Glucose-6-phosphate dehydrogenase and MEG3 controls hypoxia-induced          expression of serum response factor (SRF) and SRF-dependent genes in pulmonary smooth          muscle cell

Kitagawa, A.; Jacob, Christina; Gupte, Sachin A.

doi:10.1540/jsmr.58.34

Cited by 3 publications

(1 citation statement)

References 55 publications

(83 reference statements)

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“…Glucose-6-phosphate dehydrogenase (G6PD), the rate-limiting enzyme in the pentose phosphate pathway, has been found to regulate DNA methylation in sugen-hypoxia and hypoxia-induced PAH mouse models [ 144 , 145 ]. Studies have shown that G6PD expression and activity are increased in various cell types within the pulmonary vascular wall, including fibroblasts from IPAH patients and calves with severe hypoxic PH [ 65 , 144 , 146 , 147 ]. Collectively, these findings support the notion that elevated G6PD expression and activity, potentially induced by endothelin-1 and/or hypoxia, inhibit apoptosis and promote the proliferation of various cell types, including PASMCs, ECs, and PAAFs.…”

Section: Mechanisms Underlying Fibroblast Abnormalities In Phmentioning

confidence: 99%

Fibroblasts in Pulmonary Hypertension: Roles and Molecular Mechanisms

Zhang,

Li,

et al. 2024

Cells

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Fibroblasts, among the most prevalent and widely distributed cell types in the human body, play a crucial role in defining tissue structure. They do this by depositing and remodeling extracellular matrixes and organizing functional tissue networks, which are essential for tissue homeostasis and various human diseases. Pulmonary hypertension (PH) is a devastating syndrome with high mortality, characterized by remodeling of the pulmonary vasculature and significant cellular and structural changes within the intima, media, and adventitia layers. Most research on PH has focused on alterations in the intima (endothelial cells) and media (smooth muscle cells). However, research over the past decade has provided strong evidence of the critical role played by pulmonary artery adventitial fibroblasts in PH. These fibroblasts exhibit the earliest, most dramatic, and most sustained proliferative, apoptosis-resistant, and inflammatory responses to vascular stress. This review examines the aberrant phenotypes of PH fibroblasts and their role in the pathogenesis of PH, discusses potential molecular signaling pathways underlying these activated phenotypes, and highlights areas of research that merit further study to identify promising targets for the prevention and treatment of PH.

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Section: Mechanisms Underlying Fibroblast Abnormalities In Phmentioning

confidence: 99%

Fibroblasts in Pulmonary Hypertension: Roles and Molecular Mechanisms

Zhang,

Li,

et al. 2024

Cells

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Diagnostic Value of lncRNA FGD5-AS1 Sponge miR-223-3p in Infantile Pneumonia and Its Prognostic Effect on Rehabilitation

Ren,

Wen,

Liu

et al. 2024

J Pediatr Infect Dis

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Objective This study aimed to uncover the value of long noncoding RNA FGD5-AS1 (lncRNA FGD5-AS1) in the diagnosis of infantile pneumonia and explore its pathological mechanism in lung fibroblasts. This research may provide a potential biomarker for diagnosing patients and predicting their rehabilitation outcomes. Methods This study included 92 children with infantile pneumonia as the research object, and an equal number of healthy children were introduced as controls. The FGD5-AS1 content was detected using real-time quantitative polymerase chain reaction (RT-qPCR) assay. The diagnostic value of FGD5-AS1 was evaluated by receiver operating characteristic (ROC) and logistic analysis. The molecular mechanism of FGD5-AS1 and miR-223-3p was studied by luciferase activity assays. The impact of abnormal FGD5-AS1 expression on the proliferation and apoptosis of lung fibroblasts was analyzed using the cell counting kit-8 (CCK-8) and flow cytometry. Results FGD5-AS1 expression was decreased in the serum of infantile pneumonia patients, which may be a diagnostic marker for children with pneumonia. Furthermore, FGD5-AS1 has the ability to predict patient outcomes. FGD5-AS1 levels in lung fibroblasts (WI-38) decreased when induced by lipopolysaccharide (LPS). This decline resulted in reduced cell proliferation ability, increased apoptosis rate, and elevated inflammatory factor content. However, upregulated FGD5-AS1 counteracted the effects of LPS on WI-38 cells activity and inflammatory factors. Conclusion FGD5-AS1 may act as a potential marker in infantile pneumonia, and regulate the biological activity and inflammation level of lung fibroblasts by targeting miR-223-3p.

