Zhang Qiang, Wu Jinwei, Pan Zui, You Guofeng
Department of Pharmaceutics, Rutgers, The State University of New Jersey.
Int J Biochem Mol Biol. 2011;2(1):31-38.
Human organic anion transporter hOAT1 plays a critical role in the body disposition of environmental toxins and clinically important drugs including anti-HIV therapeutics, anti-tumor drugs, antibiotics, anti-hypertensives, and anti-inflammatories. In the current study, we investigated the role of dileucine (L6L7) at the amino terminus of hOAT1 in the expression and function of the transporter. We substituted L6L7 with alanine (A) simultaneously. The resulting mutant transporter L6A/L7A showed no transport activity due to its complete loss of expression at the cell surface. Such loss of surface expression of L6A/L7A was consistent with a complete loss of an 80 kDa mature form and a dramatic decrease in a 60 kDa immature form of the mutant transporter in the total cell lysates. Treatment of L6A/L7A-expressing cells with proteasomal inhibitor resulted in a significant increase in the immature form of hOAT1, but not its mature form, whereas treatment of these cells with lysosomal inhibitor had no effect on the expression of the mutant transporters, suggesting that the mutant transporter was degraded through proteasomal pathway. The accumulation of mutant transporter in the endoplasmic reticulum (ER) was confirmed by coimmunolocalization of L6L7 with calnexin, an ER marker. Furthermore, treatment of L6A/L7A-expressing cells with sodium 4-phenylbutyrate (4PBA) and glycerol, two chemical chaperones, could not promote the exit of the immature form of the mutant transporter from the ER. Our data suggest that L6L7 are critical for the stability and ER export of hOAT1.
人类有机阴离子转运体hOAT1在环境毒素以及包括抗HIV治疗药物、抗肿瘤药物、抗生素、抗高血压药物和抗炎药物等临床重要药物的体内处置过程中发挥着关键作用。在本研究中,我们调查了hOAT1氨基末端的双亮氨酸(L6L7)在该转运体的表达和功能中的作用。我们同时将L6L7替换为丙氨酸(A)。所得的突变转运体L6A/L7A由于在细胞表面完全丧失表达而没有转运活性。L6A/L7A这种表面表达的丧失与总细胞裂解物中突变转运体80 kDa成熟形式的完全丧失以及60 kDa未成熟形式的显著减少相一致。用蛋白酶体抑制剂处理表达L6A/L7A的细胞导致hOAT1未成熟形式显著增加,但成熟形式没有增加,而用溶酶体抑制剂处理这些细胞对突变转运体的表达没有影响,这表明突变转运体是通过蛋白酶体途径降解的。通过L6L7与内质网标记物钙连蛋白的共免疫定位证实了突变转运体在内质网(ER)中的积累。此外,用两种化学伴侣4-苯基丁酸钠(4PBA)和甘油处理表达L6A/L7A的细胞并不能促进突变转运体未成熟形式从内质网中排出。我们的数据表明,L6L7对hOAT1的稳定性和内质网输出至关重要。