Protection of hUC-MSCs against neuronal complement C3a receptor-mediated NLRP3 activation in CUMS-induced mice

Neurosci Lett. 2021 Jan 10:741:135485. doi: 10.1016/j.neulet.2020.135485. Epub 2020 Nov 5.

Abstract

Background: Hyperactivation of complement C3 and inflammation-related activation of NLR family pyrin domain containing 3 (NLRP3) inflammasome are implicated in the etiology of stress-related disorders. Studies have shown that human umbilical cord mesenchymal stromal cells (hUC-MSCs) have immunomodulatory and anti-inflammatory effects; however, the mechanism remains unclear.

Methods: hUC-MSCs were administered to chronic unpredictable mild stress (CUMS) model mice once a week for four weeks. After the administration of hUC-MSCs, several parameters were assessed, including behavioral performance, synapse-related proteins, complement C3 receptors (C3aR) in neurons, and the NLRP3 inflammasome. Then, CUMS mice were injected with SB290157, a complement C3aR antagonist, and the behavioral index and NLRP3 inflammasome activation were tested.

Results: The open-field and forced swimming behavioral tests showed an improvement in depression-like behaviors in the CUMS-exposed mice after the administration of hUC-MSCs. Treatment with hUC-MSCs significantly decreased the neuronal C3aR levels and alleviated synaptic damage. Furthermore, the levels of the NLRP3 inflammasome and inflammatory factors were reduced after hUC-MSC administration. In particular, treatment with a C3aR antagonist also decreased NLRP3 inflammasome expression and inflammation, which was consistent with the observed improvements after hUC-MSC treatment.

Conclusion: hUC-MSCs can attenuate NLRP3 activation in CUMS-induced mice, which may be correlated with C3aR in neurons.

Keywords: Chronic unpredictable mild stress; Complement C3a receptor; Human umbilical cord mesenchymal stromal cells; NLRP3 inflammasome.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Monoclonal
  • Behavior, Animal
  • Complement C3 / metabolism*
  • Disease Models, Animal
  • Hippocampus / metabolism
  • Inflammasomes / metabolism
  • Interleukin-2
  • Male
  • Mesenchymal Stem Cell Transplantation*
  • Mesenchymal Stem Cells / metabolism*
  • Mice
  • Mice, Inbred ICR
  • NLR Family, Pyrin Domain-Containing 3 Protein / metabolism*
  • Neuronal Plasticity
  • Stress, Psychological / metabolism*
  • Umbilical Cord / cytology

Substances

  • Antibodies, Monoclonal
  • Complement C3
  • Inflammasomes
  • Interleukin-2
  • NLR Family, Pyrin Domain-Containing 3 Protein
  • Nlrp3 protein, mouse
  • lorukafusp alfa