GI Research Unit, Department of Gastroenterology and Hepatology.
Department of Biochemistry and Molecular Biology.
Am J Physiol Cell Physiol. 2014 Oct 1;307(7):C622-33. doi: 10.1152/ajpcell.00086.2014. Epub 2014 Jul 30.
Hepatic stellate cells (HSCs) generate matrix, which in turn may also regulate HSCs function during liver fibrosis. We hypothesized that HSCs may endocytose matrix proteins to sense and respond to changes in microenvironment. Primary human HSCs, LX2, or mouse embryonic fibroblasts (MEFs) [wild-type; c-abl(-/-); or Yes, Src, and Fyn knockout mice (YSF(-/-))] were incubated with fluorescent-labeled collagen or gelatin. Fluorescence-activated cell sorting analysis and confocal microscopy were used for measuring cellular internalization of matrix proteins. Targeted PCR array and quantitative real-time PCR were used to evaluate gene expression changes. HSCs and LX2 cells endocytose collagens in a concentration- and time-dependent manner. Endocytosed collagen colocalized with Dextran 10K, a marker of macropinocytosis, and 5-ethylisopropyl amiloride, an inhibitor of macropinocytosis, reduced collagen internalization by 46%. Cytochalasin D and ML7 blocked collagen internalization by 47% and 45%, respectively, indicating that actin and myosin are critical for collagen endocytosis. Wortmannin and AKT inhibitor blocked collagen internalization by 70% and 89%, respectively, indicating that matrix macropinocytosis requires phosphoinositide-3-kinase (PI3K)/AKT signaling. Overexpression of dominant-negative dynamin-2 K44A blocked matrix internalization by 77%, indicating a role for dynamin-2 in matrix macropinocytosis. Whereas c-abl(-/-) MEF showed impaired matrix endocytosis, YSF(-/-) MEF surprisingly showed increased matrix endocytosis. It was also associated with complex gene regulations that related with matrix dynamics, including increased matrix metalloproteinase 9 (MMP-9) mRNA levels and zymographic activity. HSCs endocytose matrix proteins through macropinocytosis that requires a signaling network composed of PI3K/AKT, dynamin-2, and c-abl. Interaction with extracellular matrix regulates matrix dynamics through modulating multiple gene expressions including MMP-9.
肝星状细胞 (HSCs) 生成基质,而基质反过来也可能调节肝纤维化过程中 HSCs 的功能。我们假设 HSCs 可能内吞基质蛋白,以感知和响应微环境的变化。原代人 HSCs、LX2 或小鼠胚胎成纤维细胞 (MEF) [野生型;c-abl(-/-);或 Yes、Src 和 Fyn 基因敲除小鼠 (YSF(-/-))] 与荧光标记的胶原蛋白或明胶孵育。使用荧光激活细胞分选分析和共聚焦显微镜测量细胞内吞基质蛋白的情况。使用靶向 PCR 阵列和实时定量 PCR 评估基因表达变化。HSCs 和 LX2 细胞以浓度和时间依赖的方式内吞胶原蛋白。内吞的胶原蛋白与 Dextran 10K(巨胞饮的标志物)共定位,并且 5-乙基异戊基amiloride(巨胞饮抑制剂)减少了 46%的胶原蛋白内吞。细胞松弛素 D 和 ML7 分别阻止了 47%和 45%的胶原蛋白内吞,表明肌动蛋白和肌球蛋白对胶原蛋白内吞至关重要。wortmannin 和 AKT 抑制剂分别阻止了 70%和 89%的胶原蛋白内吞,表明基质巨胞饮需要磷酯酰肌醇-3-激酶 (PI3K)/AKT 信号。显性失活 dynamin-2 K44A 的过表达阻止了 77%的基质内吞,表明 dynamin-2 在基质巨胞饮中发挥作用。尽管 c-abl(-/-) MEF 显示出基质内吞受损,但 YSF(-/-) MEF 出人意料地显示出增强的基质内吞。这也与与基质动力学相关的复杂基因调控有关,包括基质金属蛋白酶 9 (MMP-9) mRNA 水平和酶谱活性的增加。HSCs 通过需要由 PI3K/AKT、dynamin-2 和 c-abl 组成的信号网络的巨胞饮内吞基质蛋白。与细胞外基质的相互作用通过调节包括 MMP-9 在内的多个基因的表达来调节基质动力学。