Matthias Schwab

Universität Ulm, Ulm, Baden-Württemberg, Germany

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Publications (394)2243.78 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Risk classification and prediction of prognosis in GIST is still a matter of debate. Data on the impact of age and gender as potential confounding factors are limited. Therefore we comprehensively investigated age and gender as independent risk factors for GIST. Two independent patient cohorts (cohort I, n = 87 [<50 years]; cohort II, n = 125 [≥50 years]) were extracted from the multicentre Ulmer GIST registry including a total of 659 GIST patients retrospectively collected in 18 collaborative German oncological centers. Based on demographic and clinicopathological parameters and a median follow-up time of 4.3 years (range 0.56; 21.33) disease-specific-survival (DSS), disease-free-survival (DFS) and overall survival (OS) were calculated. GIST patients older than fifty years showed significantly worse DSS compared to younger patients (p = 0.021; HR = 0.307, 95% CI [0.113; 0.834]). DSS was significantly more favorable in younger female GIST patients compared with elderly females (p = 0.008). Female gender resulted again in better prognosis in younger patients (p = 0.033). Patient age (<50 years) and female gender were significantly associated with a more favourable prognosis in GIST. Extended studies are warranted to confirm our clinical results and to elucidate underlying pathophysiological mechanisms.
    BMC Cancer 12/2015; 15(1):1054. DOI:10.1186/s12885-015-1054-y · 3.32 Impact Factor
  • Nature Biotechnology 05/2015; DOI:10.1038/nbt.3241 · 39.08 Impact Factor
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    ABSTRACT: Background Platelet secretion is critical to development of acute thrombotic occlusion. Platelet dense granules contain a variety of important hemostatically active substances. Nevertheless, biogenesis of platelet granules is poorly understood.ObjectivesSGK1 has been shown to be highly expressed in platelets and megakaryocytes, but its role in the regulation of platelet granule biogenesis and its impact on thrombosis has not been investigated so far.Methods and ResultsElectron microscopy analysis of platelet ultrastructure revealed significant reduction in number and packing of dense granules in platelets lacking SGK1 (sgk1-/-). In sgk1-/- platelets serotonin content was significantly reduced and activation-dependent secretion of ATP, serotonin and CD63 significantly impaired. In vivo adhesion after carotis ligation was significantly decreased in platelets lacking SGK1 and occlusive thrombus formation after FeCl3-induced vascular injury was significantly diminished in sgk1-/- mice. Transcript levels and protein abundance of dense granule biogenesis regulating GTPase Rab27b were significantly reduced in sgk1-/- platelets without affecting Rab27b mRNA stability. In MEG-01 cells transfection with constitutively active S422DSGK1 but not with inactive K127NSGK1 significantly enhanced Rab27b mRNA levels. Sgk1-/- megakaryocytes show significantly reduced expression of Rab27b and serotonin/CD63 levels compared to sgk1+/+ megakaryocytes. Proteome analysis identified 9 further vesicular transport proteins regulated by SGK1 which may have an impact on impaired platelet granules biogenesis in sgk1-/- platelets independent of Rab27b.Conclusions The present observations unravel SGK1 as a novel powerful regulator of platelet dense granule biogenesis, platelet secretion and thrombus formation. SGK1 is at least partially effective by regulating transcription of Rab27b in megakaryocytes.This article is protected by copyright. All rights reserved.
