Adipose-derived stem cells decrease pain in a rat model of oxaliplatin-induced neuropathy: Role of VEGF-A modulation

Neuropharmacology. 2018 Mar 15:131:166-175. doi: 10.1016/j.neuropharm.2017.12.020. Epub 2017 Dec 11.

Abstract

Oxaliplatin therapy of colorectal cancer induces a dose-dependent neuropathic syndrome in 50% of patients. Pharmacological treatments may offer limited relief; scientific efforts are needed for new therapeutic approaches. Therefore we evaluated in a preclinical setting the pain relieving properties of mesenchymal stem cells and its secretome. Rat adipose stem cells (rASCs) were administered in a rat model of oxaliplatin-induced neuropathy. A single intravenous injection of rASCs reduced oxaliplatin-dependent mechanical hypersensitivity to noxious and non-noxious stimuli taking effect 1 h after administration, peaking 6 h thereafter and lasting 5 days. Cell-conditioned medium was ineffective. Repeated rASCs injections every 5 days relieved pain each time with a comparable effect. Labeled rASCs were detected in the bloodstream 1 and 3 h after administration and found in the liver 24 h thereafter. In oxaliplatin-treated rats, the plasma concentration of vascular endothelial growth factor (pan VEGF-A) was increased while the isoform VEGF165b was upregulated in the spinal cord. Both alterations were reverted by rASCs. The anti-VEGF-A monoclonal antibody bevacizumab (intraperitoneally) reduced oxaliplatin-dependent pain. Studying the peripheral and central role of VEGF165b in pain, we determined that the intraplantar and intrathecal injection of the growth factor induced a pro-algesic effect. In the oxaliplatin neuropathy model, the intrathecal infusion of bevacizumab, anti-rat VEGF165b antibody and rASCs reduced pain. Adult adipose mesenchymal stem cells could represent a novel approach in the treatment of neuropathic pain. The regulation of VEGF-A is suggested as an effective mechanism in the complex response orchestrated by stem cells against neuropathy.

Keywords: Adipose stem cells; Bevacizumab; Chemotherapy-induced neuropathic pain; EGF; Intrathecal; TGF-β1; VEGF(165)b; VEGF-A; VEGF-R1.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipose Tissue / cytology*
  • Angiogenesis Inhibitors / therapeutic use
  • Animals
  • Antineoplastic Agents / toxicity
  • Bevacizumab / therapeutic use
  • Cell- and Tissue-Based Therapy / methods*
  • Cytokines / metabolism
  • Disease Models, Animal
  • Hyperalgesia / drug therapy
  • Injections, Spinal
  • Male
  • Neuralgia / chemically induced*
  • Neuralgia / therapy*
  • Organoplatinum Compounds / toxicity
  • Oxaliplatin
  • Pain Measurement
  • Rats
  • Rats, Sprague-Dawley
  • Rats, Wistar
  • Stem Cells / physiology*
  • Vascular Endothelial Growth Factor A / metabolism*
  • Vascular Endothelial Growth Factor A / therapeutic use

Substances

  • Angiogenesis Inhibitors
  • Antineoplastic Agents
  • Cytokines
  • Organoplatinum Compounds
  • VEGFA protein, human
  • Vascular Endothelial Growth Factor A
  • Oxaliplatin
  • Bevacizumab