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Biology subjects

Shaikh, G.

Publications and source records attributed to Shaikh, G..

2 recordsLinked to original sources

Temporal Vascular Endothelial Growth Factor Sub-type gene Switching in SARS-CoV Pathogenesis. Interpretation through in vivo Murine C57BL Models

This study examines temporal gene expression (GE) patterns in a murine model of SARS-CoV infection. We focused on a Temporal Gene Set (TGS) comprising pro-inflammatory genes (TNF, NFKB1, VEGF-A) and VEGF-B. A systematic search of the NCBI Geo database for MA15 (SARS-CoV) pulmonary studies using C57BL Wild (WT) mice and filtering according to TGS GE patterns eluded seven datasets for further analysis. Encompassing the GE profiles from these datasets alluded to a rising and falling pattern in TNF and NFKB1 GE. Also, our findings reveal a temporal decrease in VEGF-A GE coinciding with an increase in VEGF-B GE post-immunogenic stimulation. Notably, differential responses were observed with the MA15 dosage and in comparison, to other antigens (dORF6 and NSP16). Further, the human SARS-CoV-2 gene enrichment in this murine study confirms the MA15 murine models relevance for SARS research. Our study also suggests potential interactions between SARS-CoV-2 Spike protein and VEGF-related receptors, hinting at other pathophysiological mechanisms. Our results indicate severe inflammation may lead to a flattened VEGF-B GE response, influencing VEGF-Bs cell survival role. We underline the significance of considering VEGF-A/B interactions, particularly temporal differences, in manipulating angiogenic processes. Future research needs to consider temporal changes in VEGF-A and VEGF-B GE, in terms of time-associated gene-switching, in line with changing host inflammation.

immunology↗

Vasoactive Endothelial Growth Factor and Heat Shock Protein Gene Expression Response in Kawasaki Disease Associated Coronary Arteritis

Kawasaki Disease (KD) is a childhood vasculitis primarily affecting medium-sized arteries, which can lead to severe complications, particularly with respect to coronary artery disease (CAD). The impact of thermal stress on KD coronary artery pathogenesis, in association with prolonged fever and inflammation, remains unclear. In this study, we hypothesized that altered gene expression (GE) of angiogenesis-inducing Heat Shock Proteins (HSPs) is associated with KD-CAD through pro-inflammation. Transcriptomic analysis was performed using the three largest KD peripheral blood studies in the clinical literature (KD1-KD3), and one study direct from coronary artery tissue (KD4). The analysis revealed a significant increase in TNF and NFKB1 GE, indicating the presence of inflammation based on gene expression profiles. Gene set enrichment analysis (GSEA) of KD1-KD3 datasets identified inflammatory pathways, including TNFA signaling via NFKB, IL6 JAK STAT 3 Signalling, and p53 (Heat Shock Protein 90). The study also focused on specific HSPs known to be associated with angiogenesis, namely HSPB1, HSPA1A, and HSP90AB1. The temporal transcript model (TTM) consistently showed up-regulation of pro-inflammatory genes VEGF-A, TNF, and NFKB1, as well as up-regulation of HSPA1A. GSEA revealed gene ontology pathways associated with VEGF production. These findings suggest that the binding of VEGF-A or VEGF-B to their receptors could potentially impact the coronary artery in KD. Additionally, the up-regulation of the gene HSPAB1 in KD has not been described previously. In contrast, KD4 showed no differential GE for the studied genes potentially related to end-stage KD. This study provides valuable insights into VEGF and HSPs in KD-associated inflammation. Future research should focus on developing a VEGF-HSP CAD model to explore implications for KD biomarking as well as developing precision management strategies.

genomics↗