    Journal of Thrombosis and Haemostasis 05/2015; DOI:10.1111/jth.12998 · 5.55 Impact Factor
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    ABSTRACT: ATP-binding cassette transporter B1 (ABCB1; P-glycoprotein; multidrug resistance protein 1) is an adenosine triphosphate (ATP)-dependent efflux transporter located in the plasma membrane of many different cell types. Numerous structurally unrelated compounds, including drugs and environmental toxins, have been identified as substrates. ABCB1 limits the absorption of xenobiotics from the gut lumen, protects sensitive tissues (e.g. the brain, fetus and testes) from xenobiotics and is involved in biliary and renal secretion of its substrates. In recent years, a large number of polymorphisms of the ABCB1 [ATP-binding cassette, sub-family B (MDR/TAP), member 1] gene have been described. The variants 1236C>T (rs1128503, p.G412G), 2677G>T/A (rs2032582, p.A893S/T) and 3435C>T (rs1045642, p.I1145I) occur at high allele frequencies and create a common haplotype; therefore, they have been most widely studied. This review provides an overview of clinical studies published between 2002 and March 2015. In summary, the effect of ABCB1 variation on P-glycoprotein expression (messenger RNA and protein expression) and/or activity in various tissues (e.g. the liver, gut and heart) appears to be small. Although polymorphisms and haplotypes of ABCB1 have been associated with alterations in drug disposition and drug response, including adverse events with various ABCB1 substrates in different ethnic populations, the results have been majorly conflicting, with limited clinical relevance. Future research activities are warranted, considering a deep-sequencing approach, as well as well-designed clinical studies with appropriate sample sizes to elucidate the impact of rare ABCB1 variants and their potential consequences for effect sizes.
    Clinical Pharmacokinetics 04/2015; DOI:10.1007/s40262-015-0267-1 · 5.49 Impact Factor
  • Gastroenterology 04/2015; 148(4):S-436-S-437. DOI:10.1016/S0016-5085(15)31475-X · 13.93 Impact Factor
  • European Urology Supplements 04/2015; 193(4):e722. DOI:10.1016/j.juro.2015.02.2142 · 3.37 Impact Factor
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    ABSTRACT: Expression of genes involved in absorption, distribution, metabolism and excretion (ADME) of drugs is collectively impaired during pathophysiological conditions such as cholestasis and inflammation. The mechanism of coordinated ADME gene downregulation remains unclear. In our previous study strongly elevated levels of microRNAs (miRNA) miR-21, miR-34a, and miR-130b in cholestatic liver and of miR-21 and miR-130b during inflammation were observed. Using HepaRG cells, which retain many functional characteristics of human hepatocytes, we investigated the potential of these miRNAs to downregulate ADME genes. Cells were transfected with the corresponding miRNA mimics, chemically modified double-stranded RNAs that mimic endogenous miRNAs, followed by mRNA profiling by quantitative RT-PCR. Enzyme activities of six cytochromes P450 (CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP3A4) were determined with a liquid chromatography-tandem mass spectrometric cocktail assay. While miR-21 and miR-34a showed little effects, transfection of miR-130b lead to significantly lower expression of nuclear receptors CAR and FXRa, the CYPs 1A1, 1A2, 2A6, 2C8, 2C9, and 2C19, as well as GSTA2. Furthermore, miR-130b negatively affected activity levels of all measured P450s by more than 40%. Reporter gene assays employing the CYP2C9 3'UTR confirmed direct regulation by miR-130b. These data support miR-130b as a potential negative regulator of drug metabolism by directly and/or indirectly affecting the expression of several ADME genes. This may be of relevance in pathophysiological conditions such as cholestasis and inflammation, which are associated with increased miR-130b expression. The American Society for Pharmacology and Experimental Therapeutics.