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Elucidating the roles of SOD3 correlated genes and reactive oxygen species in rare human diseases using a bioinformatic-ontology approach

Stanworth,

Zhang

2024

PLoS ONE

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Superoxide Dismutase 3 (SOD3) scavenges extracellular superoxide giving a hydrogen peroxide metabolite. Both Reactive Oxygen Species diffuse through aquaporins causing oxidative stress and biomolecular damage. SOD3 is differentially expressed in cancer and this research utilises Gene Expression Omnibus data series GSE2109 with 2,158 cancer samples. Genome-wide expression correlation analysis was conducted with SOD3 as the seed gene. Categorical SOD3 Pearson Correlation gene lists incrementing in correlation strength by 0.01 from ρ≥|0.34| to ρ≥|0.41| were extracted from the data. Positively and negatively SOD3 correlated genes were separated for each list and checked for significance against disease overlapping genes in the ClinVar and Orphanet databases via Enrichr. Disease causal genes were added to the relevant gene list and checked against Gene Ontology, Phenotype Ontology, and Elsevier Pathways via Enrichr before the significant ontologies containing causal and non-overlapping genes were reviewed with a literature search for possible disease and oxidative stress associations. 12 significant individually discriminated disorders were identified: Autosomal Dominant Cutis Laxa (p = 6.05x10-7), Renal Tubular Dysgenesis of Genetic Origin (p = 6.05x10-7), Lethal Arteriopathy Syndrome due to Fibulin-4 Deficiency (p = 6.54x10-9), EMILIN-1-related Connective Tissue Disease (p = 6.54x10-9), Holt-Oram Syndrome (p = 7.72x10-10), Multisystemic Smooth Muscle Dysfunction Syndrome (p = 9.95x10-15), Distal Hereditary Motor Neuropathy type 2 (p = 4.48x10-7), Congenital Glaucoma (p = 5.24x210-9), Megacystis-Microcolon-Intestinal Hypoperistalsis Syndrome (p = 3.77x10-16), Classical-like Ehlers-Danlos Syndrome type 1 (p = 3.77x10-16), Retinoblastoma (p = 1.9x10-8), and Lynch Syndrome (p = 5.04x10-9). 35 novel (21 unique) genes across 12 disorders were identified: ADNP, AOC3, CDC42EP2, CHTOP, CNN1, DES, FOXF1, FXR1, HLTF, KCNMB1, MTF2, MYH11, PLN, PNPLA2, REST, SGCA, SORBS1, SYNPO2, TAGLN, WAPL, and ZMYM4. These genes are proffered as potential biomarkers or therapeutic targets for the corresponding rare diseases discussed.

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Glucose-6-phosphate dehydrogenase and MEG3 controls hypoxia-induced expression of serum response factor (SRF) and SRF-dependent genes in pulmonary smooth muscle cell

Cited by 3 publications

References 55 publications

Fibroblasts in Pulmonary Hypertension: Roles and Molecular Mechanisms

Fibroblasts in Pulmonary Hypertension: Roles and Molecular Mechanisms

Diagnostic Value of lncRNA FGD5-AS1 Sponge miR-223-3p in Infantile Pneumonia and Its Prognostic Effect on Rehabilitation

Elucidating the roles of SOD3 correlated genes and reactive oxygen species in rare human diseases using a bioinformatic-ontology approach

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