Chinese scholars have made progress in the study of the phenotypic transformation of lncRNA-coding proteins on vascular smooth muscle cells

Figure LncRNA PSR regulates the mechanism of action of vascular remodeling by encoding the novel protein Arteridin

With the funding of the National Natural Science Foundation of China (approval number: 82022005, 31771271), Professor Zeng Chunyu's team of the Department of Cardiology, Army Medical University Army Special Medical Center (Daping Hospital), discovered a new protein encoded by long-chain non-coding RNA (lncRNA), named Arteridin, and then confirmed that Arteridin protein synergies its non-coding transcript through the "transcript-protein dual effect" Promoting the phenotypic transformation of vascular smooth muscle cells is one of
the key factors leading to vascular reconstruction.
The research results are titled "LncRNA PSR Regulates Vascular Remodeling through Encoding a Novel Protein Arteridin", published online in the journal Circulation Research on September 22, 2022.
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Vascular smooth muscle cell (VSMC) phenotypic transformation is a long-term problem in the medical community, which not only leads to hypertension, coronary heart disease, stroke and other diseases, but also is an important cause of
vascular restenosis after bridge blood vessels and stents 。 Professor Zeng Chunyu's team found a piece of lncRNA with abnormally high expression of aortic expression in hypertensive reconstructed blood vessels during the detection of abnormal expression of lncRNA in rats with spontaneous hypertension, and through clinical samples, gene editing animals and cell level studies, it was further found that the lncRNA can promote the conversion of smooth muscle cells in the middle layer of the blood vessel wall from a healthy systolic phenotype to an abnormal proliferative phenotype, so it was named "Phenotypic Conversion Regulatory Factor (PSR)"
。 Although PSR was first thought to be lncRNA, the team accidentally discovered an open reading frame lurking in PSR that can code for proteins, and confirmed that PSR can encode an entirely new protein, naming it "arteridin.
"
Further studies have found that both PSR and Arteridin can worsen VSMC phenotypic transformation, thereby promoting the progression
of vascular restenosis, atherosclerosis, and hypertension.
To verify whether PSR and Arteridin proteins can be used as targets for the treatment of vascular remodeling, the research team specifically inhibited the expression of PSR/Arteridin in mouse vascular smooth muscle cells and found that it could significantly reduce vascular remodeling induced by angiotensin II (figure).

The study also found that in vascular smooth muscle cells, Arteridin protein and the PSR transcript encoding it can bind to the transcription factor YBX1, promote nuclear translocation and inhibit the expression of vascular smooth muscle cell systolic proteins, Arteridin is expected to become a new therapeutic target for
the treatment of diseases related to vascular reconstruction.
At the same time, the study found that RNA transcripts and their encoded proteins co-regulate the same molecular function, which also provides a new theoretical basis
for research in the field of lncRNA.