Transfer RNA-derived fragment tRF-36 modulates varicose vein progression via human vascular smooth muscle cell Notch signaling
Varicose veins are a prevalent vascular disorder affecting millions of individuals worldwide, and we previously reported transfer RNA-derived fragment (tRF) involvement in varicose veins. This study investigated the role of tRF-36 in varicose vein pathogenesis. Varicose veins and adjacent normal vas...
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| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
De Gruyter
2025-04-01
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| Series: | Open Life Sciences |
| Subjects: | |
| Online Access: | https://doi.org/10.1515/biol-2025-1075 |
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| Summary: | Varicose veins are a prevalent vascular disorder affecting millions of individuals worldwide, and we previously reported transfer RNA-derived fragment (tRF) involvement in varicose veins. This study investigated the role of tRF-36 in varicose vein pathogenesis. Varicose veins and adjacent normal vascular tissues were collected to measure the expression of Notch 1, 2, and 3 and the smooth muscle cell (SMC) markers SMA-α, and SM22α. Human vascular SMCs (HVSMCs) were transfected to alter tRF-36 levels and examine the effects on Notch 1–3, tRF-36, SMA-α, and SM22α expression. Notch 1–3 and tRF-36 levels were higher in varicose veins than in adjacent normal vascular tissues. tRF-36 knockdown decreased HVSMC viability, downregulated Notch 1, 2, and 3 expression, and upregulated SMC markers (SMA-α and SM22α) compared with control HVSMCs. When the Notch pathway was inhibited, the expression of tRF-36 was significantly reduced. Additionally, Notch pathway inhibition showed similar effects to tRF-36 knockdown on HVSMC viability and the expression of SMA-α and SM22α. Furthermore, a Notch pathway inhibitor reversed the effects of the tRF-36 mimic on HVSMCs. Our study suggests a critical role for tRF-36 in varicose veins and demonstrates that tRF-36 knockdown may suppress varicose vein progression by inhibiting the Notch signaling pathway. |
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| ISSN: | 2391-5412 |