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<p>Pyruvate kinases are key enzymes of glycolytic metabolism of neurons and glia. One of them, pyruvate kinase M2 (PKM2) can also act as a transcriptional regulator and in this function has been implicated in several neurodegenerative diseases. Since nuclear translocation of PKM2 induces the expression of inflammatory genes in macrophages, we hypothesized that this mechanism contributes to the neurodegenerative processes after spinal cord injury (SCI). Using a rat model of contusion SCI, quantitative RT-PCR showed a strong upregulation of PKM2 transcripts close to the lesion center. To understand the functional implication of this observation, we studied PKM2 antigen expression in different cell types. Spinal cord injury caused a significant increase of PKM2 immunoreactivity in microglia, astrocytes and motor neurons but not in interneurons and oligodendrocytes. Phagocytes were strongly PKM2-positive and displayed a marked accumulation of PKM2 in the lesion core, suggesting its involvement in the inflammatory and phagocytosis response. The expression in astrocytes increased notably in the chronic phase surrounding the lesion site, coinciding with formation of the glial scar. An analysis of the intracellular distribution revealed that microglia in various states of activation, macrophages, astrocytes and oligodendrocytes contained PKM2 in both the cytosol and nucleus. Contrary to our hypothesis, SCI did not induce a significant nuclear translocation of PKM2 in any of these cell types. Our data stress the importance of PKM2 in the CNS and its implication after traumatic injury.</p>

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Cellular Distribution of Pyruvate Kinase M2 After Spinal Cord Injury in Adult Rats

  • 期刊论文

  • 发表日期：

    2025年11月29日

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  • Alejandro Arriero-Cabañero,
  • Natalia Díaz-Rubio,
  • Cristina Talabán-Rocha,
  • Lorenzo Romero-Ramírez,
  • Vinnitsa Buzoianu-Anguiano,
  • Jörg Mey

摘要

Pyruvate kinases are key enzymes of glycolytic metabolism of neurons and glia. One of them, pyruvate kinase M2 (PKM2) can also act as a transcriptional regulator and in this function has been implicated in several neurodegenerative diseases. Since nuclear translocation of PKM2 induces the expression of inflammatory genes in macrophages, we hypothesized that this mechanism contributes to the neurodegenerative processes after spinal cord injury (SCI). Using a rat model of contusion SCI, quantitative RT-PCR showed a strong upregulation of PKM2 transcripts close to the lesion center. To understand the functional implication of this observation, we studied PKM2 antigen expression in different cell types. Spinal cord injury caused a significant increase of PKM2 immunoreactivity in microglia, astrocytes and motor neurons but not in interneurons and oligodendrocytes. Phagocytes were strongly PKM2-positive and displayed a marked accumulation of PKM2 in the lesion core, suggesting its involvement in the inflammatory and phagocytosis response. The expression in astrocytes increased notably in the chronic phase surrounding the lesion site, coinciding with formation of the glial scar. An analysis of the intracellular distribution revealed that microglia in various states of activation, macrophages, astrocytes and oligodendrocytes contained PKM2 in both the cytosol and nucleus. Contrary to our hypothesis, SCI did not induce a significant nuclear translocation of PKM2 in any of these cell types. Our data stress the importance of PKM2 in the CNS and its implication after traumatic injury.