INS-1 cells inhibit the production of extracellular matrix from pancreatic stellate cells
INS-1 cells inhibit the production of extracellular matrix from pancreatic stellate cells
复制标题
DOI：
10.1007/s10735-013-9547-y
复制
发表时间：
2014-06-01
影响因子：
3.2
通讯作者：
Sun, Zilin
中科院分区：
文献类型：
--
作者：
Li, Fengfei;Chen, Bijun;Sun, Zilin
在 2 型糖尿病中，胰腺星状细胞 (PSC) 存在于胰岛内部和周围，可能导致进行性纤维化和胰腺 β 细胞功能恶化。然而，胰腺β细胞是否影响PSC的生物学行为尚不清楚。在本研究中，我们研究了胰腺 β 细胞对 PSC 的增殖、迁移和细胞外基质 (ECM) 产生的影响。用来自 INS-1 细胞的条件培养基（上清液，SN）处理 PSC。尽管与对照相比，用 INS-1-SN 孵育的 PSC 的增殖有所增加，但 INS-1-SN 处理诱导了基质金属蛋白酶 2 活性，并减少了 ECM 和 TGF-β 1 的产生。此外，用 INS-1-SN 处理的 PSC 减少了已知介导胰腺 β 细胞死亡的细胞因子的分泌，例如 FADD、Fas、IFN-gamma、IL-1、TNF-α 和 TRAIL。我们的研究结果表明，胰腺β细胞可以改善胰岛纤维化和胰岛功能障碍的进展。
In type 2 diabetes mellitus, pancreatic stellate cells (PSCs) are present within and surrounding pancreatic islets and may cause progressive fibrosis and deterioration of pancreatic beta cell function. However, it is unknown whether pancreatic beta cells influence the biological behavior of PSCs. In the present study, we examined the impact of pancreatic beta cells on the proliferation, migration and extracellular matrix (ECM) production of PSCs. PSCs were treated with conditioned media from INS-1 cells (supernatant, SN). Although the proliferation of PSCs incubated with INS-1-SN was increased compared to control, INS-1-SN treatment induced matrix metalloproteinase-2 activity and reduced the production of ECM and TGF-beta 1. In addition, PSCs treated with INS-1-SN reduced the secretion of cytokines that are known to mediate pancreatic beta cell death, such as FADD, Fas, IFN-gamma, IL-1, TNF-alpha, and TRAIL. Our findings suggest that pancreatic beta cells may ameliorate islet fibrosis and the progression of islet dysfunction.