水通道蛋白在正常前列腺功能和良性前列腺增生发病机制中的作用

AQP is a group of small hydrophobic transmembrane protein, which can selective drive active liquid water molecules across the cell membrane TRANS-secretion and absorption. Earlier research found that human and mouse prostate epithelial and endothelial cells have high expressions of AQP1 and AQP3, speculated AQP possible infiltration of water through the cell involved in prostate secretion. New study finds AQP1 and AQP3 has an obvious promotion of cell proliferation and migration. Combined with early studies,speculated AQPs promote prostatic cell proliferation and migration. When the cell proliferation and apoptosis of imbalance occur, abnormal proliferation expressing cells and glands increase occur to benign prostatic hyperplasia (BPH). This project will used technology of AQP1 and AQP3 gene single knock-off and AQP1/AQP3 double knock-off in small rat models, which is planed to be uesd in prostate physiological and pathological physiology research. Context: 1,find roles of AQP1 and AQP3 in prostatic secretion function; 2,find roles of AQP1 and AQP3 in prostate cell proliferation, and migration process; 3,fins the relationship between AQPs and BPH;4,blocking AQPs and glycerol regulation, then observe rates of BPH occurs.To provide a theory basis of prevention and treatment of BPH.

水通道蛋白（AQP）为一组小分子疏水性跨膜蛋白，可选择性驱使水分子跨细胞膜转运进行主动液体分泌和吸收。前期研究发现人和小鼠前列腺上皮和内皮细胞有AQP1和AQP3高表达，推测AQP可能通过促进细胞对水的渗透参与前列腺液分泌功能。新近研究发现AQP1、AQP3具有明显促进细胞增殖和迁移的作用。结合前期研究推测AQPs具有促进前列腺细胞增殖和迁移作用。当细胞出现增殖与凋亡失衡，表现细胞超常增殖和腺体增大即为临床常见的良性前列腺增生（BPH）。本项目将采用AQP1、AQP3基因单敲除和AQP1/AQP3双敲除小鼠模型，进行AQP在前列腺生理和病理生理学研究，内容包括：1、AQP1和AQP3在前列腺液分泌功能的作用；2、AQP1和AQP3在前列腺细胞增殖、迁移过程的具体作用；3、AQPs与BPH发病关系；4、通过阻断AQPs转运水和甘油调控或降低BPH发生，为预防和治疗BPH寻找新靶分子提供依据。

水通道蛋白（AQP）为一组小分子疏水性跨膜蛋白，可选择性驱使水分子跨细胞膜转运进行主动液体分泌和吸收。前期研究发现人和小鼠前列腺上皮和内皮细胞有AQP1和AQP3高表达，推测AQP可能通过促进细胞对水的渗透参与前列腺液分泌功能。新近研究发现AQP1、AQP3具有明显促进细胞增殖和迁移的作用。结合前期研究推测AQPs具有促进前列腺细胞增殖和迁移作用。当细胞出现增殖与凋亡失衡，表现细胞超常增殖和腺体增大即为临床常见的良性前列腺增生（BPH）。本项目组瞄准国际前沿, 积极进行源头创新, 1年来严格按照计划任务书要求不懈努力，已引进繁育了AQP敲除小鼠模型，并进行AQP在前列腺生理和病理生理学研究，并为下一步研究AQP在前列腺细胞增殖、迁移过程的具体作用以及AQPs与BPH发病关系，最终通过阻断AQPs转运水和甘油调控或降低BPH发生，为预防和治疗BPH寻找新靶分子提供依据。