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Marta Prieto

Publications and source records attributed to Marta Prieto.

7 recordsLinked to original sources
PubMed2006

Endoglin regulates cyclooxygenase-2 expression and activity.

The endoglin heterozygous (Eng(+/-)) mouse, which serves as a model of hereditary hemorrhagic telangiectasia (HHT), was shown to express reduced levels of endothelial NO synthase (eNOS) with impaired activity. Because of intricate changes in vasomotor function in the Eng(+/-) mice and the potential interactions between the NO- and prostaglandin-producing pathways, we assessed the expression and function of cyclooxygenase (COX) isoforms. A specific upregulation of COX-2 in the vascular endothelium and increased urinary excretion of prostaglandin E(2) were observed in the Eng(+/-) mice. Specific COX-2 inhibition with parecoxib transiently increased arterial pressure in Eng(+/-) but not in Eng(+/+) mice. Transfection of endoglin in L6E9 myoblasts, shown previously to stimulate eNOS expression, led to downregulation of COX-2 with no change in COX-1. In addition, COX-2 promoter activity and protein levels were inversely correlated with endoglin levels, in doxycyclin-inducible endothelial cells. Chronic NO synthesis inhibition with N(omega)-nitro-l-arginine methyl ester induced a marked increase in COX-2 only in the normal Eng(+/+) mice. N(omega)-nitro-l-arginine methyl ester also increased COX-2 expression and promoter activity in doxycyclin-inducible endoglin expressing endothelial cells, but not in control cells. The level of COX-2 expression following transforming growth factor-beta1 treatment was less in endoglin than in mock transfected L6E9 myoblasts and was higher in human endothelial cells silenced for endoglin expression. Our results indicate that endoglin is involved in the regulation of COX-2 activity. Furthermore, reduced endoglin levels and associated impaired NO production may be responsible, at least in part, for augmented COX-2 expression and activity in the Eng(+/-) mice.

Animals↗
PubMed2006

Reduced angiogenic responses in adult Endoglin heterozygous mice.

OBJECTIVE: To determine if angiogenesis is altered in adult Endoglin heterozygous (Eng(+/-)) mice, the animal model for the vascular disorder hereditary hemorrhagic telangiectasia type 1 (HHT1). METHODS: Primary cultures of endothelial cells were generated from Eng(+/-) and Eng(+/+) mice and analyzed for proliferation, migration, and ability to form capillary-like tubes. Endothelial cells derived from umbilical veins of newborns (HUVEC) with an HHT1 genotype were also tested for capillary formation. Two in vivo models of angiogenesis were tested in the Eng(+/-) and Eng(+/+) mice: Matrigel implant-dependent angiogenesis and reperfusion following hindlimb ischemia. RESULTS: The Eng(+/-) endothelial cells displayed significantly reduced proliferation and migration, increased collagen production, and decreased NO synthase expression and vascular endothelial growth factor (VEGF) secretion. They also showed impaired capillary tube formation in vitro, as did the HHT1 HUVEC. These endothelial cell-specific abnormalities were associated with impaired Matrigel-dependent capillary tube formation in vivo and delayed reperfusion following hindlimb ischemia. CONCLUSIONS: Although vascular development is normal in Eng(+/-) mice, angiogenic abnormalities were observed in the adult mice and their isolated endothelial cells. These results suggest that a normal level of endoglin is required for full angiogenic activity.

Animals↗
PubMed2005

[Prevalence of overactive bladder in Spain: a population-based study].

OBJECTIVES: The aim of this study was to assess the prevalence of the urinary symptoms suggestive of overactive bladder (OAB) in Spain based on the International Continence Society (ICS) 2002 consensus criteria as urinary urgency, with or without urge incontinence, usually with frequency and nocturia. METHODS: 1,669 real telephone interviews were conducted to adults aged > or = 40 years. The sample size estimation was made according to the prevalence for OAB described in the Milsom paper stratified by age and gender due to the high variability observed between ranges. Appearance and prevalence of main OAB symptoms, medical diagnostic and therapy due to these symptoms data were collected. RESULTS: the sample population was 1669 aged > or = 40 years, 50.6% women and 49.4% men. The overall prevalence of symptoms suggestive of OAB according to the OAB definition from ICS report 2002 was 21.5%, significantly higher in women (25.6%) than men (17.4%)(p<0.05). Adjusting these data to Spanish National Census of year 2000, the prevalence was 19.9%, being higher as well in women (23.6%) than men (115.4%). Urge urinary incontinence and stress urinary incontinence were superior in women (16.7% vs 10.4% and 33.1% vs 7.9% respectively)(p<0.01). Urinary frequency > 8 voids/day was referred by 9.8% of women and 7.9% of men interviewed. 62% of men and 52.4% of women reported they get up at night to void. A total of 52.1% of patients with urinary symptoms suggestive of overactive bladder reported they had consulted a doctor anytime before the interview due to urinary disorders and 16.7% was currently receiving treatment for some of these symptoms. CONCLUSIONS: Prevalence of urinary symptoms suggestive of Overactive Bladder is high in this study, in accordance with data from international studies. Urinary urgency, symptom which defines the pathology, is more prevalent in Spanish women than men. Further studies are needed to better assess OAB impact in the Spanish general population.

