Long non-coding RNA SAP30-2:1 is downregulated in congenital heart disease and regulates cell proliferation by targeting
- PDF / 2,603,772 Bytes
- 10 Pages / 595.276 x 785.197 pts Page_size
- 33 Downloads / 152 Views
RESEARCH ARTICLE
Long non-coding RNA SAP30-2:1 is downregulated in congenital heart disease and regulates cell proliferation by targeting HAND2 Jing Ma1,2,*, Shiyu Chen2,*, Lili Hao2, Wei Sheng3, Weicheng Chen3, Xiaojing Ma3, Bowen Zhang2, Duan Ma (
Guoying Huang (✉)3
✉)2,3,
1
ENT Institute, Department of Facial Plastic and Reconstructive Surgery, Eye & ENT Hospital, Fudan University, Shanghai 200031, China; Research Center for Birth Defects, Institutes of Biomedical Sciences, Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China; 3Children’s Hospital of Fudan University, Shanghai 201102, China
2
© Higher Education Press 2020
Abstract Congenital heart disease (CHD) is the most common birth defect worldwide. Long non-coding RNAs (lncRNAs) have been implicated in many diseases. However, their involvement in CHD is not well understood. This study aimed to investigate the role of dysregulated lncRNAs in CHD. We used Gene Expression Omnibus data mining, bioinformatics analysis, and analysis of clinical tissue samples and observed that the novel lncRNA SAP30-2:1 with unknown function was significantly downregulated in damaged cardiac tissues from patients with CHD. Knockdown of lncRNA SAP30-2:1 inhibited the proliferation of human embryonic kidney and AC16 cells and decreased the expression of heart and neural crest derivatives expressed 2 (HAND2). Moreover, lncRNA SAP30-2:1 was associated with HAND2 by RNA immunoprecipitation. Overall, these results suggest that lncRNA SAP30-2:1 may be involved in heart development through affecting cell proliferation via targeting HAND2 and may thus represent a novel therapeutic target for CHD. Keywords congenital heart disease; Gene Expression Omnibus; lncRNA SAP30-2:1; cell proliferation; RNA immunoprecipitation; HAND2
Introduction Congenital heart disease (CHD) is the most common defect among live births, accounting for 0.8%–1.2% of all birth defects worldwide [1]. CHD is also the leading noninfectious cause of death in the first year of life [1]. Although the development of novel surgical and catheter interventions has decreased the mortality of CHD, such developments cannot resolve all the cardiac problems, and postoperative patients still face risks, such as those of arrhythmia, heart failure, and neurodevelopmental deficit [2]. Thus, the etiology and pathogenesis of CHD must be further explored to improve its prevention and treatment. Received August 31, 2019; accepted March 14, 2020 Correspondence: Guoying Huang, [email protected]; Duan Ma, [email protected] *
These authors contributed equally to this work.
CHD involves morphological, structural, functional, and metabolic abnormalities of the heart and large blood vessels caused by cardiovascular dysplasia during the embryonic period. This condition is a multifactorial, complex disease affected by environmental and genetic factors [3, 4], with genetic factors playing a le
Data Loading...
