A5031246678- Pulmonary Hypertension Research and Treatments
- Parasites and Host Interactions
- High Altitude and Hypoxia
- Renin-Angiotensin System Studies
- Hormonal Regulation and Hypertension
- Genetic diversity and population structure
- Cardiovascular Function and Risk Factors
- COVID-19 Clinical Research Studies
- Chronic Obstructive Pulmonary Disease (COPD) Research
- Cancer, Hypoxia, and Metabolism
- Eicosanoids and Hypertension Pharmacology
- Parasite Biology and Host Interactions
- Macrophage Migration Inhibitory Factor
- Neuroscience of respiration and sleep
- Extracellular vesicles in disease
- Tea Polyphenols and Effects
- Genetic Associations and Epidemiology
- Plant and Fungal Interactions Research
- Nitric Oxide and Endothelin Effects
- MicroRNA in disease regulation
- Plant Pathogens and Fungal Diseases
- Medical Imaging and Pathology Studies
- Helminth infection and control
- Sodium Intake and Health
- Vascular Anomalies and Treatments
University of California, San Francisco
2019-2025
San Francisco General Hospital
2019-2024
Employees State Insurance Post Graduate Institute of Medical Sciences and Research
2024
University of California System
2020-2024
ESIC Hospital
2024
Kettering University
2024
Memorial Sloan Kettering Cancer Center
2024
Temple University Hospital
2024
Pandit Bhagwat Dayal Sharma Post Graduate Institute of Medical Sciences
2024
St. Joseph’s University Medical Center
2021
Development of the vascular disease pulmonary hypertension (PH) involves disparate molecular pathways that span multiple cell types. MicroRNAs (miRNAs) may coordinately regulate PH progression, but integrative functions miRNAs in this process have been challenging to define with conventional approaches. Here, analysis network architecture specific predicted miR-130/301 family is a master regulator cellular proliferation via regulation subordinate miRNA unexpected connections one another. In...
Research Article30 March 2015Open Access Source Data Genetic and hypoxic alterations of the microRNA-210-ISCU1/2 axis promote iron–sulfur deficiency pulmonary hypertension Kevin White Divisions Cardiovascular Medicine Network Medicine, Department Brigham Women's Hospital, Harvard Medical School, Boston, MA, USA Search for more papers by this author Yu Lu Sofia Annis Andrew E Hale B Nelson Chau Regulus Therapeutics, San Diego, CA, James Dahlman Institute Engineering Science, Massachusetts...
Abstract Pulmonary arterial hypertension (PAH) is an obstructive disease of the precapillary pulmonary arteries. Schistosomiasis-associated PAH shares altered vascular TGF-β signalling with idiopathic, heritable and autoimmune-associated etiologies; moreover, blockade can prevent experimental (PH) in pre-clinical models. regulated at level activation, but how activated this unknown. Here we show activation by thrombospondin-1 (TSP-1) both required sufficient for development PH Schistosoma...
Hypoxia is a major cause of pulmonary hypertension (PH) worldwide, and it likely that interstitial macrophages contribute to this vascular pathology. We observed in hypoxia-exposed mice an increase resident macrophages, which expanded through proliferation expressed the monocyte recruitment ligand CCL2. also CCR2+ recruitment, express protein thrombospondin-1 functionally activates TGF-beta disease. Blockade with either CCL2 neutralizing antibody treatment or CCR2 deficiency bone marrow...
The etiology of schistosomiasis-associated pulmonary arterial hypertension (PAH), a major cause PAH worldwide, is poorly understood. Schistosoma mansoni exposure results in prototypical type-2 inflammation. Furthermore, transforming growth factor (TGF)-β signaling required for experimental (PH) caused by exposure. We hypothesized inflammation driven IL-4 and IL-13 necessary Schistosoma-induced TGF-β-dependent vascular remodeling. Wild-type, IL-4(-/-), IL-13(-/-), IL-4(-/-)IL-13(-/-) mice...
Background: Deficiencies of iron-sulfur (Fe-S) clusters, metal complexes that control redox state and mitochondrial metabolism, have been linked to pulmonary hypertension (PH), a deadly vascular disease with poorly defined molecular origins. BOLA3 (BolA Family Member 3) regulates Fe-S biogenesis, mutations in result multiple dysfunction syndrome, fatal disorder associated PH. The mechanistic role PH remains undefined. Methods: In vitro assessment regulation gain- loss-of-function assays were...
Transforming growth factor-β (TGF-β) signalling is required for chronic hypoxia-induced pulmonary hypertension (PH). The activation of TGF-β by thrombospondin-1 (TSP-1) contributes to the pathogenesis PH. However, neither cellular source pathologic TSP-1 nor downstream pathway that link activated PH have been determined. In this study, we hypothesized circulating monocytes, which are recruited become interstitial macrophages (IMs), major in hypoxia-exposed mice, and activates with increased...
In severe pulmonary hypertension (SPH), prior studies have shown an increase in right ventricle (RV) uptake of glucose, but it is unclear whether there a change the relative utilization fatty acids. We hypothesized that RV SPH, as left ventricular (LV) failure, altered substrate utilization, with increased glucose and decreased acid uptake. SPH was induced rats by treatment VEGF receptor inhibitor SU5416 3 wk hypoxia (10% Fi O 2 ), followed additional 4 normoxia (SU-Hx group). Control were...
Abstract Altered metabolism in pulmonary artery smooth muscle cells (PASMCs) and endothelial (PAECs) contributes to the pathology of hypertension (PH), but changes substrate uptake how substrates are utilized have not been fully characterized. We hypothesized stable isotope metabolomics would identify increased glucose, glutamine fatty acid utilization human PASMCs PAECs from PH versus control specimens, that TGF-β treatment phenocopy these metabolic changes. used 13 C-labeled or a...
Introduction Hypoxia is a common pathological driver contributing to various forms of pulmonary vascular diseases leading hypertension (PH). Pulmonary interstitial macrophages (IMs) play pivotal roles in immune and dysfunction, inflammation, abnormal remodeling, fibrosis PH. However, IMs’ response hypoxia their role PH progression remain largely unknown. We utilized murine model hypoxia-induced investigate the repertoire functional profiles IMs acute prolonged hypoxia, aiming elucidate...
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Optimal right ventricular (RV) function in pulmonary hypertension (PH) requires structural and functional coupling between the RV cardiomyocyte its adjacent capillary network. Prior investigations have indicated that vascular rarefaction occurs PH, which could contribute to failure by reduced delivery of oxygen or other metabolic substrates. However, it has not been determined if results from relative underproliferation setting tissue hypertrophy actual loss vessels. It is also unknown...
The interactions among various biomarkers remained unexplored under the stressful environment of high-altitude. Present study evaluated to susceptibility for high altitude pulmonary edema (HAPE) in HAPE-patients (HAPE-p) and adaptation highland natives (HLs); both comparison HAPE-free sojourners (HAPE-f). All subjects were recruited at 3500 m. We measured clinical parameters, biochemical levels plasma gene expression using RNA from blood; analyzed correlations between especially arterial...
Tea Unigene-derived MicroSatellite (TUGMS) markers were identified from the publicly available EST data in Camellia sinensis for characterization and future genome mapping studies tea.One hundred twelve novel TUGMS 4356 unigenes derived by clustering of 12788 random ESTs C. sinensis. Amplification-based validation loci proved them to be highly polymorphic [an average (av.) 5.24 alleles], heterozygous (H(E), av. 0.746; H(o), 0.566) informative (PIC, 0.392). 100% transferable cultivated...