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Peer-reviewedCC BY 4.0Cell Proliferation

A Specific tRNA Half, 3'tiRNA‐GlyGCC, Regulates Hypoxic Pulmonary Artery Smooth Muscle Cell Proliferation via Myrf‐Mediated Endoplasmic Reticulum Stress

  • Lixin Zhang1,2
  • Xiaoyu Guan2,3
  • Xiangrui Zhu4
  • Yingying Hao2,5
  • Ya Xu2,3
  • Hao Yuan2,3
  • Danni Gao2,3
  • Hongxia Du2,3
  • Jiayu Li2,3
  • Weiwei Cao5
  • Cui Ma4
  • Xiaoying Wang2,5,6
6 affiliations
  1. 1College of Medical Laboratory Science and Technology Harbin Medical University, Daqing Campus Daqing P. R. China
  2. 2Central Laboratory of Harbin Medical University, Daqing Campus Daqing P. R. China
  3. 3College of Pharmacy, Harbin Medical University Harbin P. R. China
  4. 4Institute of Cardiovascular Diseases, Xiamen Cardiovascular Hospital, School of Medicine, Xiamen University, Fujian Branch of National Clinical Research Center for Cardiovascular Diseases Xiamen P. R. China
  5. 5College of Pharmacy, Harbin Medical University, Daqing Campus Daqing P. R. China
  6. 6Key Laboratory of Frigid Zone Exercise Health Research and Translation in Heilongjiang Province Daqing P. R. China
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Abstract

Pulmonary artery smooth muscle cell (PASMC) proliferation is a hallmark of the pathogenesis of hypoxic pulmonary hypertension (PH), and endoplasmic reticulum stress (ERS) plays a crucial role. Many studies have implicated that tRNA‐derived fragment, tiRNAs, in a variety of biological processes, but their roles in hypoxia‐induced PASMC ERS and proliferation have not been investigated. In this study, we identified a significantly upregulated 3′tiRNA‐GlyGCC in hypoxic mouse lung tissues using Arraystar small RNA microarray analysis. Functional assays, including CCK8, EdU incorporation, Western blot, and immunofluorescence, demonstrated that inhibition of 3′tiRNA‐GlyGCC reversed hypoxia‐induced ERS and proliferation in PASMCs. Mechanistically, 3′tiRNA‐GlyGCC interacts with the eukaryotic translation elongation factor 1 alpha 1 (Eef1a1) protein and reduces the binding capacity between Eef1a1 and myelin regulatory factor (Myrf) mRNA, leading to decreased stability of Myrf mRNA. Additionally, 3′tiRNA‐GlyGCC targets Myrf mRNA and inhibits its expression. We further verified that angiogenin (Ang) mediated the biogenesis of 3′tiRNA‐GlyGCC under hypoxic conditions. Collectively, these findings highlight a novel mechanism underlying PASMC ERS and proliferation and suggest that 3′tiRNA‐GlyGCC could serve as a potential therapeutic target for hypoxic PH.

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Cite

BibTeXRIS
BibTeX
@article{zhang2026specific,
  title = {{A Specific tRNA Half, 3'tiRNA‐GlyGCC, Regulates Hypoxic Pulmonary Artery Smooth Muscle Cell Proliferation via Myrf‐Mediated Endoplasmic Reticulum Stress}},
  author = {Lixin Zhang and Xiaoyu Guan and Xiangrui Zhu and Yingying Hao and Ya Xu and Hao Yuan and Danni Gao and Hongxia Du and Jiayu Li and Weiwei Cao and Cui Ma and Xiaoying Wang},
  journal = {Cell Proliferation},
  year = {2026},
  month = may,
  doi = {10.1111/cpr.70238},
  url = {https://doi.org/10.1111/cpr.70238},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - A Specific tRNA Half, 3'tiRNA‐GlyGCC, Regulates Hypoxic Pulmonary Artery Smooth Muscle Cell Proliferation via Myrf‐Mediated Endoplasmic Reticulum Stress
AU  - Lixin Zhang
AU  - Xiaoyu Guan
AU  - Xiangrui Zhu
AU  - Yingying Hao
AU  - Ya Xu
AU  - Hao Yuan
AU  - Danni Gao
AU  - Hongxia Du
AU  - Jiayu Li
AU  - Weiwei Cao
AU  - Cui Ma
AU  - Xiaoying Wang
PY  - 2026
DA  - 2026/05/29
JO  - Cell Proliferation
DO  - 10.1111/cpr.70238
UR  - https://doi.org/10.1111/cpr.70238
AB  - Pulmonary artery smooth muscle cell (PASMC) proliferation is a hallmark of the pathogenesis of hypoxic pulmonary hypertension (PH), and endoplasmic reticulum stress (ERS) plays a crucial role. Many studies have implicated that tRNA‐derived fragment, tiRNAs, in a variety of biological processes, but their roles in hypoxia‐induced PASMC ERS and proliferation have not been investigated. In this study, we identified a significantly upregulated 3′tiRNA‐GlyGCC in hypoxic mouse lung tissues using Arraystar small RNA microarray analysis. Functional assays, including CCK8, EdU incorporation, Western blot, and immunofluorescence, demonstrated that inhibition of 3′tiRNA‐GlyGCC reversed hypoxia‐induced ERS and proliferation in PASMCs. Mechanistically, 3′tiRNA‐GlyGCC interacts with the eukaryotic translation elongation factor 1 alpha 1 (Eef1a1) protein and reduces the binding capacity between Eef1a1 and myelin regulatory factor (Myrf) mRNA, leading to decreased stability of Myrf mRNA. Additionally, 3′tiRNA‐GlyGCC targets Myrf mRNA and inhibits its expression. We further verified that angiogenin (Ang) mediated the biogenesis of 3′tiRNA‐GlyGCC under hypoxic conditions. Collectively, these findings highlight a novel mechanism underlying PASMC ERS and proliferation and suggest that 3′tiRNA‐GlyGCC could serve as a potential therapeutic target for hypoxic PH.
SN  - 0960-7722
SN  - 1365-2184
ER  -