A. Estellés

Hospital Universitari i Politècnic La Fe

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Francisco España

Instituto de Investigación Sanitaria La Fe

J Aznar

Leitat Technological Center

J. Gilabert

Universidad Complutense de Madrid

Juan Gilabert–Estellés

Memorial Sloan Kettering Cancer Center

José A. Aznar

Instituto de Investigación Sanitaria La Fe

Pilar Medina

Instituto de Investigación Sanitaria La Fe

Luis Ramón

Valencian Infertility Institute

Esther Zorio

Instituto de Investigación Sanitaria La Fe

Amparo Vayá

Hospital Universitari i Politècnic La Fe

Salvador Grancha

Grifols (Spain)

Cooperative Institutions

Hospital Universitari i Politècnic La Fe

Instituto de Investigación Sanitaria La Fe

Leitat Technological Center

Universitat de València

Universidad de Murcia

Instituto de Salud Carlos III

Centro de Investigación Biomédica en Red

University of Rochester Medical Center

Sociedad Española de Trombosis y Hemostasia

Leiden University Medical Center

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Assay of protein c in human plasma: Comparison of amidolytic, coagulation, and immunochemical assays

Thrombosis Research (1986)

Francisco España A. Estellés J Aznar J. Gilabert

Unstable angina

10.1016/0049-3848(86)90023-x

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Citations (36)

Insights Into the Role of microRNAs in Cardiac Diseases: From Biological Signalling to Therapeutic Targets

Cardiovascular & Hematological Agents in Medicinal Chemistry (2009)

Esther Zorio Pilar Medina J. Rueda José M. Millán María Rosa Arnau

microRNAs have recently opened new pathways to explain gene expression and disease biology in many scenarios, including cardiac diseases. microRNAs are endogenous small non-coding RNAs that mediate post-transcriptional repression or messenger RNA degradation. By annealing to inexactly complementary sequences in the 3 untranslated region of the target messenger RNA, protein level is down-regulated. Several microRNAs appear to act cooperatively through multiple target sites in one gene and, conversely, most microRNAs can target several genes. miR-133 and miR-1 are specifically expressed in cardiac and skeletal muscle and control myogenesis, cardiac development, cardiac performance and cardiomyocyte hypertrophy (mainly by tuning transcription factors and other growth-related targets). They also modulate the expression of certain cardiac ion channels and related proteins with proarrhythmic effect. Besides them, other microRNAs have been shown to exert influence on the myocardial growth, the electrical balance and the angiogenesis processes that take place in the heart. Bioinformatics is a useful tool to identify potential targets of a given microRNA, although there is still substantial concern about their reliability. Experimental manipulation of microRNAs has provided a tantalizing basis to speculate that future research on microRNAs may yield important progress in the prevention of sudden cardiac death and in the treatment of cardiac heart failure. However, the final effect of the blockage of microRNAs in vivo remains unclear, since each of them can target hundreds of genes with different intensity. The era of the microRNAs in cardiovascular diseases has just started. Keywords: microRNA, gene expression, differentiation, cardiac hypertrophy, ion channel, repolarization, connexin, angiogenesis

10.2174/187152509787047676

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Citations (48)

Changes in molecular forms of prostate‐specific antigen during treatment with finasteride

BJU International (2002)

Francisco España Manuel Martı́nez M. Royo A. Estellés J.M. Alapont

Objective To study the influence of finasteride treatment on the molecular forms of prostate‐specific antigen (PSA) in patients with benign prostatic hyperplasia (BPH). Patients and methods Total PSA, free PSA and PSA complexed to α 1 ‐antichymotrypsin (PSA‐α 1 ACT) were measured in plasma and serum from 40 men with BPH and a total PSA of < 20 ng/mL, using in‐house and commercial immunoassays, before and during treatment with finasteride (30 men) or placebo (10 men). Results The baseline values were not significantly different between the groups, with mean ( sd ) total plasma PSA levels of 3.6 (4.3) and 4.8 (5.9) ng/mL in the finasteride and placebo groups, respectively. Finasteride, but not placebo, induced a significant reduction in total PSA, free PSA and PSA‐α 1 ACT levels in plasma and serum ( P < 0.001). However, complexed‐to‐total (c/t) and free‐to‐total (f/t) PSA ratios remained constant in both groups, both in plasma and serum, during the follow‐up. Conclusion The decrease in total PSA after finasteride treatment results from a proportional reduction in its two major molecular forms, free PSA and PSA‐α 1 ACT, which explains why the c/t and f/tPSA ratios do not change significantly despite treatment. This suggests that routine analysis of molecular forms of PSA could improve the utility of the change in total PSA associated with finasteride for the early diagnosis of prostate cancer. It also suggests that any subsequent change in both ratios, particularly an increase in c/tPSA or a decrease in f/tPSA ratio, could be considered an early sign of neoplastic degeneration rather than a therapeutic consequence.

10.1046/j.1464-410x.2002.03002.x

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Citations (20)

Fibrinogen, plasma viscosity and blood viscosity in obesity. Relationship with insulin resistance.

