Different expression of circulating microRNA profile in Tibetan OSAHS with Metabolic Syndrome patients
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE274563 | GEO | 2025/01/29
REPOSITORIES: GEO
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Project description:Long term-exposed to high altitude, the increased numbers of red blood cells tend to stabilize to a certain extend in most people, but someone will occur over-increasing in number of red blood cells, which cause a serious of clinical symptoms and signs, and this is high altitude polycythemia. EPO-EPOR system may be the main reasons for erythroid progenitor cell proliferation and differentiation in early exposion to plateau, but, in the late, there may be other factors involved in the regulation of erythropoiesis in bone marrow, multiple factors working together lead to excessive red blood cell proliferation. We compared gene expression profiling of leukocytes in peripheral blood from high altitude polycythemia patients with those from matched controls. Subjects consisting of 5 masculine Han Chinese patients with HAPC (diagnosed according to international consensus statement on HAPC) and 5 matched controls, were migrants at River of TUOTUO area (Qinghai-Tibetan Plateau, 4550 m). Each of the five HAPC patients was matched to each of the control: gender, nationality, birthplace, duration migrating to plateau, height of location, work intensity. Peripheral blood samples were obtained at 4550m plateau from above subjects. Total RNA was extracted from peripheral blood leucocytes. The gene expression profilings were analysed by Human Genome U133 Plus 2.0 Array.
2014-06-15 | E-GEOD-29977 | biostudies-arrayexpress
Project description:The study aimed to investigate molecular signatures in peripheral blood of individuals affected by metabolic syndrome (MetS) and different degrees of obesity. Metabolic health of 1204 individuals was assessed, and 32 subjects were recruited to four study groups: MetS lean, MetS obese, “healthy obese” and healthy lean. Whole-blood transcriptome next generation sequencing with functional data analysis was carried out.
2020-02-18 | GSE145412 | GEO
Project description:The metabolic syndrome (MetS), a collective cluster of disease risk factors that includes dyslipidemia, obesity, inflammation, hypertension, and insulin resistance, affects numerous people worldwide. Accumulating studies have shown that long-noncoding RNAs (lncRNA) serve as competing endogenous RNA (ceRNA) to play essential roles in regulating gene expression in various diseases. To explore the role of lncRNAs as ceRNAs in MetS, we examined a MetS-associated network in circulating extracellular vesicles (EVs) collected from systemic blood of MetS and control patients (n=5 each). MetS patients showed elevated body-weight, glucose, blood pressure, insulin, liver injury and inflammatory markers levels. In total, 191 differentially-expressed (DE) lncRNAs, 1389 mRNAs, and 138 miRNAs were selected for further analysis. Biological processes and pathway functional enrichment analysis were performed based on the Database for Annotation, Visualization, and Integrated Discovery (DAVID) database. LncRNA/mRNA/miRNA ceRNA network was constructed by Cytoscape v3.8 based on the DE-RNAs, and included 13 lncRNAs, 8 miRNAs, and 64 mRNAs. We found that the lncRNA-associated ceRNA network members potentially serve as regulators of central cellular processes and complications of MetS, including cancer. These findings suggest that MetS alters the interactions among the ceRNA network components in circulating EV-specific ceRNA network, and implicate the cargo of circulating EVs in ramifications of MetS.
2021-02-10 | GSE166474 | GEO
Project description:RNA was extracted from 57 LUAD patients hospitalized from 2004 to 2010 at the Pasteur Hospital (Departments of Pulmonary Medicine, and Thoracic Surgery, CHU de Nice, France) and 11 normal lung tissue specimens taken from areas at standard distance (3 cm) from the same cohort of patients.The diagnosis of LUAD patients was based on examination of all tumor specimens using the 7th pTNM classification and on the last histological classification of NSCLC. Written informed consent was obtained from participants after explaining the nature of the study, which was approved by the research ethics board of the Nice University hospital and was performed according to the guidelines of the Declaration of Helsinki. The main clinical and pathological data are summarized. Enrollment of patients in our study was conditioned by stringent criteria such as obtained signed consent, availability of resected surgical specimens, good quality RNA and time of follow-up for surviving patients (min 40 months for surviving patients).
