Publications by authors named "Gabriela Diaz-Pina"
Double-stranded RNA adenosine deaminase 1 (ADAR1) is significantly down-regulated in fibroblasts derived from Idiopathic Pulmonary Fibrosis (IPF) patients, and its overexpression restored levels of , , and . There are two ADAR1 isoforms in humans, ADAR1-p110 and ADAR1-p150, generated by an alternative promoter. is considered an essential microRNA in Pulmonary Fibrosis (PF).
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- Chronic obstructive pulmonary disease (COPD) is increasingly common among older adults and is characterized by an inflammatory response.
- A specific population of blood cells affected by genetic changes, known as clonal hematopoiesis of indeterminate potential (CHIP), has been studied for its link to COPD, though its effects are not well understood.
- Research on 125 COPD patients revealed that about 20% had CHIP mutations, particularly linked to decreased DNA methylation in a gene associated with lung function, leading to higher levels of harmful substances and inflammation.
Introduction: Idiopathic pulmonary fibrosis (IPF) is a lethal disease with an unclear pathogenic mechanism. Components of the renin-angiotensin system (RAS) have a role in the pathogenesis of IPF, specifically, the aspartyl protease renin acts as a profibrotic factor in the lung. However, the concentration of the RAS components renin and soluble (pro)renin receptor (sPRR) have not been previously evaluated neither in serum nor in bronchoalveolar lavage fluid (BAL) of patients with IPF or chronic Hypersensitivity pneumonitis (cHP), a disease which may be confused with IPF.
View Article and Find Full Text PDFIntroduction: microRNAs (miRNAs) are small non-coding 1RNAs that post-transcriptionally regulate gene expression. Recent evidence shows that adenosine deaminases that act on RNA (ADAR) can edit miRNAs. miRNAs are involved in the development of different diseases, such as idiopathic pulmonary fibrosis (IPF).
View Article and Find Full Text PDFObjective: The objective of this study is to determine the effect of two angiotensin-converting enzyme inhibitors (ACEi) (Enalapril and Captopril), an angiotensin-II receptor inhibitor (Losartan) and a renin inhibitor (Aliskiren) on renin, TGF-β1 and collagen expressions in human lung fibroblast cultures through real-time PCR and ELISA.
Materials And Methods: Normal commercial fibroblasts (CCD25) were exposed to 10(-6) M of enalapril, captopril, losartan, or aliskiren for 6 h. Subsequently, media were recovered and proteins were concentrated; RNA was extracted from the cells.