Search bioRxiv⌕ Search

Biology subjects

Hwang, H. S.

Publications and source records attributed to Hwang, H. S..

2 recordsLinked to original sources

Assessing Long-Term Stored Tissues for Multi-Omics Data Quality and Proteogenomics Suitability

As research into the complexities of cancer biology deepens, the integration of multi-omics analyses has emerged as a powerful approach to unravel the complex molecular basis of cancers. However, challenges related to sample availability, including size, collection procedures, and storage duration, hinder the broad application of this methodology. Despite these limitations, there is a growing interest in exploring the potential of archived samples to expand the scope of multi-omics research. Our study aims to investigate the impact of storage duration on the measurment in genomic, transcriptomic, and proteomic profiles of archived samples, demonstrating their viability for advancing our understanding of cancer biology. To comprehensively address these trends and limitations, we systematically examined archived samples collected over a decade, focusing on their transcriptomic, proteomic, and phosphoproteomic attributes. Analysis revealed intricate patterns and dynamic shifts, especially in long-term transcriptomic data, with observed declines in read counts related to protein coding and gene coverage. However, these changes did not compromise the fundamental gene expression landscape. Proteomic result also demonstrated that storage period did not significantly influence proteomic measurement. Comparisons of housekeeping gene (HKG) and housekeeping protein (HKP) expressions unveiled consistent transcriptomic levels across samples, while distinctive proteomic disparities between tumor and normal tissues. In conclusion, the challenges posed by limited sample availability in multi-omics studies can be partially overcome through the strategic integration of archived samples. While technical shifts were evident in certain aspects of transcriptomic data, core gene expression patterns remained robust, and the functionality of essential transcription factors (TFs) and kinases remained unaffected. These findings underscore the potential of archived samples as valuable resources for multi-omics research, providing a broader landscape for investigating cancer biology and paving the way for more comprehensive insights into this intricate field.

cancer biology↗

The Role of Sex in the Effects of Smoking and Nicotine in Cardiovascular Function, Atherosclerosis, and Inflammation

cigarette smoke (CS) invokes an inflammatory response involving increased levels of circulating cytokines and chemokines, vascular dysfunction, and atherosclerosis. The role of sex and nicotine in CS effects in cardiovascular function and atherosclerosis is unexplored. To assess the role of sex, male and female C57Bl/6 WT (wild type) and ApoE-/- mice were exposed to CS and nicotine for 16 weeks to bridge this literature gap. Heart rate and endothelial function were measured in the aorta of WT mice, while plasma levels of lipids, cytokines and chemokines and aortic plaque burden was assessed in ApoE-/- mice. CS increased heart rate to similar levels in both sexes and induced a stronger impairment in endothelial function in males and more plaque in females than nicotine. Females showed a higher necrotic core area at basal compared with males, while males had a higher calcification area than females by CS. Senescence-associated GLB1/-galactosidase (SA-GLB1) activity was elevated similarly in both sexes by both treatments. Total cholesterol (TC) was elevated by CS in both sexes. CS increased triglycerides (TG), very-low density lipoprotein (VLDL) and high-density lipoprotein (HDL) only in males and low-density lipoprotein (LDL) only in females. Interleukin 17A (IL17A) was upregulated by CS and nicotine in both sexes, while CS upregulated C-X-C motif chemokine ligand 5 (CXCL5/LIX) and interleukin 1 alpha (IL1A) in males and females, respectively. Additionally, nicotine metabolism showed sex specific responses to nicotine, but not smoking. Overall, we identified sex-specific pro-atherogenic responses to CS in the lipid profile, plaque area and composition and inflammatory markers. Males present a stronger impairment in endothelia dysfunction in WT mice, while females a stronger plaque burden in ApoE-/- mice exposed to CS. Elevated HDL and estrogens in males may offer partial protection against the harmful effects of CS. In contrast, elevated LDL and a pro-inflammatory state may promote a stronger pro-atherogenic phenotype in females exposed to CS.

cell biology↗