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Genetic and Pharmacological Modulation of P75 Neurotrophin Receptor Attenuate Brain Damage After Ischemic Stroke in Mice. | LitMetric

Genetic and Pharmacological Modulation of P75 Neurotrophin Receptor Attenuate Brain Damage After Ischemic Stroke in Mice.

Mol Neurobiol

Department of Anatomy and Neurobiology, College of Medicine, The University of Tennessee Health Science Center, 875 Monroe Avenue, Wittenborg Bldg, Room-231, Memphis, TN, 38163, USA.

Published: January 2024

AI Article Synopsis

  • * Two experimental approaches were used: one involving the administration of a p75 inhibitor (LM11A-31) after inducing stroke in mice, and the other comparing p75 knockout mice to wild-type mice to assess the impact on stroke outcomes.
  • * Results showed that inhibiting or knocking down p75 reduced brain damage and improved motor function post-stroke, suggesting that targeting p75 might be a promising strategy for enhancing recovery from ischemic stroke, although further research is necessary to confirm these findings. *

Article Abstract

The precursor nerve growth factor (ProNGF) and its receptor p75 neurotrophin receptor (p75) are upregulated in several brain diseases, including ischemic stroke. The activation of p75 is associated with neuronal apoptosis and inflammation. Thus, we hypothesized that p75 modulation attenuates brain damage and improves functional outcomes after ischemic stroke. Two sets of experiments were performed. (1) Adult wild-type (WT) C57BL/6 J mice were subjected to intraluminal suture-middle cerebral artery occlusion (MCAO) to induce cerebral ischemia. Pharmacological inhibitor of p75, LM11A-31 (50 mg/kg), or normal saline was administered intraperitoneally (IP) 1 h post-MCAO, and animals survived for 24 h. (2) Adult p75 heterozygous knockout (p75) and WT were subjected to photothrombotic (pMCAO) to induce ischemic stroke, and the animals survived for 72 h. The sensory-motor function of animals was measured using Catwalk XT. The brain samples were collected to assess infarction volume, edema, hemorrhagic transformation, neuroinflammation, and signaling pathway at 24 and 72 h after the stroke. The findings described that pharmacological inhibition and genetic knocking down of p75 reduce infarction size, edema, and hemorrhagic transformation following ischemic stroke. Additionally, p75 modulation significantly decreased several anti-apoptosis markers and improved sensory motor function compared to the WT mice following ischemic stroke. Our observations exhibit that the involvement of p75 in ischemic stroke and modulation of p75 could improve the outcome of ischemic stroke by increasing cell survival and enhancing motor performance. LM11A-31 has the potential to be a promising therapeutic agent for ischemic stroke. However, more evidence is needed to illuminate the efficacy of LM11A-31 in ischemic stroke.

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Source
http://dx.doi.org/10.1007/s12035-023-03550-1DOI Listing

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