Abstract
Background: Spinal cord injury (SCI) is a challenge worldwide, but there are no effective treatments or therapeutic methods in the clinic. Recent studies have shown that type I arginase (Arginase1, Arg1) is closely associated with the treatment of SCI. The classical treatment for SCI involves filling the local area of SCI with activated M2a macrophages to allow the repair and regeneration of some synapses, but the specific mechanism of action of Arg1 is not clear.Method: In the present study, we first induced the polarization of RAW264.7 macrophages to M2a-type cells using IL-4 and constructed an Arg1 knockout cell line through the use of shRNA; we used these cells to treat a rat model of SCI. Finally, the present study explored the mechanism and pathway by which Arginase 1 regulates spinal repair by immunoblotting and immunohistochemistry.Result: Suspended M2a (Arg1-/+) macrophages were transplanted into the injury site in a rat model of contusion SCI. Compared with the model group and the shArg1 group, the shScramble (shSc) group exhibited higher Basso, Beattie, Bresnahan motor function scores, more compact structures and more Nissl bodies. Immunohistochemical results showed that the shSc group expressed higher levels of NeuN (a neuronal marker) and tau (an axonal marker), as well as the up-regulation of Cdc42, N-WASP, Arp2/3 and tau, as determined by Western blot.Conclusion: The study found that the polarization of M2a macrophages promoted the expression of Arginase 1, which restored axonal regeneration, promoted axonal regeneration, and promoted the structural and functional recovery of the contused spinal cord.
Highlights
Spinal cord injury (SCI) is a catastrophic event for patients; it can profoundly affect a patient’s quality of life and has profound social and economic impacts [1]
The results showed that the expression of Cdc42, N-Wiskott Aldrich syndrome protein (WASP), Arp2 and tau was significantly increased in the shSc group compared with the model group, while in the shArg1 group, these expression levels were not different from those in the model group, and the grayscale analysis showed the same conclusion (Figure 6B-E)
One of the difficulties in the treatment of spinal cord injury is the difficulties with axonal regeneration, which is associated with a large number of necrotic or apoptotic neurons in the spinal cord, difficulties with neuronal regeneration and a reduction in the levels of nutrient factors secreted by nerve cells, which disrupt beneficial microflora regeneration [15,16]
Summary
Spinal cord injury (SCI) is a challenge worldwide, but there are no effective treatments or therapeutic methods in the clinic. Method: In the present study, we first induced the polarization of RAW264.7 macrophages to M2a-type cells using IL-4 and constructed an Arg knockout cell line through the use of shRNA; we used these cells to treat a rat model of SCI. The present study explored the mechanism and pathway by which Arginase 1 regulates spinal repair by immunoblotting and immunohistochemistry. Result: Suspended M2a (Arg1-/+) macrophages were transplanted into the injury site in a rat model of contusion SCI. Conclusion: The study found that the polarization of M2a macrophages promoted the expression of Arginase 1, which restored axonal regeneration, promoted axonal regeneration, and promoted the structural and functional recovery of the contused spinal cord. Accepted Manuscript online: 29 January 2020 Version of Record published: 11 February 2020
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