MicroRNA-135a participates in the development of astrocytes derived from bacterial meningitis by downregulating...

Accumulating evidence has highlighted the potential of microRNAs (miRs) as biomarkers in various human diseases. However, the roles of miRs in bacterial meningitis (BM), a severe infectious condition, still remain unclear. Thus, the present study aimed to investigate the effects of miR-135a on proliferation and apoptosis of astrocytes in BM. Neonatal rats were injected with Streptococcus pneumoniae to establish the BM model. The expression of miR-135a and hypoxia-inducible factor 1α (HIF-1α) in the BM rat models were characterized, followed by determination of their interaction. Using gain- and loss-of-function approaches, the effects of miR-135a on proliferation, apoptosis, and expression of glial fibrillary acidic protein (GFAP), in addition to apoptosis-related factors in astrocytes were examined accordingly. The regulatory effect of HIF-1α was also determined along with the overexpression or knockdown of HIF-1α. The results obtained indicated that miR-135a was poorly expressed, whereas HIF-1α was highly expressed in the BM rat models. In addition, restored expression levels of miR-135a were determined to promote proliferation while inhibiting the apoptosis of astrocytes, along with downregulated Bax and Bad, as well as upregulated Bcl-2, Bcl-XL, and GFAP. As a target gene of miR-135a, HIF-1α expression was determined to be diminished by miR-135a. The upregulation of HIF-1α reversed the miR-135a-induced proliferation of astrocytes. Taken together, the key findings of the current study present evidence suggesting that miR-135a can downregulate HIF-1α and play a contributory role in the development of astrocytes derived from BM, providing a novel theoretical perspective for BM treatment approaches.