2. Academic Validation
  3. Deficiency of CD93 exacerbates inflammation-induced activation and migration of BV2 microglia by regulating the TAK1/NF-κB pathway

Deficiency of CD93 exacerbates inflammation-induced activation and migration of BV2 microglia by regulating the TAK1/NF-κB pathway

  • Neurosci Lett. 2022 Oct 18;136914. doi: 10.1016/j.neulet.2022.136914.
Xin Hong 1,  Mingjie Xia 2,  Qinyang Zhang 3,  Tianyu Zhao 3,  Yanan Zhang 3,  Zhanyang Qian 4,  Junping Bao 5,  Haijun Li 6
Affiliations

Affiliations

  • 1 Spine center, Zhongda Hospital of Southeast University, Nanjing, China.
  • 2 Department of Orthopedics, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.
  • 3 Department of Orthopedics, Taizhou People's Hospital of Nanjing Medical University, Taizhou, China; Postgraduate School, Dalian Medical University, Dalian, China.
  • 4 Spine center, Zhongda Hospital of Southeast University, Nanjing, China; School of Medicine, Southeast University, Nanjing, China. Electronic address: [email protected].
  • 5 Spine center, Zhongda Hospital of Southeast University, Nanjing, China; School of Medicine, Southeast University, Nanjing, China.
  • 6 Department of Orthopedics, Taizhou People's Hospital of Nanjing Medical University, Taizhou, China.
PMID: 36270452 DOI: 10.1016/j.neulet.2022.136914
Abstract

The role of CD93 in inflammatory response has been reported in multiple previous studies. However, the underlying mechanism of CD93 in microglial activation and migration during neuroinflammation post spinal cord injury (SCI) remains elusive. In the current study, we performed western blot, qRT-PCR, immunofluorescence analyses Transwell assay, and ELISA to determine the expression change and in-depth molecular mechanism of CD93 in microglia post inflammatory initiation. We found that CD93 expression was increased in microglia after SCI in vivo or lipopolysaccharide (LPS) stimuli in vitro. Additionally, CD93 interacted with TAK1 to inhibit NF-κB activation, thus attenuating inflammation and migration of microglia after treatment with LPS. These findings indicate that CD93 might participate in microglia-induced neuroinflammation development post SCI, suggesting that CD93 is a promising target for neuroimmunological regulation.

Keywords

CD93; Inflammation; Microglia; NF-κB; Spinal cord injury.

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