2 is the primary eicosanoid produced by the uterine and systemic vasculature [3,17,22]. We and others have reported the vasodilatory effects of estrogen with and without progesterone administration on uterine and systemic blood flows [4][5][6][7][9][10][11][12] and the roles that these steroids play during the cardiovascular adaptations to pregnancy (reviewed in [1,2,5,7]). These complex and integrated vasodilatory effects of estrogen treatment and their modification by progesterone may be modulated by PGI 2 that is locally produced within the endothelium and/or VSM via these enzymes.…”

Section: Discussionmentioning

confidence: 99%

“…Prolonged systemic estrogen administration to ovariectomized ewes acutely and dramatically elevates UBF within 120 min; however, UBF falls on Days 1-3 and remains slightly elevated above basal levels through 10 days of treatment [5][6][7][8]. Progesterone alone does not stimulate UBF; however, it can partially attenuate the acute (ϳ120 min) increase in UBF in estrogen-treated ovariectomized sheep [6,[9][10][11]. During prolonged estrogen infusion, concomitant progesterone treatment did not alter the estrogen-mediated elevation in UBF [6,12] but may redistribute UBF in favor of the caruncles, i.e., the future site of ovine placentation [12].…”

Section: Introductionmentioning

confidence: 99%

Endothelial Vasodilator Production by Uterine and Systemic Arteries. VIII. Estrogen and Progesterone Effects on cPLA2, COX-1, and PGIS Protein Expression1

Rupnow

Phernetton

Modrick

et al. 2002

Biology of Reproduction

View full text Add to dashboard Cite

During ovine pregnancy, when both estrogen and progesterone are elevated, prostacyclin (PGI2) production by uterine arteries and the key enzymes for PGI2 production, phospholipase A2 (cPLA2), cyclooxygenase 1 (COX-1), and prostacyclin synthetase (PGIS), are increased. This study was conducted to determine whether exogenous estradiol-17beta (E2beta) with or without progesterone (P4) treatment would increase cPLA2, COX-1, and PGIS protein expression in ovine uterine, mammary, and systemic (renal, mental, and coronary) arteries. Nonpregnant ovariectomized sheep received vehicle (n = 10), P(4) (0.9-g controlled internal drug release vaginal implants; n = 13), E2beta (5 microg/kg bolus followed by 6 microg x kg(-1) x day(-1); n = 10), or P4 + E2beta (n = 12). Arteries were procured on Day 10, and cPLA2, COX-1, and PGIS protein were measured by Western immunoblot analysis in endothelial isolated proteins and vascular smooth muscle (VSM). The levels of cPLA2 was increased in uterine artery endothelium in ewes treated with P4 + E2beta but was not altered by any steroid treatment in renal, coronary, mammary, or omental artery endothelium or in VSM of any evaluated artery. Similarly, COX-1 was increased in uterine artery endothelium with P4 + E2beta but was not significantly altered by treatment in other endothelium or VSM. E2beta treatment increased PGIS protein in uterine and renal artery endothelium but did not alter PGIS in other endothelial tissue. P4 increased PGIS expression in the uterine, mammary, omental, and renal artery VSM, and E2beta increased PGIS expression in the uterine and omental artery VSM. Both E2beta and P4 treatments differentially alter protein expression of the key enzymes involved in PGI2 production in different artery types and may play an important role in the control of blood flow redistribution during hormone replacement therapy.

show abstract

“…It is known that progesterone abolishes or alters the effect of estrogen on lipoproteins (Newnham 1993;Psaty et al 1993) and reendothelialization after vascular injury (Levine et al 1996). It is thought that progesterone decreases estrogen receptor expression in the human uterine vascular endothelium (Perrot-Applanat et al 1994;McDonnell et al 1995), thereby attenuating estrogen-induced angiogenic responses (Resnik et al 1977;Magness et al 1998).…”

Section: Discussionmentioning

confidence: 99%

Endometrial Injury Increases Side Population Cells in the Uterine Endometrium: A Decisive Role of Estrogen

Hyodo

Matsubara

Kameda

et al. 2011

Tohoku J. Exp. Med.

View full text Add to dashboard Cite

Normal endometrial growth is essential for embryonic implantation and maintenance of pregnancy. The uterine endometrium contains stem cells that are involved in tissue regeneration. Side population cells (SP cells) are an emerging cell population that may be responsible for the regeneration process of uterine endometrium. In this study, we investigated the changes in the distribution of SP cells using a mouse model of uterine endometrial injury that was induced by peritoneal injection of lipopolysaccharide (LPS). The uterine horns were collected 0, 6, 12, and 18 hours after LPS injection. ATP-binding cassette and sub-family G member 2 (Abcg2) is highly expressed on the cellular membrane of some stem and progenitor cells, and was used as a marker for SP cells. Immunohistochemistry demonstrated that Abcg2-positive cells were increased around the uterine endometrial glands from 6 to 12 h after LPS injection. The percentage of Abcg2-positive cells was calculated using flow cytometry. The percentage of stromal SP cells was significantly higher at 6 h after LPS injection, compared with the value before the injection (3.01 ± 0.41% vs. 1.63 ± 0.31%, P < 0.05). To evaluate the influence of ovarian hormones, we implanted pellets containing 17β-estradiol (0.1 mg), progesterone (10 mg), or a combination of 17β-estradiol and progesterone in the bilaterally ovariectomized mice. Ovariectomy abolished the increase in SP cells, which was restored by estradiol, but not by progesterone or the combination treatment. In conclusion, estrogen is required for the increase of SP cells, thereby leading to the regeneration of the uterine endometrium.

show abstract

The effect of progesterone on estrogen-induced uterine blood flow

Cited by 63 publications

References 9 publications

Global Protein Expression Profiling Underlines Reciprocal Regulation of Caveolin 1 and Endothelial Nitric Oxide Synthase Expression in Ovariectomized Sheep Uterine Artery by Estrogen/Progesterone Replacement Therapy1

Global Protein Expression Profiling Underlines Reciprocal Regulation of Caveolin 1 and Endothelial Nitric Oxide Synthase Expression in Ovariectomized Sheep Uterine Artery by Estrogen/Progesterone Replacement Therapy1

Endothelial Vasodilator Production by Uterine and Systemic Arteries. VIII. Estrogen and Progesterone Effects on cPLA2, COX-1, and PGIS Protein Expression1

Endometrial Injury Increases Side Population Cells in the Uterine Endometrium: A Decisive Role of Estrogen

Contact Info

Product

Resources

About