Turner Douglas J, Martin Paul C, Rao Jaladanki N, Greenspon Jose, Zou Tongtong, Bass Barbara L, Wang Jian-Ying, Strauch Eric D
Cell Biology Group, Department of Surgery, University of Maryland School of Medicine, Baltimore, MD, USA.
Ann Surg. 2007 Mar;245(3):408-14. doi: 10.1097/01.sla.0000245549.57076.db.
The current study examined the effect of substance P (SP) upon intestinal epithelial cells and the mechanistic details of this interaction.
Intestinal epithelial cells must be capable of migration to reseal mucosal wounds for several vital intestinal functions. This process is incompletely understood; however, recent evidence implicates the neurotransmitter SP in this process.
Normal rat intestinal epithelial cells (IEC-6 cells) were studied to identify the presence of the SP receptor (NK-1 subtype) and then exposed to physiologic doses of SP and antagonists to assess for increased migration.
Examination IEC-6 cells revealed the presence of the SP receptor. Wounding of these cells followed by subsequent exposure to SP (10 mol/L) resulted in increased migration. Similarly, SP-induced increases in intracellular calcium concentration and actomyosin stress fiber formation. These effects were all blocked through specific NK-1 receptor antagonists.
These results indicate that SP stimulates intestinal epithelial migration and increases in calcium concentration. These data support a beneficial role for SP in the maintenance of intestinal mucosal homeostasis.
本研究探讨了P物质（SP）对肠上皮细胞的作用及其相互作用的机制细节。
肠上皮细胞必须能够迁移以重新封闭黏膜伤口，以实现多种重要的肠道功能。这个过程尚未完全了解；然而，最近的证据表明神经递质SP参与了这个过程。
研究正常大鼠肠上皮细胞（IEC-6细胞）以确定SP受体（NK-1亚型）的存在，然后用生理剂量的SP和拮抗剂处理，以评估细胞迁移是否增加。
对IEC-6细胞的检测发现了SP受体的存在。这些细胞受伤后再暴露于SP（10摩尔/升）会导致迁移增加。同样，SP可诱导细胞内钙浓度升高和肌动球蛋白应激纤维形成。这些作用均被特异性NK-1受体拮抗剂阻断。
这些结果表明SP刺激肠上皮细胞迁移并增加钙浓度。这些数据支持SP在维持肠黏膜稳态中发挥有益作用。