Adult↗
PubMed2004

Effect of the long-term treatment with trandolapril on endoglin expression in rats with experimental renal fibrosis induced by renal mass reduction.

BACKGROUND: Endoglin is a membrane glycoprotein that regulates TGF-beta1 signaling. Previous studies have revealed that endoglin is upregulated in several models of experimental fibrosis, and that endoglin expression can counteract the fibrogenic effects of TGF-beta1. As treatment with angiotensin converting enzyme (ACE) inhibitors reduces renal fibrosis by mechanisms that are, in part, not dependent on angiotensin II blockade, we have assessed the hypothesis that this effect could be mediated by endoglin upregulation. METHODS: We have used the 5/6-nephrectomy renal mass reduction (RMR) model of renal fibrosis in rats treated (RMR+T) or not treated with the ACE inhibitor trandolapril (0.7 mg/kg/day). One, 3 and 5 months after RMR, mean arterial pressure and renal function were measured. In addition, renal fibrosis was evaluated quantitatively and endoglin, TGF-beta1, collagen type I and collagen type IV expression was assessed by Northern blot and immunohistochemistry. RESULTS: RMR induced a progressive increase in mean arterial pressure, urinary protein excretion and glomerular and tubulointerstitial fibrosis, which is accompanied by an increased expression of TGF-beta1, endoglin and collagen types I and IV. Trandolapril treatment reduced systemic blood pressure and lessened proteinuria after RMR, as well as expression of TGF-beta1, endoglin and collagens. CONCLUSION: The present study demonstrates an increased TGF-beta1, endoglin, collagen type I and collagen type IV expression in rats with severe hypertension and renal damage. The effect of trandolapril to decrease renal fibrosis seems to be based in a reduced TGF-beta1 expression but not in an increased expression of endoglin.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2004

Endoglin regulates nitric oxide-dependent vasodilatation.

Endoglin is a membrane glycoprotein that plays an important role in cardiovascular development and angiogenesis. We examined the role of endoglin in the control of vascular tone by measuring nitric oxide (NO)-dependent vasodilation in haploinsufficient mice (Eng+/-) and their Eng+/+ littermates. The vasodilatory effect of acetylcholine, bradykinin, and sodium nitroprusside was assessed in anesthetized mice; in isolated, perfused hindlimbs; and in aortic rings. The substantial hypotensive and vasodilatory response induced by acetylcholine and bradykinin in Eng+/+ was markedly reduced in Eng+/- mice. Both kinds of animals had similar responses to sodium nitroprusside, suggesting that the deficient vasodilatory effect is not due to a NO response impairment. Urinary and plasma concentrations of nitrites, a NO metabolite, were lower in Eng+/- than in Eng+/+ mice. The levels of endothelial nitric oxide synthase (eNOS) in kidneys and femoral arteries were about half in Eng+/- than in Eng+/+ mice and were also reduced in primary cultures of aortic endothelial cells from Eng+/- compared with those from Eng+/+ mice. Furthermore, overexpression or suppression of endoglin in cultured cells induced a marked increase or decrease in the protein levels of eNOS, respectively. Thus, our results in vivo and in vitro demonstrate a relationship between endoglin and NO-dependent vasodilation mediated by the regulation of eNOS expression.

Acetylcholine↗
PubMed2003

Cancer care in Chile.

Cancer is responsible for 22% of deaths in Chile and this proportion is increasing every year. After years of comparative neglect, the Chilean government is now attempting to implement a systematic anticancer policy rooted in evidence-based medicine. Major reform of the national health system promises to guarantee healthcare for those affected by "catastrophic" illnesses. However, budgetary constraints mean that only some cancers will count as catastrophic. This Reportage considers how cancer care has evolved in Chile over recent years and examines the rationale behind the allocation of scarce resources.

Adult↗