Objective      To determine the expression of miR-210 in PC12 cells exposed to hypoxia and the regulatory mechanisms of hypoxia on mitochondria function.        Methods      PC12 cells were cultured in hypoxic condition (94% N

2

5% CO

2

and 1% O

2

) at 37 ℃. CCK-8 assay was carried out to analyze cell vitality. The expression of miR-210 was tested by qRT-PCR. Western blotting was used to detect

the expression of mitochondrial proteins

iron-sulfur cluster assembly proteins (ISCU1/2) and cytochrome oxidase (COX10). Rhodamine 123-indicated mitochondrial membrane potential (MMP) was detected with flow cytometry. The concentrations of ATP

ADP and AMP in PC12 cells were measured by high performance liquid chromatography (HPLC).        Results      After hypoxia exposure for 24 h and 48 h

the viability of PC12 cells was decreased to (63.2±0.1)% and (48.7±0.4)% of normally cultured cells (

P

0.05)

respectively. The expression of miR-210 was up-regulated at 12

24 and 48 h after hypoxia exposure. A sharp and transient increase of MMP at 12 h was followed by significant attenuation at 24 and 48 h. Cellular contents of ADP and AMP were increased while ATP level was declined. Western blot results showed the expression of ISCU1/2 and COX10

target genes of miR-210

was dramatically reduced after hypoxia challenge in an obvious time-effect relationship.       Conclusion      Hypoxia induces mitochondrial dysfunction in PC12 cells. The impact of hypoxia-upregulated miR-210 expression on its target genes

ISCU1/2 and COX10

may be one of the possible key pathways.