Dataset Information

The novel long noncoding RNA lncRNA-Adi regulates adipogenesis.

ABSTRACT: Adipogenesis participates in many physiological and pathological processes, such as obesity and diabetes, and is regulated by a series of precise molecular events. However, the molecules involved in this regulation have not been fully characterized. In this study, we identified a long noncoding (lnc)RNA, lncRNA-Adi, which is highly expressed in adipose tissue-derived stromal cells (ADSCs) that are differentiating into adipocytes. Knockdown of lncRNA-Adi impaired the adipogenic differentiation ability of ADSCs. Moreover, lncRNA-Adi was found to interact with microRNA (miR)-449a to enhance the expression of cyclin-dependent kinase (CDK)6 during adipogenesis. The mechanism by which lncRNA-Adi regulates adipogenesis was determined to involve an lncRNA-Adi-miR-449a interaction that competes with the CDK6 3' untranslated region to increase CDK6 translation and activate the pRb-E2F1 pathway to promote adipogenesis. These findings provide valuable information and a new study angle to search for therapeutic targets against metabolic disorders such as obesity and diabetes.

SUBMITTER: Chen Y

PROVIDER: S-EPMC7445023 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

The novel long noncoding RNA lncRNA-Adi regulates adipogenesis.

Chen Yuanwei Y Li Kaide K Zhang Xiao X Chen Jinlong J Li Meisheng M Liu Lei L

Stem cells translational medicine 20200501 9

Adipogenesis participates in many physiological and pathological processes, such as obesity and diabetes, and is regulated by a series of precise molecular events. However, the molecules involved in this regulation have not been fully characterized. In this study, we identified a long noncoding (lnc)RNA, lncRNA-Adi, which is highly expressed in adipose tissue-derived stromal cells (ADSCs) that are differentiating into adipocytes. Knockdown of lncRNA-Adi impaired the adipogenic differentiation ab ...[more]

PMID: 32356938

Similar Datasets

Project description:The study was designed to determine the role of long noncoding RNA (lncRNA), metastasis-associated lung adenocarcinoma transcript 1 (Malat1), in ischemic stroke outcome. Primary mouse brain microvascular endothelial cells (BMECs) were cultured and treated with Malat1 GapmeR before 16 h oxygen and glucose depravation (OGD). Cell death was assayed by LDH and MTT methods. Malat1 knock-out and wild-type mice were subjected to 1 h of middle cerebral artery occlusion (MCAO) and 24-72 h of reperfusion. To explore the underlying mechanism, apoptotic and inflammatory factors were measured by qPCR, ELISA, and Western blotting. The physical interaction between Malat1 and apoptotic or inflammatory factors was measured by RNA immunoprecipitation. Increased Malat1 levels were found in cultured mouse BMECs after OGD as well as in isolated cerebral microvessels in mice after MCAO. Silencing of Malat1 by Malat1 GapmeR significantly increased OGD-induced cell death and Caspase 3 activity in BMECs. Silencing of Malat1 also significantly aggravated OGD-induced expression of the proapoptotic factor Bim and proinflammatory cytokines MCP-1, IL-6, and E-selectin. Moreover, Malat1 KO mice presented larger brain infarct size, worsened neurological scores, and reduced sensorimotor functions. Consistent with in vitro findings, significantly increased expression of proapoptotic and proinflammatory factors was also found in the cerebral cortex of Malat1 KO mice after ischemic stroke compared with WT controls. Finally, we demonstrated that Malat1 binds to Bim and E-selectin both in vitro and in vivo Our study suggests that Malat1 plays critical protective roles in ischemic stroke.SIGNIFICANCE STATEMENT Accumulative studies have demonstrated the important regulatory roles of microRNAs in vascular and neural damage after ischemic stroke. However, the functional significance and mechanisms of other classes of noncoding RNAs in cerebrovascular pathophysiology after stroke are less studied. Here we demonstrate a novel role of Malat1, a long noncoding RNA that has been originally identified as a prognostic marker for non-small cell lung cancer, in cerebrovascular pathogenesis of ischemic stroke. Our experiments have provided the first evidence that Malat1 plays anti-apoptotic and anti-inflammatory roles in brain microvasculature to reduce ischemic cerebral vascular and parenchymal damages. Our studies also suggest that lncRNAs can be therapeutically targeted to minimize poststroke brain damage.

Dataset Information

The novel long noncoding RNA lncRNA-Adi regulates adipogenesis.

Publications

The novel long noncoding RNA lncRNA-Adi regulates adipogenesis.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets