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Abstract: PO0393

Macrophage Heterogeneity in Progression and Regression Phages of Cisplatin-Induced AKI Mice Model: A Single-Cell RNA Sequencing Study

Session Information

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Authors

  • Li, Shensen, Sir Run Run Hospital Nanjing Medical University, Nanjing, Jiangsu, China
  • Deng, Bingquan, Sir Run Run Hospital Nanjing Medical University, Nanjing, Jiangsu, China
  • Liu, Qingqing, Sir Run Run Hospital Nanjing Medical University, Nanjing, Jiangsu, China
  • Shen, Haiyan, Sir Run Run Hospital Nanjing Medical University, Nanjing, Jiangsu, China
  • Li, Wenwen, Sir Run Run Hospital Nanjing Medical University, Nanjing, Jiangsu, China
  • Cao, Changchun, Sir Run Run Hospital Nanjing Medical University, Nanjing, Jiangsu, China
Background

Immune cells, especially innate immune cells, play an important role in the pathogenesis of AKI. However heterogeneous of macrophage (M) and its dynamic change during progression and regression of cisplatin induced AKI (cis-AKI) remain uncertain.

Methods

8-week-old male C57BL/6 mice were randomly divided into sham, cis3d and cis7d groups (Fig.1A). Single-cell analysis were conducted based on 10×Chromium platform. Differentially expressed genes were analysed.

Results

36 cell clusters were identified and integrated into 11 cell types according to cell-specific markers in murine kidneys (Fig.1B). 4 clusters were identified as macrophage (Fig.1C). Cluster 4 (Cx3cr1+M) was defined as embryonic derived renal resident macrophage (EMRM) for its high expression of F4/80, Cd74, Cx3cr1 (Fig.1D). Cluster 15 (Itgam+M) was defined as recruit M due to its high expression of Itgam (Fig.1D). Cluster 26 (Cd74+M) was defined as bone marrow derived resident macrophage according to its high expression of Cd74 (Fig.1D). Cluster 30 (Cx3cr1+Mki67+M) was the proliferation subset of EMRM (Fig.1D).
The proportion of Itgam+MΦ was increased in the injury stage, and restored in repair stage (Fig.1E). Resident-M (Cx3cr1+M, Cd74+M and Cx3cr1+Mki67+M) slightly decreased in injury period and recovered in the repair period (Fig.1E). KEGG analysis showed Itgam+M mainly enriched in apoptosis and damage-related pathway, while Cx3cr1+M and Cd74+ enriched in phagocytosis and antigen presentation pathway (Fig.1F).

Conclusion

A total of 4 clusters were classified as M, while recruit-M and resident-M shown opposite dynamic trends in the injury and repair stages. KEGG analysis demonstrated that recruit-M may dominant injury phage while resident-M contribute to regression phages in cis-AKI.