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Journal of neuroinflammation
Jun 20, 2022;19 (1): 160.

Apelin alleviated neuroinflammation and promoted endogenous neural stem cell proliferation and differentiation after spinal cord injury in rats.

Qing Liu, Shuai Zhou, Xiao Wang, Chengxu Gu, Qixuan Guo, Xikai Li, Chunlei Zhang, Naili Zhang, Luping Zhang, Fei Huang
Author Information
  1. Qing Liu: Institute of Neurobiology, Binzhou Medical University, 346 Guanhai Road, Laishan, 264003, Shandong, China.
  2. Shuai Zhou: Institute of Neurobiology, Binzhou Medical University, 346 Guanhai Road, Laishan, 264003, Shandong, China.
  3. Xiao Wang: Institute of Neurobiology, Binzhou Medical University, 346 Guanhai Road, Laishan, 264003, Shandong, China.
  4. Chengxu Gu: Institute of Neurobiology, Binzhou Medical University, 346 Guanhai Road, Laishan, 264003, Shandong, China.
  5. Qixuan Guo: Institute of Neurobiology, Binzhou Medical University, 346 Guanhai Road, Laishan, 264003, Shandong, China.
  6. Xikai Li: Institute of Neurobiology, Binzhou Medical University, 346 Guanhai Road, Laishan, 264003, Shandong, China.
  7. Chunlei Zhang: Institute of Neurobiology, Binzhou Medical University, 346 Guanhai Road, Laishan, 264003, Shandong, China.
  8. Naili Zhang: Institute of Neurobiology, Binzhou Medical University, 346 Guanhai Road, Laishan, 264003, Shandong, China.
  9. Luping Zhang: Institute of Neurobiology, Binzhou Medical University, 346 Guanhai Road, Laishan, 264003, Shandong, China. zhangluping3000@163.com.
  10. Fei Huang: Institute of Neurobiology, Binzhou Medical University, 346 Guanhai Road, Laishan, 264003, Shandong, China. hfei22518@163.com.
PMID: 35725619 DOI: 10.1186/s12974-022-02518-7

Abstract

BACKGROUND: Spinal cord injury (SCI) causes devastating neurological damage, including secondary injuries dominated by neuroinflammation. The role of Apelin, an endogenous ligand that binds the G protein-coupled receptor angiotensin-like receptor 1, in SCI remains unclear. Thus, our aim was to investigate the effects of Apelin in inflammatory responses and activation of endogenous neural stem cells (NSCs) after SCI.
METHODS: Apelin expression was detected in normal and injured rats, and roles of Apelin in primary NSCs were examined. In addition, we used induced pluripotent stem cells (iPSCs) as a carrier to prolong the effective duration of Apelin and evaluate its effects in a rat model of SCI.
RESULTS: Co-immunofluorescence staining suggested that Apelin was expressed in both astrocytes, neurons and microglia. Following SCI, Apelin expression decreased from 1 to 14 d and re-upregulated at 28 d. In vitro, Apelin promoted NSCs proliferation and differentiation into neurons. In vivo, lentiviral-transfected iPSCs were used as a carrier to prolong the effective duration of Apelin. Transplantation of transfected iPSCs in situ immediately after SCI reduced polarization of M1 microglia and A1 astrocytes, facilitated recovery of motor function, and promoted the proliferation and differentiation of endogenous NSCs in rats.
CONCLUSION: Apelin alleviated neuroinflammation and promoted the proliferation and differentiation of endogenous NSCs after SCI, suggesting that it might be a promising target for treatment of SCI.

Keywords

Apelin Astrocytes Endogenous neural stem cells Neuroinflammation SCI

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Grants

  1. 81870985/National Natural Science Foundation of China
  2. 81171142/National Natural Science Foundation of China
  3. ZR201702140355/Natural Science Foundation of Shandong Province

MeSH Term

Animals
Apelin
Cell Differentiation
Cell Proliferation
Neuroinflammatory Diseases
Rats
Recovery of Function
Spinal Cord
Spinal Cord Injuries

Chemicals

Apelin
Journal Article
Article has an altmetric score of 2

Word Cloud

Created with Highcharts 10.0.0ApelinSCIendogenousNSCsstempromotedproliferationdifferentiationneuroinflammationneuralcellsratsiPSCscordinjuryreceptor1effectsexpressionusedcarrierprolongeffectivedurationastrocytesneuronsmicrogliaalleviatedBACKGROUND:SpinalcausesdevastatingneurologicaldamageincludingsecondaryinjuriesdominatedroleligandbindsGprotein-coupledangiotensin-likeremainsunclearThusaiminvestigateinflammatoryresponsesactivationMETHODS:detectednormalinjuredrolesprimaryexaminedadditioninducedpluripotentevaluateratmodelRESULTS:Co-immunofluorescencestainingsuggestedexpressedFollowingdecreased14 dre-upregulated28 dvitrovivolentiviral-transfectedTransplantationtransfectedsituimmediatelyreducedpolarizationM1A1facilitatedrecoverymotorfunctionCONCLUSION:suggestingmightpromisingtargettreatmentcellspinalAstrocytesEndogenousNeuroinflammation

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