Long intergenic noncoding RNA antisense to S1PR1 (S1PR1-DT)

Long intergenic noncoding RNA antisense to S1PR1, abbreviated as S1PR1-DT and also known as LISPR1, is a long noncoding RNA positioned antisense to the S1PR1 gene and partially sharing its promoter[2][5][8]. It does not encode a protein and is localized in both the cytoplasm and nucleus of endothelial cells[2][8]. LISPR1 plays a critical role in controlling the expression level of S1PR1, the main receptor mediating sphingosine-1-phosphate (S1P) signaling in endothelium, by influencing transcriptional regulation; knockdown of LISPR1 leads to reduced S1PR1 expression via increased recruitment of the transcriptional repressor ZNF354C to the S1PR1 promoter and reduced RNA polymerase II activity, resulting in attenuated S1P signaling and impaired endothelial migration and angiogenic response[2][8]. LISPR1 is highly expressed in normal lung and endothelium, but decreased in diseases such as COPD, and is upregulated by inflammatory stimuli, shear stress, and statins[2][8]. There are no known drugs that directly interact with LISPR1, and it is not itself a classical therapeutic target (e.g., receptor, enzyme), but rather a regulatory lncRNA relevant for vascular biology and disease.

Other names

LISPR1S1PR1 divergent transcriptNONHSAT004848