DNA microarrays were used to identify new targets of estrogen in the vasculature. Ovariectomized rats were treated with estradiol, genistein or daidzein, for four days. [33P]dCTP-labelled probes synthesized from mesenteric artery RNA were hybridized with DNA microarrays. Analysis of the microarray data identified endothelin converting enzyme-1 (ECE-1) as a gene whose expression was inhibited by treatment with estrogen, genistein, or daidzein. Semi-quantitative RT-PCR was used to confirm the data from the DNA microarrays. Reversal of the estrogen and phytoestrogen effect on ECE-1 expression by ICI 182,780 suggested that the inhibition was an estrogen receptor response. An inhibition of ECE-1 mRNA expression by estrogen or the phytoestrogens has not been previously reported. These data highlight the power of DNA microarray technology to identify new gene expression targets of estrogen in the vasculature. Moreover, the data suggest that genistein and daidzein inhibit ECE-1 expression by an estrogen receptor-mediated mechanism.
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http://dx.doi.org/10.1016/j.lfs.2003.05.001 | DOI Listing |
J Korean Med Sci
January 2025
Division of Rheumatology, Department of Internal Medicine, Kangwon National University School of Medicine, Chuncheon, Korea.
Background: Gout is a type of inflammatory arthritis caused by monosodium urate crystal deposits, and the prevalence of this condition has been increasing. This study aimed to determine the combined effects of genetic risk factors and lifestyle habits on gout, using data from a Korean cohort study. Identifying high-risk individuals in advance can help prevent gout and its associated disorders.
View Article and Find Full Text PDFRen Fail
December 2025
Division of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, Rochester, Minnesota, USA.
Identifying risk factors for disease onset and progression has been a core focus in nephrology research. Mendelian Randomization (MR) has emerged as a powerful genetic epidemiological approach, utilizing genome-wide association studies (GWAS) to establish causal relationships between modifiable risk factors and kidney disease outcomes. MR uses genetic variants as instrumental variables to infer causal relationships between exposures and disease outcomes.
View Article and Find Full Text PDFRespir Res
January 2025
Department of Pulmonary and Critical Care Medicine, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Background: The emergence of new molecular targeted drugs marks a breakthrough in asthma treatment, particularly for severe cases. Yet, options for moderate-to-severe asthma treatment remain limited, highlighting the urgent need for novel therapeutic drug targets. In this study, we aimed to identify new treatment targets for asthma using the Mendelian randomization method and large-scale genome-wide association data (GWAS).
View Article and Find Full Text PDFJ Transl Med
January 2025
Department of Rheumatology and Immunology, Peking University Third Hospital, No. 49, North Garden Road, Beijing, 100191, China.
Background: Sjogren syndrome (SS) is a chronic systemic autoimmune disease and its pathogenesis often involves the participation of numerous immune cells and inflammatory factors. Despite increased researches and studies recently focusing on this area, it remains to be fully elucidated. We decide to incorporate genetic insight into investigation of the causal link between various immune cells, inflammatory factors and pathogenesis of Sjogren syndrome (SS).
View Article and Find Full Text PDFNat Commun
January 2025
Department of Neurology and National Center for Neurological Disorders, Huashan Hospital, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Shanghai Medical College, Fudan University, Shanghai, China.
Brain glymphatic activity, as indicated by diffusion-tensor imaging analysis along the perivascular space (ALPS) index, is involved in developmental neuropsychiatric and neurodegenerative diseases, but its genetic architecture is poorly understood. Here, we identified 17 unique genome-wide significant loci and 161 candidate genes linked to the ALPS-indexes in a discovery sample of 31,021 individuals from the UK Biobank. Seven loci were replicated in two independent datasets.
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