    Drug metabolism and disposition: the biological fate of chemicals 03/2015; 43(6). DOI:10.1124/dmd.114.062844 · 3.33 Impact Factor
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    ABSTRACT: Surface expression of stromal cell-derived factor-1 (SDF-1, CXCL12) on platelets is enhanced during ischaemic events and plays an important role in peripheral homing of stem cells and myocardial repair mechanisms. SDF-1 effects are mediated through CXCR4 and CXCR7. Both CXCR4 and CXCR7 are surface expressed on human platelets and to a higher degree in patients with coronary artery disease (CAD) when compared with healthy controls. In this study, we investigated the prognostic role of platelet CXCR4- and CXCR7 surface expression in patients with symptomatic CAD. In a cohort study, platelet surface expression of CXCR4 and CXCR7 was measured by flow cytometry in 284 patients with symptomatic CAD at the time of percutaneous coronary intervention (PCI). The primary combined endpoint was defined as all-cause death and/or MI during 12 month follow-up. Secondary endpoints were defined as the single events of all-cause death and myocardial infarction (MI). We found significant differences of CXCR4 values in patients who developed a combined endpoint compared to event-free patients (mean MFI 3.17 vs. 3.44, 95% CI 0.09 - 0.45) and in patients who subsequently died (mean MFI 3.10 vs. 3.42, 95% CI 0.09 - 0.56). In multivariate Cox regression analysis lower platelet CXCR4 levels were independently and significantly associated with all cause mortality (HR 0.24, 95% CI 0.07 - 0.87) and the primary combined endpoint of all-cause death and/or MI (HR 0.30, 95% CI 0.13 - 0.72). These findings highlight a potential prognostic value of platelet expression CXCR4 on clinical outcomes in patients with CAD. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Journal of Thrombosis and Haemostasis 02/2015; 13(5). DOI:10.1111/jth.12870 · 5.55 Impact Factor
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    ABSTRACT: Currently available data on prognostic implication of additional neoplasms in GIST miss comprehensive information on patient outcome with regard to overall or disease specific and disease free survival. Registry data of GIST patients with and without additional neoplasm were compared in retrospective case series. We investigated a total of 836 patients from the multi-center Ulmer GIST registry. Additionally, a second cohort encompassing 143 consecutively recruited patients of a single oncology center were analyzed. The frequency of additional malignant neoplasms in GIST patients was 31.9% and 42.0% in both cohorts with a mean follow-up time of 54 and 65 months (median 48 and 60 months), respectively. The spectrum of additional neoplasms in both cohorts encompasses gastrointestinal tumors (43.5%), uro-genital and breast cancers (34.1%), hematological malignancies (7.3%), skin cancer (7.3%) and others. Additional neoplasms have had a significant impact on patient outcome. The five year overall survival in GIST with additional malignant neoplasms (n = 267) was 62.8% compared to 83.4% in patients without other tumors (n = 569) (P < .001, HR=0.397, 95% CI: 0.298-0.530). Five-year disease specific survival was not different between both groups (90.8% versus 90.9%). 34.2% of all deaths (n = 66 of n = 193) were GIST-related. The presented data suggest a close association between the duration of follow-up and the rate of additional malignancies in GIST patients. Moreover the data indicate a strong impact of additional malignant neoplasms in GIST on patient outcome. A comprehensive follow-up strategy of GIST patients appears to be warranted. Copyright © 2014. Published by Elsevier Inc.
    Neoplasia (New York, N.Y.) 01/2015; 17(1):134-40. DOI:10.1016/j.neo.2014.12.001 · 5.40 Impact Factor
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    ABSTRACT: BACKGROUND/AIMS: Sterol regulatory element-binding protein (SREBP) 1, the master regulator of lipogenesis, was shown to be associated with non-alcoholic fatty liver disease, which is attributed to its major isoform SREBP1c. Based on studies in mice, the minor isoform SREBP1a is regarded as negligible for hepatic lipogenesis. This study aims to elucidate the expression and functional role of SREBP1a in human liver. METHODS: mRNA expression of both isoforms was quantified in cohorts of human livers and primary human hepatocytes. Hepatocytes were treated with PF-429242 to inhibit the proteolytic activation of SREBP precursor protein. SREBP1a-specifc and pan-SREBP1 knock-down were performed by transfection of respective siRNAs. Lipogenic SREBP-target gene expression was analyzed by real-time RT-PCR. RESULTS: In human liver, SREBP1a accounts for up to half of the total SREBP1 pool. Treatment with PF-429242 indicated SREBP-dependent auto-regulation of SREBP1a, which however was much weaker than of SREBP1c. SREBP1a-specifc knock-down also reduced significantly the expression of SREBP1c and of SREBP-target genes. Regarding most SREBP-target genes, simultaneous knock-down of both isoforms resulted in effects of only similar extent as SREBP1a-specific knock-down. CONCLUSION: We here showed that SREBP1a is significantly contributing to the human hepatic SREBP1 pool and has a share in human hepatic lipogenic gene expression.
