Long non‐coding RNA small nucleolar RNA host gene 7 facilitates cardiac hypertrophy via stabilization of SDA1 domain containing 1 mRNA

Abstract

Cardiac hypertrophy is a result of cardiac response to excessive heart burden. The sustention of hypertrophic stress indicates a higher risk of cardiac failure or even sudden death. Despite the increasing research works on cardiac hypertrophy, there remains a considerable space left for further mechanism exploration. Long noncoding RNAs (lncRNAs) are a cluster of transcripts lacking in protein coding potential. Past decades have witnessed the increasing identification of their significant roles in cardiac hypertrophy. Small nucleolar RNA host gene 7 (SNHG7) has been identified as an oncogene in human cancers, but its function in cardiac hypertrophy remains unknown. SDA1 domain containing 1 (SDAD1) is newly discovered to exert procancer function in several cancers, whose role in cardiac hypertrophy remains elusive. Present study sought to investigate the biological function of SNHG7 in cardiac hypertrophy. First, the expressions of SNHG7 and SDAD1 were found to be upregulated in Ang II‐induced cardiac hypertrophy model in the neonatal rat cardiomyocytes (NRCMs). Functionally, loss‐of‐function assays verified that silencing SNHG7 and SDAD1 attenuated the inductive effect of Ang II on cardiac hypertrophy. Mechanistically, we proved that SNHG7 interacted with Hu Antigen R so as to stabilize SDAD1 messenger RNA (mRNA). In conclusion, this study proved that SNHG7 facilitates cardiac hypertrophy via the stabilization of SDAD1 mRNA, indicating SNHG7 as a novel regulator for cardiac hypertrophy.

Transcriptome analysis of long noncoding RNAs reveals their potential roles in anthracycline-induced cardiotoxicity

“…Through these databases, the association of DE lncRNAs with heart disease was detected, especially the H19 and FTX genes were mentioned in both databases ( Table S5, S6 ). Furthermore, other studies also highlighted the potential causal relationships between the DE lncRNAs and heart diseases [ [40] , [41] , [42] , [43] , [44] ]. Based on this prior knowledge, a network was established to represent the relationship between DE lncRNAs and corresponding heart diseases ( Fig.…”

NAP1L5 Promotes Nucleolar Hypertrophy and Is Required for Translation Activation During Cardiomyocyte Hypertrophy

“…Thus, our findings indicate that the NAP1L proteins might form SDAD1 (SDA1 domain containing 1) is a shared hub protein interacting with both NAP1L1 and NAP1L5 (Figures 6A,B). It has been involved in the development of cardiac hypertrophy and tumor diseases through binding with long non-coding RNAs or microRNAs (64)(65)(66). Interestingly, the yeast homolog of SDAD1 has been shown to interact with NAP1 and facilitates the export of 60S pre-ribosomal subunits from nucleus to cytoplasm (67,68).…”

Activation of Hypoxia-Inducible Factor Signaling Modulates the RNA Protein Interactome in Caenorhabditis elegans

“…SDAD1 is implicated in regulation of tumor progression and metastasis (Ding et al., 2018, Zeng et al., 2017). There is an indication that HuR, an RBP targeting HIF-1 mRNA (Galban et al., 2008), also binds to SDAD1 mRNA (Jing et al., 2019). It will now be of great interest to focus on the function of specific hypoxia-modulated RBPs such as SDAD1 and TCP1 and to further characterize their differential RNA-binding, e.g.…”