The central nervous system (CNS) is a crucial anatomical compartment for brain functions where cellular mechanisms are tightly regulated. One such regulatory agent is PTPσ (Protein Tyrosine Phosphatase-sigma), a transmembrane enzyme that also plays the role of a receptor in the signaling cascade involved in the immune response in the CNS and neuronal plasticity (reviewed in 1). PTPσ is known to be the receptor for CSPG (chondroitin sulfate proteoglycans), a regulatory molecule for the maturation and differentiation of oligodendrocyte progenitor cells (OPCs) (2). Thus, PTPσ is directly involved in brain tissue development and regeneration. At the neonatal stage, the absence of PTPσ interferes with axogenesis, leading to neurological deficits and a high mortality rate (3).
A team from Shanghai has recently demonstrated its role as a double agent in tissue regeneration, for example following white matter injury. Indeed, in the days following prenatal hypoxic ischemia, PTPσ levels increase considerably, having the impact of limiting the inflammatory response of microglia as well as tissue repair (4). On the other hand, by inhibiting the action of PTPσ using ISP (Intracellular Signal Protein) (5), they demonstrated that the use of this peptide allowed the differentiation of oligodendrocytes and that it resulted in a significant improvement in neurological functions (4).
These observations suggest that PTPσ inhibition could become a therapeutic avenue for the treatment of brain lesions in humans. To evaluate the impact of this inhibition, target-specific antibodies such as anti-RPTPσ MM-0020 (6) can be a useful tool for your studies.