Abstract
[Purpose]Recent studies have shown that glucose-6-phosphate isomerase (GPI)—which is a glycolysis interconversion enzyme—reduces oxidative stress. However, these studies are limited to tumors such as fibrosarcoma, and there are no studies that have examined the effects of exercise on GPI expression in mice skeletal muscle. Furthermore, GPI acts in an autocrine manner thorough its receptor, autocrine motility factor receptor (AMFR); therefore, we investigated expression level changes of secreted GPI from skeletal muscle in in vitro study to examine the potential role of GPI on skeletal muscle.[Methods]First, we performed an in vitro study, to identify the condition that upregulates GPI levels in skeletal muscle cells; we treated C2C12 muscle cells with an exercise-mimicking chemical, AICAR. AICAR treatment upregulated GPI expression level in C2C12 cell and its secretomes. To confirm the direct effect of GPI on skeletal muscle cells, we treated C2C12 cells with GPI recombinant protein.[Results]We found that GPI improved the viability of C2C12 cells. In the in vivo study, the exercise-treated mice group showed upregulated GPI expression in skeletal muscle. Based on the in vitro study results, we speculated that expression level of GPI in skeletal muscle might be associated with muscle function. We analyzed the association between GPI expression level and the grip strength of the all mice group. The mice group’s grip strengths were upregulated after 2 weeks of treadmill exercise, and GPI expression level positively correlated with the grip strength.[Conclusion]These results suggested that the exercise-induced GPI expression in skeletal muscle might have a positive effect on skeletal muscle function.
Highlights
Glucose-6-phosphate isomerase (GPI) plays an important role in glycolysis, where it catalyzes the interconversion between glucose-6-phosphate and fructose-6-phosphate[1]
According to a previous study, treatment with aminoimidazole-4-carboxamide ribonucleotide (AICAR)—which is a type of exercise mimetic molecule that upregulates AMPK signaling pathway19—upregulated GPI secretion by L6 skeletal muscle cells[9]
GPI acts in an autocrine manner with its own receptor, known as autocrine motility factor receptor (AMFR)[23,24], and secreted GPI from skeletal muscle can act on the skeletal muscle itself directly
Summary
Glucose-6-phosphate isomerase (GPI) plays an important role in glycolysis, where it catalyzes the interconversion between glucose-6-phosphate and fructose-6-phosphate[1]. AMF acts like cytokines, and is known to be a stimulator of vascular proliferation[5]. These signaling pathways are initiated by its binding to specific glycoproteins proteins present on the cell surface[6], by means of which it acts in an autocrine manner[7]. A previous study showed that GPI mRNA level decreased with aging in gastrocnemius muscle. They confirmed the upregulation of GPI mRNA in caloric-restricted state[8]. It was reported that knockdown of GPI induces downregulation of aging markers, p21 and p5310
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