PubMed (2007)

Eva Solá Amparo Vayá María Simó Antonio Hernández‐Mijares Carlos Morillas

Plasma viscosity (PV) and blood viscosity (BV) have been scarcely evaluated in morbid obese patients with no other concomitant cardiovascular risk factors. Contradictory results have been published regarding the influence of insulin resistance on these rheological parameters in obesity. In 67 severe or morbid obese patients without other cardiovascular risk factors (51 women and 11 men, aged 34+/-11 years), fibrinogen, PV and BV at native (nBV) and corrected 45% hematocrit (cBV) have been determined, and insulin resistance has been calculated with homeostasis model assessment (HOMA) index, in basal conditions and after a three month diet period. The same determinations were performed in 67 healthy volunteers (45 women, 22 men, aged 32+/-10 years) at baseline and three months later. When cases and controls were compared, obese patients showed higher fibrinogen levels (P<0.001), PV (P=0.050) and cBV (P=0.035), and showed a higher insulin resistance than the control group (P<0.001). Differences in PV were maintained after adjusting for BMI (P=0.001), but disappeared after adjusting for HOMA (P=0.391) fibrinogen (P=0.367) and LDL-chol (P=0.097). Differences between obese patients and the control group for cBV disappeared after adjusting for BMI (P=0.739), HOMA (P=0.744), fibrinogen (P=0.907), LDL-chol (P=0.283) and PV (P=0.112). The achieved weight loss (8.7+/-3.53%) was not accompanied by any changes in these rheological parameters (P>0.050). Obese patients show increased fibrinogen levels, PV and cBV. These rheological disturbances seem to be associated with insulin resistance and the metabolic syndrome, and do not seem to improve with moderate weight loss.

Hyperviscosity

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Interaction of plasma kallikrein with protein C inhibitor in purified mixtures and in plasma

Fibrinolysis and Proteolysis (1990)

Francisco España A. Estellés John H. Griffin J Aznar

Prekallikrein

10.1016/0268-9499(90)90101-o

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Citations (0)

The Journal of Urology (1999)

Francisco España M. Royo Manuel Martı́nez M J Enguídanos C.D. Vera Donoso

10.1097/00005392-199908000-00074

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Citations (10)

108 Relationship between PAI-1 promoter polymorphism and PAI-1 circulating levels in postmenopausal women with coronary artery disease (CAD)

Fibrinolysis & proteolysis/Fibrinolysis and proteolysis (1997)

Salvador Grancha A. Estellés J. Gilabert Guillermo Sáez Tormo C. Falcó

10.1016/s0268-9499(97)80224-x

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Functional Analysis of Two Haplotypes of the Human Endothelial Protein C Receptor Gene

Arteriosclerosis Thrombosis and Vascular Biology (2014)

Pilar Medina Silvia Navarro Elena Bonet Laura Martos A. Estellés

Objective— To confirm the effect of the endothelial protein receptor gene ( PROCR ) haplotypes H1 and H3 on venous thromboembolism (VTE), to study their effect on endothelial protein C receptor (EPCR) expression in human umbilical vein endothelial cells, and to investigate the functionality of H1 tagging single-nucleotide polymorphisms in an in vitro model. Approach and Results— Protein C (PC), activated PC, and soluble EPCR (sEPCR) levels were measured in 702 patients with VTE and 518 healthy individuals. All subjects were genotyped for PROCR H1 and H3. Human umbilical vein endothelial cells isolated from 111 umbilical cords were used to study the relation between PROCR haplotypes, PROCR mRNA, cellular distribution of EPCR, and rate of PC activation. Finally, the functionality of the intragenic PROCR H1 single-nucleotide polymorphisms was analyzed using a luciferase-based method. We confirmed that individuals carrying H1 have reduced VTE risk, increased plasma activated PC levels, and reduced plasma sEPCR levels and that individuals with the H3H3 genotype have an increased VTE risk and increased plasma sEPCR levels. In cultured human umbilical vein endothelial cells, H1 is associated with increased membrane-bound EPCR, increased rate of PC activation, and reduced sEPCR in conditioned medium, but does not significantly influence PROCR mRNA levels. In contrast, H3 is associated with reduced membrane-bound EPCR and increased sEPCR in human umbilical vein endothelial cell–conditioned medium, higher levels of a truncated mRNA isoform, and a lower rate of PC activation. Finally, we identified the g.2132T>C single-nucleotide polymorphism in intron 1 as an intragenic H1-specific functional single-nucleotide polymorphism. Conclusions— These results support a protective role of PROCR H1 against VTE and an increased risk of VTE associated with the H3 haplotype.

10.1161/atvbaha.113.302518

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Citations (32)

[Assessment of amniotic fluid fibrinolytic activity (author's transl)].

PubMed (1975)

Alberto Hernández Parrilla Jj J Aznar Juan Gilabert–Estellés A. Estellés

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Intracardiac thrombosis in a case of Behcet's disease associated with the prothrombin 20210G-A mutation.

PubMed (2000)

Amparo Vayá MJ Forner A. Estellés Paola Villa Yolanda Mira

Thrombosis occurs in 20 to 30% of patients with Behçet's disease (BD), but the precise pathogenic mechanism underlying the thrombotic tendency in these patients is not well known. Venous thromboses are commonly located in the lower extremities, but right intracardiac thrombi are extremely rare. We report for the first time on a young patient with BD associated the 20210G-A prothrombin gene mutation and right intracardiac thrombosis. We suggest that the association of BD with this newly recognized prothrombotic genetic mutation may have contributed to the development of the thrombotic event in this patient.

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Citations (35)