2019-09-04 | GSE116959 | GEO
Project description:Metabolic syndrome (MetS) is the name of cluster of risk factors that increases the risk for heart disease and other health problems by which several organs are affected, but research is lacking for those not involved directly in metabolism. The cluster is integrated by central obesity, insulin resistance, dyslipidemia (elevated triglycerides and low density lipoprotein and decreased high density lipoprotein), and high blood pressure, according to the consensus released by the International Diabetes Federation [1]. This problem could be as the result of an unbalanced diets (high-fat and carbohydrates), and genetic background [2, 3]. There is evidence that suggests that MetS is a condition that increases the risk of different lung diseases. It have been reported in some MetS patients a diminished lung function, as assessed by spirometry, in addition, there is an association with insulin resistance, increase in body mass index; abdominal obesity and systemic inflammation (high levels of C reactive protein) [4-6]. In other cases, like asthma, some components of MetS such as abdominal obesity, hypertension and pro-inflammatory cytokines have been with related with this disease [7-9]. Also, a few clinical studies reported that abdominal obesity, hyperglycemia and elevated levels of systemic inflammatory markers, which are components of MetS, were significantly more prevalent in patients with chronic obstructive pulmonary disease [10-13]. In the present work we evaluated the transcriptomic changes of lung tissue in an animal model of MetS induced by diet.
2017-07-01 | GSE73910 | GEO
Project description:The metabolic syndrome (MetS) is a collection of co-occurring complex disorders including obesity, hypertension, dyslipidemia, and insulin resistance. The Lyon Hypertensive (LH) and Lyon Normotensive (LN) rats are models of MetS sensitivity and resistance, respectively. To identify genetic determinants and mechanisms underlying MetS, 169 rats from an F2 intercross between LH and LN were studied. Multi-dimensional data were obtained including genotypes of 1536 SNPs, 23 physiological traits including blood pressure, plasma lipid and leptin levels, and body weight/adiposity, and more than 150 billion nucleotides of RNA-seq reads from the livers of 36 F2 individuals, 6 LH and 6 LN individuals. We identified 17 pQTLs (physiological quantitative trait loci) and 1200 eQTLs (gene expression quantitative trait loci). Systems biology methods were applied to identify 18 candidate MetS genes, including genes (Prcp and Aqp11) previously shown to be MetS-related. We found an eQTL hotspot on RNO17, which was also located within pQTLs for MetS-related traits. The genes regulated by this eQTL hotspot were mainly in two co-expression network modules (a mitochondria related module and a gene regulation related module) and were predicted to causally affect many MetS-related traits. Multiple evidences strongly and consistently support RGD1562963, a gene regulated in cis by this eQTL hotspot and possibly related to RNA stability, as the eQTL driver gene directly affected by genetic variation between LH and LN rats; the expression of this gene is also correlated with MetS-related traits. Our study sheds light on the intricate pathogenesis of MetS and proved that systems biology with high-throughput sequencing is a powerful method to study the etiology of complicated diseases. RNA-Seq of the liver of 6 LH (Lyon Hypertensive) rats and 6 LN (Lyon Normotensive) rats and 36 F2 rats.
2014-10-31 | E-GEOD-50027 | biostudies-arrayexpress
Project description:objection: The immune inflammatory disorders rheumatoid arthritis (RA), psoriatic arthritis (PsA) and psoriasis (Ps) share common pathologic features and show responsiveness to anti-tumor necrosis factor (TNF) agents yet they are phenotypically distinct. The aim of this study was to examine if anti-TNF therapy is associated with divergent gene expression profiles in circulating cells and target tissues of patients with these diseases Method: Peripheral blood CD14+ and CD14- cells were isolated from 9 RA, 12 PsA and 10 Ps patients before and after infliximab (IFX) treatment. Between April 2007 and June 2009, 31 patients with active RA, PsA and Ps who were naïve to anti-TNF agents, were recruited from the Faculty Rheumatology Clinics at the University of Rochester Medical Center after informed, written consent was obtained in a protocol approved by the Research Subjects Review Board at the University of Rochester Medical Center. Of the 31 subjects, 9 had active RA and 12 had PsA despite treatment with Disease Modifying Anti-Rheumatic Drugs (DMARDs). Also, 10 patients with extensive Ps (>5% BSA) documented by a dermatologist, were enrolled and they were examined by a rheumatologist to exclude the presence of inflammatory arthritis. Nineteen healthy controls were also recruited.
