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. 2023 Feb 8;8(3):e165369. doi: 10.1172/jci.insight.165369

Figure 2. Hepatocyte-derived MCP-1 is necessary and sufficient to induce liver fibrosis.

Figure 2

(A) Experimental schematic for hepatocyte-specific MCP-1 gain of function by hydrodynamic injection of control (pLive-empty) or MCP-1 (pLive-MCP1) vectors in WT male mice (n = 8 mice/group). (B) Liver MCP-1 protein and quantitation from hepatocyte-specific MCP-1 gain of function by hydrodynamic injection of control (pLive-empty) or MCP-1 (pLive-MCP1) vectors in WT male mice (n = 4 mice/group). MCP-1 and actin blots are derived from the same samples run contemporaneously in parallel gels. (C) Gene expression for markers of hepatic stellate cell (HSC) activity from hepatocyte-specific MCP-1 gain of function by hydrodynamic injection of control (pLive-empty) or MCP-1 (pLive-MCP1) vectors in WT male mice (n = 8 mice/group). (D) Representative IHC image of Col1a1 protein expression from hepatocyte-specific MCP-1 gain of function by hydrodynamic injection of control (pLive-empty) or MCP-1 (pLive-MCP1) vectors in WT male mice. (E) Sirius red staining and quantitation from hepatocyte-specific MCP-1 gain of function by hydrodynamic injection of control (pLive-empty) or MCP-1 (pLive-MCP1) vectors in WT male mice (n = 6 mice/group). Scale bars: 50 μm. All data are shown with group means ± SEM; *, P < 0.05, **, P < 0.01, ***, P < 0.001 by 2-tailed t test.