    Cellular Physiology and Biochemistry 01/2015; 35(2):803-815. DOI:10.1159/000369739 · 3.55 Impact Factor
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    ABSTRACT: Objectives This study was designed to identify the multivariate effect of clinical risk factors on high on-treatment platelet reactivity (HPR) and 12 months major adverse events (MACE) under treatment with aspirin and clopidogrel in patients undergoing non-urgent percutaneous coronary intervention (PCI). Methods 739 consecutive patients with stable coronary artery disease (CAD) undergoing PCI were recruited. On-treatment platelet aggregation was tested by light transmittance aggregometry. Clinical risk factors and MACE during one-year follow-up were recorded. An independent population of 591 patients served as validation cohort. Results Degree of on-treatment platelet aggregation was influenced by different clinical risk factors. In multivariate regression analysis older age, diabetes mellitus, elevated BMI, renal function and left ventricular ejection fraction were independent predictors of HPR. After weighing these variables according to their estimates in multivariate regression model, we developed a score to predict HPR in stable CAD patients undergoing elective PCI (PREDICT-STABLE Score, ranging 0-9). Patients with a high score were significantly more likely to develop MACE within one year of follow-up, 3.4% (score 0-3), 6.3% (score 4-6) and 10.3% (score 7-9); odds ratio 3.23, P=0.02 for score 7-9 vs. 0-3. This association was confirmed in the validation cohort. Conclusions Variability of on-treatment platelet function and associated outcome is mainly influenced by clinical risk variables. Identification of high risk patients (e.g. with high PREDICT-STABLE score) might help to identify risk groups that benefit from more intensified antiplatelet regimen. Additional clinical risk factor assessment rather than isolated platelet function-guided approaches should be investigated in future to evaluate personalized antiplatelet therapy in stable CAD-patients.
    PLoS ONE 01/2015; 10(3):e0121620. DOI:10.1371/journal.pone.0121620 · 3.53 Impact Factor
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    ABSTRACT: Human infection with Puumala virus (PUUV), the most common hantavirus in Central Europe, causes nephropathia epidemica (NE), a disease characterized by acute kidney injury and thrombocytopenia. To determine the clinical phenotype of hantavirus-infected patients and their long-term outcome and humoral immunity to PUUV, we conducted a cross-sectional prospective survey of 456 patients in Germany with clinically and serologically confirmed hantavirus-associated NE during 2001-2012. Prominent clinical findings during acute NE were fever and back/limb pain, and 88% of the patients had acute kidney injury. At follow-up (7-35 mo), all patients had detectable hantavirus-specific IgG; 8.5% had persistent IgM; 25% had hematuria; 23% had hypertension (new diagnosis for 67%); and 7% had proteinuria. NE-associated hypertension and proteinuria do not appear to have long-term consequences, but NE-associated hematuria may. All patients in this study had hantavirus-specific IgG up to years after the infection.
    Emerging infectious diseases 01/2015; 21(1). DOI:10.3201/eid2101.140861 · 7.33 Impact Factor
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    ABSTRACT: Background and Objectives: To elucidate diagnostic criteria, clinicopathological features and clinical out-come in patients with esophageal gastrointestinal stromal tumors (GIST), representing an extremely rare subform of GIST with an estimated incidence of about 0.1 to 0.3 per million people. Patients and methods: Esophageal GIST cases from the Ulmer GIST registry consisting of 1077 cases were pooled with case reports and case series of esophageal GIST extracted from MEDLINE. Data were compared with those from 683 cases with gastric GIST from the Ulmer GIST registry. Results: In comparison to gastric GIST, esophageal GIST (n = 55) occurred significantly more frequent in men (p = 0.035) as well as in patients younger than 60 at diagnosis (p < 0.001). Primary tumor sizes were significantly larger (p < 0.001), thereby resulting more frequently in a high-risk classification (OR = 4.53, CI 95% 2.41-8.52, p < 0.001). The 5-year rates of disease-specific survival (DSS), disease-free survival (DFS), and over-all survival (OS) were 50.9%, 65.3% and 48.3%, respectively. The prognosis of esophageal GIST was less favorable compared with gastric GIST (DSS: p < 0.001, HR = 0.158, 95% CI: 0.087-0.288; DFS: p = 0.023, HR 0.466, 95% CI: 0.241-0.901; OS p = 0.003, HR = 0.481, 95% CI: 0.294-0.785; univariate Cox model) after a median follow-up time of 28 months (range 1.9 to 202). Mutational analysis for KIT showed more frequently wild-type status in esophageal GIST (OR = 10.13, CI 95% 3.02-33.96, p < 0.001). Conclusions: Esophageal GIST differ significantly from gastric GIST in respect to clinicopathological features and clinical outcome. To optimize treatment options further prospec-tive data on patients with esophageal GIST are urgently warranted. Introduction Gastrointestinal stromal tumors (GIST) are the most common mesenchymal neoplasms of the gastrointestinal tract with an annual incidence of 7 to 20 per million [1-6]. There is substantial evidence that GISTs differentiate parallel to the gut pacemaker cells, the interstitial cells of Cajal suggesting an origin from the Cajal cells or their progenitor cells [7-9]. Despite prognos-tic relevance of metastases at primary stage and tumor rupture, risk stratification in GIST is related to tumor size, mitotic rate and as recent-ly recognized also to tumor location. The major-ity of GISTs are located in the stomach (60-70%) and the small intestine (25-30%), whereas GISTs of the colo-rectum (up to 5%) and extra-gastrointestinal manifestations (< 5%) are less common [10-12]. Esophageal GIST is a very rare entity of GIST and represents < 1% of all cases. Therefore data on clinicopathological characteristics and clinical outcome are limit-ed. The aim of the present study was to eluci-date comprehensively demographic and
    American Journal of Cancer Research 01/2015; 5(1):333-343. · 3.97 Impact Factor
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    ABSTRACT: To elucidate diagnostic criteria, clinicopathological features and clinical outcome in patients with esophageal gastrointestinal stromal tumors (GIST), representing an extremely rare subform of GIST with an estimated incidence of about 0.1 to 0.3 per million people. Esophageal GIST cases from the Ulmer GIST registry consisting of 1077 cases were pooled with case reports and case series of esophageal GIST extracted from MEDLINE. Data were compared with those from 683 cases with gastric GIST from the Ulmer GIST registry. In comparison to gastric GIST, esophageal GIST (n = 55) occurred significantly more frequent in men (p = 0.035) as well as in patients younger than 60 at diagnosis (p < 0.001). Primary tumor sizes were significantly larger (p < 0.001), thereby resulting more frequently in a high-risk classification (OR = 4.53, CI 95% 2.41-8.52, p < 0.001). The 5-year rates of disease-specific survival (DSS), disease-free survival (DFS), and overall survival (OS) were 50.9%, 65.3% and 48.3%, respectively. The prognosis of esophageal GIST was less favorable compared with gastric GIST (DSS: p < 0.001, HR = 0.158, 95% CI: 0.087-0.288; DFS: p = 0.023, HR 0.466, 95% CI: 0.241-0.901; OS p = 0.003, HR = 0.481, 95% CI: 0.294-0.785; univariate Cox model) after a median follow-up time of 28 months (range 1.9 to 202). Mutational analysis for KIT showed more frequently wild-type status in esophageal GIST (OR = 10.13, CI 95% 3.02-33.96, p < 0.001). Esophageal GIST differ significantly from gastric GIST in respect to clinicopathological features and clinical outcome. To optimize treatment options further prospective data on patients with esophageal GIST are urgently warranted.
  • Emerging infectious diseases 01/2015; 21(1). DOI:10.3201/eid2101.140861. · 7.33 Impact Factor
  • David Zakim, Matthias Schwab
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    ABSTRACT: Basic life science research holds the promise of personalizing medical care. However, translation steps from the laboratory to the bedside are not trivial. Results from clinical research are difficult to replicate in part because study cohorts are poorly defined phenotypically. Here, we discuss how computer technology can improve the collection of clinical data to enable translation of insights from basic science to validated clinical guidelines. Copyright © 2014 Elsevier Ltd. All rights reserved.
