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Differential Regulation of Endothelium Behavior by Progesterone and Medroxyprogesterone Acetate

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Differential Regulation of Endothelium Behavior by Progesterone and Medroxyprogesterone Acetate P H CUTINI and others Progestins and vascular function 220:3 179–193 Research Differential regulation of endothelium behavior by progesterone and medroxyprogesterone acetate Pablo H Cutini1,2, Adria´n E Campelo1,2 and Virginia L Massheimer1,2 Correspondence should be addressed 1Ca´ tedra de Bioquı´mica Clı´nica II, Departamento de Biologı´a, Bioquı´mica y Farmacia, Universidad Nacional to V L Massheimer del Sur (UNS), San Juan 670, B8000ICN, Bahı´a Blanca, Argentina Email 2Consejo Nacional de Investigaciones Cientı´ficas y Te´ cnicas (CONICET), Argentina, Buenos Aires, Argentina [email protected] Abstract Medroxyprogesterone acetate (MPA) is a synthetic progestin commonly used in hormone Key Words replacement therapy (HRT). The aim of this research was to study and compare the effect of " cell migration progesterone (Pg) and MPA on the regulation of cellular events associated with vascular " medroxyprogesterone homeostasis and disease. Platelet adhesion to endothelial cells (ECs), nitric oxide (NO) acetate production, and cell migration were studied using murine ECs in vitro exposed to the " nitric oxide progestins. After 7 min of treatment, MPA significantly inhibited NO synthesis with respect " progesterone to control values; meanwhile, Pg markedly increased vasoactive production. In senile ECs, " vascular tissue the stimulatory action of Pg decreases; meanwhile, MPA maintained its ability to inhibit Journal of Endocrinology NO synthesis. The presence of RU486 antagonized the action of each steroid. When ECs were preincubated with PD98059 (MAPK inhibitor) or chelerythrine (protein kinase C (PKC) inhibitor) before Pg or MPA treatment, the former totally suppressed the steroid action, but the PKC antagonist did not affect NO production. In the presence of a PI3K inhibitor (LY294002), a partial reduction in Pg effect and a reversal of MPA action were detected. Using indomethacin, the contribution of the cyclooxygenase (COX) pathway was also detected. On platelet adhesion assays, Pg inhibited and MPA stimulated platelet adhesion to ECs. Under inflammatory conditions, Pg prevented platelet adhesion induced by lipopoly- saccharide (LPS); meanwhile, MPA potentiated the stimulatory action of LPS. Finally, although both steroids enhanced migration of ECs, MPA exhibited a greater effect. In conclusion, the data presented in this research provide evidence of a differential regulation of vascular function by Pg and MPA. Journal of Endocrinology (2014) 220, 179–193 Introduction The endothelium is the main regulator of vascular properties. NO is a potent vasodilator that prevents physiology that contributes to maintaining vascular tone platelet aggregation (Ignarro 1989) and leukocyte and non-thrombogenic properties of the endothelial sur- adhesion to the endothelium (Tsao et al. 1995)and face. Endothelial nitric oxide (NO) is a key factor in vascular decreases the expression of proinflammatory genes homeostasis with antiatherogenic and antithrombotic (Harrison et al. 2006). Several cardiovascular risk factors http://joe.endocrinology-journals.org Ñ 2014 Society for Endocrinology Published by Bioscientifica Ltd. DOI: 10.1530/JOE-13-0263 Printed in Great Britain Downloaded from Bioscientifica.com at 09/25/2021 01:15:08AM via free access Research P H CUTINI and others Progestins and vascular function 220:3 180 such as oxidative stress, alterations in plasmatic lipid resulted in a substantial increase in the risk of myocardial profile, hypertension, viral infections, and diabetes melli- infarction (Rossouw et al. 2002). In contrast, another tus promote endothelial dysfunction and consequently study also performed in healthy postmenopausal women vascular diseases, mainly atherosclerosis. The genesis of showed that oral administration of E2 plus Pg improved atheromatous lesions has a multifactorial pattern charac- circulating levels of coagulation factors and vascular terized by impaired synthesis of vasoactive molecules health (van Baal et al. 1999). (NO and prostacyclin), enhanced synthesis and expression Vascular function is regulated by several hormones of cell adhesion molecules (CAMs) involved in leukocyte and factors including sex steroids. Both ECs and vascular infiltration and platelet adhesion, as well as an altered smooth muscle cells (VSMCs) possess estrogen receptor profile of cell proliferation and migration. The initial and Pg receptor (PgR; Joswig et al. 1999, Vazquez et al. response to vascular injury includes activation, adhesion, 1999). Current knowledge about the biochemical action and aggregation of platelets to endothelium, which are of natural Pg and other progestins at the vascular level the events that release cytokines and enhance leukocyte is quite low in contrast to the large amount of evi- recruitment (Ross 1999). In vascular diseases, endothelial dence reported regarding E2. In recent years, potential cell (EC) turnover is altered (Choy et al. 2001). After vascular effects of Pg have been described. In rabbit endothelium damage, vessel repair is achieved by coronary arteries and rat aorta, Pg induces endothelium- migration and proliferation of adjacent ECs (Cartwright independent vasorelaxation (Jiang et al. 1992). Moreover, et al et al . 