Aging-US: MiR-520d-5p modulates chondrogenesis and chondrocyte metabolism through targeting HDAC1


Aging-US recently published "MiR-520d-5p modulates chondrogenesis and chondrocyte metabolism through targeting HDAC1" which reported that this study aimed to determine miRNAs associated with chondrogenesis of human mesenchymal stem cells and chondrocyte metabolism.

MiRNAs were screened in hMSCs during chondrogenesis by RNA-seq and qRT-PCR.

Histone deacetylase 1 was decreased in hMSCs chondrogenesis, and HDAC1 was a targeting gene of miR-520d-5p.

CI994, HDAC1 inhibitor, elevated cartilage-specific gene expressions and promoted hMSCs chondrogenesis.

Taken together, these results suggest that miR-520d-5p promotes hMSCs chondrogenesis and regulates chondrocyte metabolism through targeting HDAC1.

This Aging-USAging-US study provides a novel understanding of the molecular mechanism of OA progression.

Dr. Aimin Chen from The Department of Orthopedics and Trauma Surgery at Changzheng Hospital said, "Osteoarthritis (OA) is the most widespread joint degenerative disease around the world and a leading cause of pain and severe impairment of mobility in adults."

Figure 8. Expressions of miR-520d-5p and HDAC1 in the degraded cartilage. (A, B) Expression of miR-520d-5p and HDAC1 in non-degraded and degraded cartilages, respectively. (C) In situ hybridization for miR-520d-5p in non-degraded and degraded cartilages. MiR-520d-5p was labeled by green fluorescence, and the nuclei were labeled by blue fluorescence. Scalar bar = 50 μm. For each experiment, at least three replicates were available for the analysis. Data were expressed as mean ± standard deviation (SD). *P < 0.05; ** P < 0.01; *** P < 0.001.

To date, the detailed mechanisms underlying OA progression remain to be thoroughly investigated, and there are no effective interventions to cure degraded cartilage or slow OA progression.

Therefore, much attention so far is being drawn toward investigating the cellular and molecular mechanisms underlying the cartilage degeneration and chondrogenesis in OA.

For example, the expression of miR-194 decreases during the chondrogenesis of human adipose-derived stem cells, and the downregulation of miR-194 promotes the expression of SOX5, leading to enhanced chondrogenic differentiation .

Higher expressions of HDAC1 and HDAC2 are found in the chondrocytes of diseased cartilages of patients with OA, which inhibit the expressions of matrix proteins, such as AGGRECAN and COL2A1.

By bioinformatic prediction, they found that miR-520d-5p might directly target HDAC1. In addition, the authors demonstrated that miR-520d-5p plays an essential role in chondrogenesis and cartilage degradation by inhibiting HDAC1, thereby modulating the expressions of cartilage-specific genes.

The Chen Research Team concluded in their Aging-US Research Paper, "the results suggest that miR-520d-5p promotes hMSCs chondrogenesis and regulates chondrocyte metabolic activities through regulating the expressions of the cartilage-specific genes via targeting HDAC1. These observations provide a novel understanding of the mechanism underlying OA progression and insight into developing therapeutic treatments for OA."

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Correspondence to: Aimin Chen email:

Keywords: osteoarthritis, chondrogenesis, chondrocytes metabolism, human mesenchymal stem cells, miR-520d-5p

About Aging-US:

Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

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