Related Experiment Video
Updated: Jan 20, 2026

Measuring Proliferation of Vascular Smooth Muscle Cells Using Click Chemistry
Published on: October 30, 2019
Long non-coding RNA SNHG16 regulates human aortic smooth muscle cell proliferation and migration via sponging miR-205
Yongqing Lin1, Guoping Tian2, Haifeng Zhang1
1Department of Cardiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Abstract:
The present study investigated the role of long non-coding RNA (lncRNA) small nucleolar RNA host gene 16 (SNHG16) in the human aortic smooth muscle cell (HASMC) proliferation and migration and explored the potential link between SNHG16 and atherosclerosis. Our results showed that platelet-derived growth factor (PDGF)-bb treatment promoted cell proliferation and migration with concurrent up-regulation of SNHG16 in HASMCs. Small nucleolar RNA host gene 16 overexpression promoted HASMC proliferation and migration, while SNHG16 knockdown suppressed cell proliferation and migration in PDGF-bb-stimulated HASMCs. The bioinformatic analyses showed that SNHG16 possessed the complementary binding sequence with miR-205, where the interaction was confirmed by luciferase reporter assay and RNA pull-down assay in HASMCs, and SNHG16 inversely regulated miR-205 expression. MiR-205 overexpression attenuated the enhanced effects of PDGF-bb treatment on HASMC proliferation and migration. Moreover, Smad2 was targeted and inversely regulated by miR-205, while being positively regulated by SNHG16 in HASMCs. Smad2 knockdown attenuated PDGF-bb-mediated actions on HASMC proliferation and migration. Both miR-205 overexpression and Smad2 knockdown partially reversed the effects of SNHG16 overexpression on HASMC proliferation and migration. Moreover, SNHG16 and Smad2 mRNA were up-regulated, while miR-205 was down-regulated in the plasma from patients with atherosclerosis. Small nucleolar RNA host gene 16 expression was inversely correlated with miR-205 expression and positively correlated with Smad2 expression in the plasma from atherosclerotic patients. In conclusion, our data showed the up-regulation of SNHG16 in pathogenic-stimulated HASMCs and clinical samples from atherosclerotic patients. Small nucleolar RNA host gene 16 regulated HASMC proliferation and migration possibly via regulating Smad2 expression by acting as a competing endogenous RNA for miR-205.
More Related Videos
06:14Murine Aortic Crush Injury: An Efficient In Vivo Model of Smooth Muscle Cell Proliferation and Endothelial Function
Published on: June 11, 2017
11:47Construction of a Human Aorta Smooth Muscle Cell Organ-On-A-Chip Model for Recapitulating Biomechanical Strain in the Aortic Wall
Published on: July 6, 2022
Related Concept Videos
lncRNA - Long Non-coding RNAs
Functions of Smooth Muscles
Function of visceral smooth muscles
Visceral smooth muscle is found in the walls of all hollow organs, except the heart, and is a key player in the involuntary movements that drive the functioning of these internal organs. This tissue is arranged in...
Smooth Muscle Contraction
The onset of contraction is triggered by an increase in calcium ions within the sarcoplasm, similar to the process in striated muscle. However, smooth muscles have a relatively smaller reservoir of the sarcoplasmic...
Structure and Organization of Smooth Muscles
Structure of smooth muscle cell
Smooth muscle cells are spindle-shaped with tapering ends and a...
Alternative RNA Splicing
There are five types of alternative RNA splicing that vary in the ways the pre-mRNA segments are removed or retained in the mature mRNA. The first...
Regulation of Expression Occurs at Multiple Steps
Transcription results in the generation of precursor (pre-mRNA) that consists of both exons and introns, which needs further processing before being translated to a...