Aplastic anemia (AA) is a bone marrow failure syndrome with high morbidity and mortality. Bone marrow (BM)‑mesenchymal stem cells (MSCs) are the main components of the BM microenvironment, and dysregulation of BM‑MSC adipogenic differentiation is a pathologic hallmark of AA. MicroRNAs (miRNAs/miRs) are crucial regulators of multiple pathological processes such as AA. However, the role of miR‑30a‑5p in the modulation of BM‑MSC adipogenic differentiation in AA remains unclear. The present study aimed to explore the effect of miR‑30a‑5p on AA BM‑MSC adipogenic differentiation and the underlying mechanism. The levels of miR‑30a‑5p expression and family with sequence similarity 13, member A (F... More
Aplastic anemia (AA) is a bone marrow failure syndrome with high morbidity and mortality. Bone marrow (BM)‑mesenchymal stem cells (MSCs) are the main components of the BM microenvironment, and dysregulation of BM‑MSC adipogenic differentiation is a pathologic hallmark of AA. MicroRNAs (miRNAs/miRs) are crucial regulators of multiple pathological processes such as AA. However, the role of miR‑30a‑5p in the modulation of BM‑MSC adipogenic differentiation in AA remains unclear. The present study aimed to explore the effect of miR‑30a‑5p on AA BM‑MSC adipogenic differentiation and the underlying mechanism. The levels of miR‑30a‑5p expression and family with sequence similarity 13, member A (FAM13A) mRNA expression in BM‑MSCs were quantified using reverse transcription‑quantitative (RT‑q) PCR. The mRNA expression levels of adipogenesis‑associated factors [fatty acid‑binding protein 4 (FABP4), lipoprotein lipase (LPL), perilipin‑1 (PLIN1), peroxisome proliferator‑activated receptor γ (PPARγ) and CCAAT/enhancer binding protein α (C/EBPα)] were analyzed using RT‑qPCR. Lipid droplet accumulation was evaluated using Oil Red O staining in BM‑MSCs. The interaction between miR‑30a‑5p and the FAM13A 3'‑untranslated region was identified by TargetScan, and a dual‑luciferase reporter assay was used to confirm the interaction. The expression levels of FAM13A and Wnt/β‑catenin pathway‑related proteins were examined via western blotting. The results showed that miR‑30a‑5p expression levels were significantly elevated in BM‑MSCs from patients with AA compared with those in control subjects (iron deficiency anemia). miR‑30a‑5p expression levels were also significantly increased in adipose‑induced BM‑MSCs in a time‑dependent manner. miR‑30a‑5p significantly promoted AA BM‑MSC adipogenic differentiation, and significantly enhanced the mRNA expression levels of FABP4, LPL, PLIN1, PPARγ and C/EBPα as well as lipid droplet accumulation. miR‑30a‑5p was also demonstrated to target FAM13A in AA BM‑MSCs. FAM13A significantly reduced BM‑MSC adipogenic differentiation by activating the Wnt/β‑catenin signaling pathway. In conclusion, miR‑30a‑5p was demonstrated to serve a role in AA BM‑MSC adipogenic differentiation by targeting the FAM13A/Wnt/β‑catenin signaling pathway. These findings suggest that miR‑30a‑5p may be a therapeutic target for AA.
