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Abstract
Objectives We aim to identify the key biomarker of acute rejection (AR) after kidney transplantation via bioinformatics methods. Methods The gene expression data GSE75693 of 30 samples with stable kidney transplantation recipients and 15 AR samples were downloaded and analyzed by the limma package to identify differentially expressed genes (DEGs). Then, Gene Ontology (GO) functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were done to explore the biological functions and potential important pathways of DEGs. Finally, protein-protein interactions (PPIs) and literature mining were applied to construct the cocitation network and to select the hub protein. Results A total of 437 upregulated genes and 353 downregulated genes were selected according to P < 0.01 and |log2(fold change)| > 1.0. DEGs of AR are mainly located on membranes and impact the activation of receptors in immune responses. In the PPI network, Src kinase, lymphocyte kinase (LCK), CD3G, B2M, interferon-γ, CD3D, tumor necrosis factor, VAV1, and CD3E in the T cell receptor signaling pathway were selected as important factors, and LCK was identified as the hub protein. Conclusion LCK, via acting on T-cell receptor, might be a potential therapeutic target for AR after kidney transplantation.
Highlights
Kidney transplantation is widely accepted as a standard life-saving therapy for end-stage chronic kidney disease [1]
According to the distinct key players in the pathogenesis, acute rejection (AR) is classified into two types, i.e., acute T cell-mediated rejection (TCMR) and acute antibody-mediated rejection (AMR)
By Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) in differentially expressed genes (DEGs) enrichment analysis, we further investigated the potential mechanisms of AR
Summary
Kidney transplantation is widely accepted as a standard life-saving therapy for end-stage chronic kidney disease [1]. As the last resort, kidney transplantation may prolong patients’ survival and improve their life quality [2]. Immunosuppressants are routinely prescribed to recipients to promote graft survival after transplantation [3]. Despite the standard use of immunosuppressants, acute rejection (AR) is sometimes inevitable, which usually occurs days to months after transplantation [4]. According to the distinct key players in the pathogenesis, AR is classified into two types, i.e., acute T cell-mediated rejection (TCMR) and acute antibody-mediated rejection (AMR). AMR is caused by circulating antibodies of recipients, which are mainly antibodies against donor human leukocyte antigen (HLA). T cells play important roles in both TCMR and AMR
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