Related Experiment Video
Updated: Nov 16, 2025
Tissue-specific miRNA Expression Profiling in Mouse Heart Sections Using In Situ Hybridization
Published on: September 15, 2018
MicroRNA-21-containing microvesicles from tubular epithelial cells promote cardiomyocyte hypertrophy
1Department of Nephrology, The First People's Hospital of Changzhou, Changzhou, China.
Insights
Chronic kidney disease (CKD) can cause heart problems. Microvesicles (MVs) carrying microRNA-21 (miR-21) from kidney cells induce heart muscle cell (cardiomyocyte) growth, contributing to cardiac dysfunction in CKD.
Area of Science:
- Molecular Biology
- Cardiovascular Research
- Nephrology
Background:
- Cardiomyocyte hypertrophy is a key factor in cardiovascular disease (CVD) associated with chronic kidney disease (CKD).
- MicroRNA-21 (miR-21) is implicated in myocardial hypertrophy, but its role via microvesicles (MVs) in CKD is understudied.
Purpose of the Study:
- To investigate the role of microvesicles (MVs) containing miR-21 in the development of cardiomyocyte hypertrophy in the context of chronic kidney disease (CKD).
- To explore the mechanism by which kidney tubular cells influence cardiomyocyte hypertrophy through MV-mediated miR-21 transfer.
Main Methods:
- Renal tubular epithelial cells were stimulated with transforming growth factor-beta 1 (TGF-β1) to induce microvesicle (MV) production.
- MVs were isolated, and their miR-21 content was quantified using qRT-PCR.
- Cardiomyocytes were exposed to MVs, and changes in cell size, protein content, and atrial natriuretic peptide (ANP) levels were measured. The effect of miR-21 inhibitors on MV-induced hypertrophy was assessed.
Main Results:
- Stimulation with TGF-β1 induced renal tubular cells to release MVs that were taken up by cardiomyocytes, leading to increased cardiomyocyte size, protein concentration, and ANP levels.
- Elevated miR-21 levels were observed in MVs derived from stimulated renal tubular cells and in recipient cardiomyocytes.
- Inhibition of miR-21 in cardiomyocytes attenuated the hypertrophic response induced by MVs.
Conclusions:
- Tubular cells secrete miR-21 via MVs, which can be transferred to cardiomyocytes, promoting cardiomyocyte hypertrophy.
- This MV-mediated transfer of miR-21 represents a novel mechanism contributing to cardiac dysfunction in CKD.
- Targeting this pathway may offer new therapeutic strategies for CKD-related cardiac complications.
Background:
Cardiomyocyte hypertrophy has been reported as one of the important mechanisms for cardiovascular disease (CVD) in patients with chronic kidney disease (CKD). MiroRNA-21(miR-21) was determined to play an important role in myocardial hypertrophy. However, the role of microvesicles (MVs) containing miR-21 in CKD-related cardiomyocyte hypertrophy remains largely unexplored.
Methods:
Renal tubular epithelial cells were stimulated by transforming growth factor (TGF-β1), and the conditioned medium was extracted by differential centrifugation. Renal tubular epithelial cells were labeled with Dil-C18 dye and the recipient cardiomyocytes were observed by fluorescence microscope. MiR-21 level in MVs was detected by qRT-PCR, and the length and diameter of cardiomyocytes were measured by microscope. BCA protein kit and ANP kit were used to detect the content of cell protein and the level of ANP. MiR-21 inhibitor was transfected into cardiomyocytes to observe the effect of miR-21 on myocardial hypertrophy.
Results:
TGF-β1 could induce donor renal tubular epithelial cells to produce MVs and delivered into cardiomyocytes, followed by the diameter, protein concentration and ANP content of cardiomyocytes significantly increased. Meanwhile, MiR-21 levels were markedly increased in MVs isolated from donor renal tubular epithelial cells and recipient cardiomyocytes. Pre-transfection of miR-21 inhibitors could inhibit MV-induced cardiomyocyte hypertrophy.
Conclusion:
Tubular cells could secrete miR-21 by MVs and deliver it into recipient cardiomyocytes to induce cardiomyocyte hypertrophy. It might shed a new light on the mechanism and treatment of CKD-related cardiac dysfunction.