    Trends in Pharmacological Sciences 12/2014; 36(2). DOI:10.1016/j.tips.2014.11.002 · 9.99 Impact Factor
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    ABSTRACT: The incidence of acid-base disorders (ABDs) is high, especially in hospitalized patients. ABDs are often indicators for severe systemic disorders. In everyday clinical practice, analysis of ABDs must be performed in a standardized manner. Highly sensitive diagnostic tools to distinguish the various ABDs include the anion gap and the serum osmolar gap. Drug-induced ABDs can be classified into five different categories in terms of their pathophysiology: (1) metabolic acidosis caused by acid overload, which may occur through accumulation of acids by endogenous (e.g., lactic acidosis by biguanides, propofol-related syndrome) or exogenous (e.g., glycol-dependant drugs, such as diazepam or salicylates) mechanisms or by decreased renal acid excretion (e.g., distal renal tubular acidosis by amphotericin B, nonsteroidal anti-inflammatory drugs, vitamin D); (2) base loss: proximal renal tubular acidosis by drugs (e.g., ifosfamide, aminoglycosides, carbonic anhydrase inhibitors, antiretrovirals, oxaliplatin or cisplatin) in the context of Fanconi syndrome; (3) alkalosis resulting from acid and/or chloride loss by renal (e.g., diuretics, penicillins, aminoglycosides) or extrarenal (e.g., laxative drugs) mechanisms; (4) exogenous bicarbonate loads: milk-alkali syndrome, overshoot alkalosis after bicarbonate therapy or citrate administration; and (5) respiratory acidosis or alkalosis resulting from drug-induced depression of the respiratory center or neuromuscular impairment (e.g., anesthetics, sedatives) or hyperventilation (e.g., salicylates, epinephrine, nicotine).
    Pediatric Nephrology 11/2014; DOI:10.1007/s00467-014-2958-5 · 2.88 Impact Factor
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    ABSTRACT: At present the global diabetes epidemic is affecting 347 million individuals, 90% of whom are diagnosed with type II diabetes mellitus (T2DM). T2DM is commonly treated with more than one type of therapy, including oral antidiabetic drugs (OADs) and agents used in the treatment of diabetic complications. Several pharmacological classes of OADs are currently available for the treatment of T2DM, of which insulin secretagogues (i.e. sulphonylureas and meglitinides), insulin sensitizers (thiazolidinediones) and biguanides are the most commonly prescribed. Although many of these OADs have been used for more than half a century in the treatment of T2DM, the pharmacogenomic characteristics of these compounds have only recently been investigated, primarily in retrospective studies. Recent advances in pharmacogenomics have led to the identification of polymorphisms that affect the expression and function of drug-metabolizing enzymes and drug transporters, as well as drug targets and receptors. These polymorphisms have been shown to affect the therapeutic response to and side effects associated with OADs. The aim of this review was to provide an up-to-date summary of some of the pharmacogenomic data obtained from studies of T2DM treatment, with a focus on polymorphisms in genes affecting pharmacokinetics, pharmacodynamics and treatment outcome of the most commonly prescribed OADs. In addition, the implications of pharmacogenomics in the use of the OAD metformin in cancer will be briefly discussed. Finally, we will focus on recent advances in novel ‘omics’ technologies and discuss how these might aid in the personalized management of T2DM.This article is protected by copyright. All rights reserved.
