- Pulmonary Hypertension Research and Treatments
- Single-cell and spatial transcriptomics
- RNA Research and Splicing
- Kruppel-like factors research
- RNA modifications and cancer
- Congenital heart defects research
- Cardiovascular Disease and Adiposity
- Genomics and Rare Diseases
- Genetic Associations and Epidemiology
- Cardiovascular Function and Risk Factors
- Cancer-related molecular mechanisms research
Stanford University
2024
Lucile Packard Children's Hospital
2024
Institute of Genetics
2024
Pathological high shear stress (HSS, 100 dyn/cm
Long noncoding RNAs (lncRNAs) are a class of RNA molecules exceeding 200 nucleotides in length that lack long open-reading frames. Transcribed predominantly by polymerase II (>500nt), lncRNAs can undergo splicing and produced from various regions the genome, including intergenic regions, introns, antisense orientation to protein-coding genes. Aberrations lncRNA expression or function have been associated with wide variety diseases, cancer, cardiovascular diabetes, neurodegeneration. Despite...
BACKGROUND: Pulmonary arterial hypertension (PAH) is characterized by obliteration of distal pulmonary arteries (PA) in association with endothelial cell (EC) dysfunction, leading to smooth muscle proliferation. SOX17 a transcription factor (TF) expressed EC that critical vascular development. Deleterious variants causing reduced expression are linked PAH, particularly congenital heart defects (CHD) cause increased PA flow and high shear stress (HSS). HYPOTHESIS: deficiency additive HSS...
Computational modeling indicated that pathological high shear stress (HSS; 100 dyn/cm2) is generated in pulmonary arteries (PAs; 100-500 µm) congenital heart defects causing PA hypertension (PAH) and idiopathic PAH with occlusive vascular remodeling. Endothelial-to-mesenchymal transition (EndMT) a feature of PAH. We hypothesize HSS induces EndMT, contributing to the initiation progression used Ibidi perfusion system determine whether applied human endothelial cells (ECs) EndMT when compared...