2014-10-29 | E-GEOD-57405 | biostudies-arrayexpress
Project description:objection: The immune inflammatory disorders rheumatoid arthritis (RA), psoriatic arthritis (PsA) and psoriasis (Ps) share common pathologic features and show responsiveness to anti-tumor necrosis factor (TNF) agents yet they are phenotypically distinct. The aim of this study was to examine if anti-TNF therapy is associated with divergent gene expression profiles in circulating cells and target tissues of patients with these diseases Method: Peripheral blood CD14+ and CD14- cells were isolated from 9 RA, 12 PsA and 10 Ps patients before and after infliximab (IFX) treatment Between April 2007 and June 2009, 31 patients with active RA, PsA and Ps who were naïve to anti-TNF agents, were recruited from the Faculty Rheumatology Clinics at the University of Rochester Medical Center after informed, written consent was obtained in a protocol approved by the Research Subjects Review Board at the University of Rochester Medical Center. Of the 31 subjects, 9 had active RA and 12 had PsA despite treatment with Disease Modifying Anti-Rheumatic Drugs (DMARDs). Also, 10 patients with extensive Ps (>5% BSA) documented by a dermatologist, were enrolled and they were examined by a rheumatologist to exclude the presence of inflammatory arthritis. Nineteen healthy controls were also recruited.
2014-10-29 | E-GEOD-57383 | biostudies-arrayexpress
Project description:The understanding of metastatic spread is limited and molecular mechanisms causing particular characteristics of metastasis, like varying dormancy periods of Mets originating from the same primary tumor entity or the differing number of Mets in patients with the same primary tumor, are largely unknown. Knowing the molecular fundamentals of these phenomena would support the prognosis of patients´ outcome and facilitate the decision for an appropriate therapy regime. We analyzed the transcriptome-wide expression profiles of 20 pulmonary metastases of renal cell carcinoma in order to identify expression patterns associated with two important prognostic factors in RCC: the disease-free interval after nephrectomy (DFI) and the number of Mets per patient. Keywords: comparison of pulmonary metastases from patients with different clinical characteristics metastases manifested early or late after nephrectomy (DFI less than or equal to 9 vs. greater than or equal to 60 months) metastases derived from patients with only few or multiple pulmonary metastases (less than or equal to 8 vs. greater than or equal to 16)
2009-01-13 | E-GEOD-14378 | biostudies-arrayexpress
Project description:TMPRSS2-ERG fusion is the most common genetic alteration in prostate cancer (PCa) and TP53 is the most frequently mutated gene in human cancers. However, their precise roles in PCa pathogenesis remain elusive. Here we showed that TMPRSS2-ERG fusion co-occurred with TP53 deletion/mutation in PCa patient specimens. ERG overexpression and Trp53 knockout/R172H mutant knockin induced pyrimidine synthesis gene (PSG) expression and prostate tumorigenesis in mice. Gain-of-function p53 mutants bound to the CTNNB1 promoter and upregulated β-Catenin. Overexpressed ERG and β-Catenin co-occupied PSG loci and mediated PSG expression, and high PSG expression associated with increased β-Catenin level and poor overall survival of PCa patients. β-Catenin inhibition by proteolysis-targeting chimeras (PROTACs) of its co-activator CBP and partner proteins LEF1/TCFs blocked ERG/p53-mutant PCa growth. Our study identifies CTNNB1 as a transcriptional target of p53 GOF-mutants, and reveals a druggable dependency on β-Catenin and pyrimidine synthesis in p53-mutated cancers with or without TMPRSS2-ERG fusion.
2023-06-27 | GSE184625 | GEO