Global expression profiling identifies a novel hyaluronan synthases 2 gene in the pathogenesis of lower extremity varicose veins.

doi:10.3390/jcm7120537

淡江大學機構典藏 > 理學院 > 化學學系暨研究所 > 期刊論文 > Item 987654321/116957

Please use this identifier to cite or link to this item: https://tkuir.lib.tku.edu.tw/dspace/handle/987654321/116957

Title:	Global expression profiling identifies a novel hyaluronan synthases 2 gene in the pathogenesis of lower extremity varicose veins.
Authors:	CS, Hsieh;CT, Tsai;YH, Chen;SN, Chang;JJ, Hwang;EY, Chuang;IH, Wu
Keywords:	varicose veins;HAS2;RNA seq
Date:	2018-12-11
Issue Date:	2019-09-11 12:10:28 (UTC+8)
Abstract:	Lower extremities varicose veins (VV) are among the most easily recognized venous abnormalities. The genetic mechanism of VV is largely unknown. In this study, we sought to explore the global expressional change of VV and identify novel genes that might play a role in VV. We used next-generation ribonucleic acid (RNA) sequence (RNA seq) technology to study the global messenger RNA expressional change in the venous samples of five diseased and five control patients. We identified several differentially expressed genes, which were further confirmed by conventional reverse transcription polymerase chain reaction (RT-PCR). Using these significant genes we performed in silico pathway analyses and found distinct transcriptional networks, such as angiogenesis, cell adhesion, vascular injury, and carbohydrate metabolisms that might be involved in the mechanism of VV. Among these significant genes, we also found hyaluronan synthases 2 gene (HAS2) played a pivotal role and governed all these pathways. We further confirmed that HAS2 expression was decreased in the venous samples of patients with VV. Finally, we used a zebrafish model with fluorescence emitting vasculature and red blood cells to see the morphological changes of the venous system and blood flow. We found that HAS2 knockdown in zebrafish resulted in dilated venous structural with static venous flow. HAS2 may modulate the transcriptional networks of angiogenesis, cell adhesion, vascular injury, and carbohydrate metabolisms in venous tissues and downregulation of HAS2 may underlie the mechanism of VV.
Relation:	Journal of Clinical Medicine 7(12), p.537
DOI:	10.3390/jcm7120537
Appears in Collections:	[化學學系暨研究所] 期刊論文

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