2000, Moreno . 2009). Pg regulates vascular cell growth (Glusa et al. 1997, Menopause hypoestrogenism represents a physiologi- Simoncini et al. 2003) and inhibits expression of adhesion cal risk factor for cardiovascular disease, which is molecules induced by tumor necrosis factor-a (TNF-a) attributed to the loss of 17b-estradiol (E ) cardioprotec- 2 and lipopolysaccharide (LPS) (Glusa et al. 1997, Otsuki tion. However, besides the decrease of circulating E2 et al. 2001, Simoncini et al. 2004). We have previously levels, synthesis of ovarian progesterone (Pg) is also demonstrated that in rat aortic tissue, Pg non-genomically affected during menopause. Hormone replacement induces NO synthase (NOS) and cyclooxygenase (COX) therapy (HRT) based on estrogen, or combined with stimulation through a mechanism of action that involves natural or synthetic progestins like medroxyprogesterone MAPK and phosphatidylinositol-3-kinase (PI3K) signaling acetate (MPA), has emerged as an option to relieve the pathways and a cross talk between NOS and COX systems. signs and symptoms associated with menopause. Journal of Endocrinology The rapid action of the steroid also includes inhibition Although there is a large body of information derived of platelet aggregation (IPA) dependent on NOS and from in vitro experimental studies that confer a relevant phospholipase C (PLC) transduction systems (Mendiberri cardioprotective action to E2, this cannot be translated et al. 2006). The fast effects elicited by the hormone are into health benefit when HRT is applied to postmenopau- required for the regulation of EC growth (Cutini et al. sal women. This raises the controversy about the risk/benefit of HRT with respect to cardiovascular disease. 2009). Pg also enhances cell proliferation, migration, Historically, progestins were included in the HRT and apoptosis of VSMCs. The regulation of muscle cell protocols to counteract the endometrial dysplasia caused growth matched with the two-step model of steroid action that integrates genomic and non-genomic actions (Cutini by E2. It has been reported that administration of MPA improves the effectiveness of HRT (Manson et al. 2003). et al. 2009, Cutini & Massheimer 2010). However, other studies have shown that coadministration There is evidence in the literature that Pg and MPA of progestins blocks the atheroprotective effect of estrogen are not equivalent in terms of molecular signaling in (Sitruk-Ware 2000). The secondary cardiovascular preven- human and murine vascular tissues. It has been reported tion study Heart and Estrogen/progestin Replacement that Pg and MPA activate different signaling events in vitro Study showed that HRT performed by oral administration (L’hermite et al. 2008). MPA and other synthetic proges- of conjugated equine estrogen (CEE) and MPA for 4 years tins exert different inflammatory and anti-inflammatory was not able to reduce the incidence of coronary events effects in vitro when compared with Pg (Simoncini et al. and, in turn, increased the risk of thromboembolic events 2004). Therefore, the aim of this research was to study in postmenopausal women with established coronary and compare the effect of Pg and MPA on the regulation artery disease (Hulley et al. 1998, Grady et al. 2002). of cellular events associated with vascular homeostasis Indeed, in the Women’s Health Initiative trial, CEE plus and disease: platelet adhesion to ECs, NO production, and MPA administration to healthy postmenopausal women cell migration. http://joe.endocrinology-journals.org Ñ 2014 Society for Endocrinology Published by Bioscientifica Ltd. DOI: 10.1530/JOE-13-0263 Printed in Great Britain Downloaded from Bioscientifica.com at 09/25/2021 01:15:08AM via free access Research P H CUTINI and others Progestins and vascular function 220:3 181 Materials and methods establish a pure EC culture, after 3 days of culture, the ring explants were removed and ECs were allowed to reach Materials confluency. The identity of the ECs was determined Pg was obtained from Calbiochem-Novabiochem Inter- i) by phase-contrast microscope observation of the national (San Diego, CA, USA). Griess reagents were characteristic morphology of cobblestone shape growth purchased from Britania Laboratories (Buenos Aires, in confluent monolayer, ii) by positive immunocytochem- Argentina). Trypsin/EDTA
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