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PRMT6 deficiency or inhibition alleviates neuropathic pain by decreasing glycolysis and inflammation in microglia.
Hua, Tong; Kong, Erliang; Zhang, Hailing; Lu, Jinfang; Huang, Kesheng; Ding, Ruifeng; Wang, Haowei; Li, Jian; Han, Chaofeng; Yuan, Hongbin.
Afiliação
  • Hua T; Department of Anesthesiology, Changzheng Hospital, Naval Medical University, Shanghai, China.
  • Kong E; Department of Anesthesiology, Changzheng Hospital, Naval Medical University, Shanghai, China; Department of Anesthesiology, The No. 988 Hospital of Joint Logistic Support Force of Chinese People's Liberation Army, Zhengzhou, China.
  • Zhang H; Department of Neurology, Changhai Hospital, Naval Medical University, Shanghai, China.
  • Lu J; Department of Anesthesiology, Changzheng Hospital, Naval Medical University, Shanghai, China.
  • Huang K; Department of Anesthesiology, Changzheng Hospital, Naval Medical University, Shanghai, China.
  • Ding R; Department of Anesthesiology, Changzheng Hospital, Naval Medical University, Shanghai, China.
  • Wang H; Department of Anesthesiology, Changzheng Hospital, Naval Medical University, Shanghai, China.
  • Li J; Department of Anesthesiology, Changzheng Hospital, Naval Medical University, Shanghai, China.
  • Han C; Department of Histology and Embryology, and Shanghai Key Laboratory of Cell Engineering, Naval Medical University, Shanghai, China. Electronic address: hcf@immunol.org.
  • Yuan H; Department of Anesthesiology, Changzheng Hospital, Naval Medical University, Shanghai, China. Electronic address: jfjczyy@aliyun.com.
Brain Behav Immun ; 118: 101-114, 2024 May.
Article em En | MEDLINE | ID: mdl-38402915
ABSTRACT
Microglia induced chronic inflammation is the critical pathology of Neuropathic pain (NP). Metabolic reprogramming of macrophage has been intensively reported in various chronic inflammation diseases. However, the metabolic reprogramming of microglia in chronic pain remains to be elusive. Here, we reported that immuno-metabolic markers (HIF-1α, PKM2, GLUT1 and lactate) were related with increased expression of PRMT6 in the ipsilateral spinal cord dorsal horn of the chronic construction injury (CCI) mice. PRMT6 deficiency or prophylactic and therapeutic intrathecal administration of PRMT6 inhibitor (EPZ020411) ameliorated CCI-induced NP, inflammation and glycolysis in the ipsilateral spinal cord dorsal horn. PRMT6 knockout or knockdown inhibited LPS-induced inflammation, proliferation and glycolysis in microglia cells. While PRMT6 overexpression exacerbated LPS-induced inflammation, proliferation and glycolysis in BV2 cells. Recent research revealed that PRMT6 could interact with and methylate HIF-1α, which increased HIF-1α protein stability. In sum, increased expression of PRMT6 exacerbates NP progress by increasing glycolysis and neuroinflammation through interacting with and stabilizing HIF-1α in a methyltransferase manner, which outlines novel pathological mechanism and drug target for NP.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Microglia / Neuralgia Limite: Animals Idioma: En Revista: Brain Behav Immun Assunto da revista: ALERGIA E IMUNOLOGIA / CEREBRO / PSICOFISIOLOGIA Ano de publicação: 2024 Tipo de documento: Article País de afiliação: China

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Microglia / Neuralgia Limite: Animals Idioma: En Revista: Brain Behav Immun Assunto da revista: ALERGIA E IMUNOLOGIA / CEREBRO / PSICOFISIOLOGIA Ano de publicação: 2024 Tipo de documento: Article País de afiliação: China