Evaluation of CD93hi macrophage on atherosclerosis through dynamic cells adoptive transfer

  • Impact factors: 6.212
  • Publication: Arabian Journal of Chemistry
  • Author:Chen Su, Ting Liang, Bin Qu, Chao Zhang, Yeming Han, Guihua Hou, Feng Gao
  • DOI citation-doi:10.1016/j.arabjc.2023.104796
  • Date:2023-03-17

Macrophage (MΦ) with different surface marker exhibits diversity effect on the development of atherosclerosis (AS). Recently CD93 high MΦ was reported tightly related with inflammatory diseases, however, its effect on the development of AS remains unclear. Here, we adoptive transferred with prepared CD93 high and low expressed (CD93 hi , CD93 lo ) MΦ in establishing ApoE -/- mice AS model at the week of 1, 4, 8, 12, 16, respectively. At w12 and 20, pathology change and the expression of CD93, F4/80, CD31, ApoE in related vessels were detected. Pro-inflammatory cytokines and related signal pathway were also analyzed. Finally, CD93 targeting radionuclide imaging in AS model was performed with prepared 125 I-anti-CD93 mAb injection. The results showed that all pathological changes in diseased vessels showed much severe in w20 (the time that AS model was established successfully) than w12. In contrast to group with CD93 lo MΦ adoptive transferred, much serious inflammatory infiltration, increased pro-inflammatory factors and elevated CD93, F4/80, CD31 expression in clamped carotid artery were detected, and also higher Tumor necrosis factor-α (TNF-α) and Interleukin-1β (IL-1β) in serum were measured in ApoE -/- model with CD93 hi MΦ adoptive transferred in w20. Furthermore, obviously high expressed p-STAT3 and p-NF-κB were detected in CD93 hi MΦ, compared with CD93 lo MΦ. Ex vivo phosphor-autoradiography showed higher radioactivity accumulation in diseased vessels in ApoE -/- model with CD93 hi MΦ adoptive transferred after 125 I-anti-CD93 mAb injection, compared with CD93 lo MΦ adopted group in w20. In conclusion, CD93 hi MΦ subset promoted the development of AS and aggravated the disease severity mainly through p-STAT3/p-NF-κB pathways. CD93 on MΦ may be as a novel target for AS modulation.

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