hUC-MSCs Attenuate Acute Graft-Versus-Host Disease through Chi3l1 Repression of Th17 Differentiation

Figure 1

Chi3l1 is highly expressed in hUC-MSCs. (a) Heat map of differential gene expression in various MSCs, including BM-MSCs, hP-MSCs, hM-MSCs, and hUC-MSCs. (b) A volcano plot was used to analyze the DEGs (red indicates upregulated genes). (c) KEGG pathway indicating that Chi3l1 is highly associated with the JAK-STAT signaling pathway and graft-versus-host disease (GvHD) in hUC-MSCs. (d) Chi3l1 expression in different MSCs by qPCR. (e) hUC-MSCs were treated with IFN-γ and TNF-α (20 ng/ml) for 24 h, 48 h, and 72 h, and Chi3l1 mRNA levels were measured by qPCR. (f) The protein expression of Chi3l1 in IFN-γ- and TNF-α-pretreated hUC-MSC supernatants was analyzed by western blot. (g) The Chi3l1 protein expression levels in IFN-γ- and TNF-α-pretreated hUC-MSCs determined by western blot. JAK: Janus kinase; STAT: signal transducer and activator of transcription; IFN-γ: interferon-gamma; TNF-α: tumor necrosis factor-alpha.

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