    Journal of Internal Medicine 11/2014; 277(2). DOI:10.1111/joim.12330 · 5.79 Impact Factor
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    ABSTRACT: Background. Functional recovery and prognosis after acute coronary syndromes (ACS) are mainly driven by the extent of reperfusion injury and myocardial repair mechanisms. Transforming growth factor-beta 1 (TGF-β1) is critically involved in cardiac injury, repair and remodeling. In this study, we investigated the prognostic role of platelet TGF-β1 surface expression and circulating TGF-β1 levels in patients with coronary artery disease (CAD). Methods and results. Expression of TGF-β1 in platelets and circulating TGF-β1 levels were investigated by flow cytometry and ELISA, respectively, among patients with ACS and stable CAD undergoing percutaneous coronary intervention (PCI). In a cohort study, platelet and circulating TGF-β1 was measured in 299 patients with symptomatic CAD (stable CAD = 145, ACS = 154) at the time of PCI. The primary combined endpoint was defined as death and/or STEMI during 12-month follow-up. Platelets expressed TGF-β1 and circulating TGF-β1 showed a weak, but significant negative correlation. TGF-β1 surface expression was significantly elevated on platelets in ACS patients compared to patients with stable CAD (median MFI 13.4 vs. median MFI 11.7, p = 0.003). During follow-up, lower platelet expression of TGF-β1 was associated with all-cause mortality (median MFI 11.0 vs. median MFI 13.9, p = 0.011) as well as for the combined endpoint of death and/or STEMI, (median MFI 10.8 vs. median MFI 13.9, p = 0.006). In multivariate analysis platelet TGF-β1 expression was independently associated with the combined primary endpoint in the overall cohort (Hazard Ratio 0.31, 95% Confidence Interval 0.11-0.89, p = 0.029) and was strongly associated with prognosis in ACS patients. There was no significant association of circulating TGF-β1 levels neither with the presence of ACS nor the occurrence of the primary endpoint. Conclusion. These findings highlight a potential role of platelet expressed TGF-β1 in ACS and indicate a prognostic value of TGF-β1 on clinical outcomes in patients with acute coronary syndromes. Large scale studies are warranted to further evaluate the regulatory mechanisms of platelet TGF-β1 expression- and its prognostic impact in CAD. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.
    Atherosclerosis 10/2014; 237(2):754-759. DOI:10.1016/j.atherosclerosis.2014.10.021 · 3.97 Impact Factor
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Publication Stats

13k Citations
2,243.78 Total Impact Points

Institutions

  • 2015
    • Universität Ulm
      • Institute of Pathology
      Ulm, Baden-Württemberg, Germany
  • 2007–2015
    • University of Tuebingen
      Tübingen, Baden-Württemberg, Germany
    • Universität Regensburg
      Ratisbon, Bavaria, Germany
  • 2003–2015
    • Universitätsklinikum Tübingen
      • • Division of Clinical Pharmacology
      • • Division of Neurogastroenterology
      Tübingen, Baden-Württemberg, Germany
    • Klinikum Stuttgart
      Stuttgart, Baden-Württemberg, Germany
  • 2004–2014
    • Universität Stuttgart
      Stuttgart, Baden-Württemberg, Germany
    • Dr. Falk Pharma GmbH
      Freiburg, Baden-Württemberg, Germany
  • 1997–2014
    • Institut für klinische Pharmakologie
      Stuttgart, Baden-Württemberg, Germany
  • 2013
    • University of Greifswald
      Griefswald, Mecklenburg-Vorpommern, Germany
    • McGill University
      Montréal, Quebec, Canada
  • 2012
    • Binghamton University
      • Department of Biological Sciences
      Binghamton, New York, United States
  • 2011
    • Children's National Medical Center
      Washington, Washington, D.C., United States
  • 2009
    • University of Iowa Children's Hospital
      Iowa City, Iowa, United States
  • 2002–2007
    • Humboldt-Universität zu Berlin
      • Department of Biology
      Berlín, Berlin, Germany
    • Universität Heidelberg
      • Department of Urology
      Heidelberg, Baden-Wuerttemberg, Germany
  • 2006
    • University of California, Davis
      • Department of Medical Microbiology and Immunology
      Davis, California, United States
    • University of Bonn
      Bonn, North Rhine-Westphalia, Germany
  • 2005
    • Hannover Medical School
      • Department of Paediatric Haematology and Oncology
      Hannover, Lower Saxony, Germany
    • Medical University of Vienna
      • Klinische Abteilung für Gastroenterologie und Hepatologie
      Vienna, Vienna, Austria
    • Goethe-Universität Frankfurt am Main
      • Center for Internal Medicine
      Frankfurt, Hesse, Germany
  • 2001–2004
    • Robert-Bosch Krankenhaus
      Stuttgart, Baden-Württemberg, Germany
    • Bundesärztekammer
      Berlín, Berlin, Germany
  • 1999–2004
    • Philipps University of Marburg
      Marburg, Hesse, Germany