Expression of PDS/Pds, the Pendred syndrome gene, in endometrium

被引：50

作者：

Suzuki, K

Royaux, IE

Everett, LA

Mori-Aoki, A

Suzuki, S

Nakamura, K

Sakai, T

Katoh, R

Toda, S

Green, ED

Kohn, LD

机构：

[1] Natl Inst Infect Dis, Dept Microbiol, Leprosy Res Ctr, Tokyo 1890002, Japan

[2] NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA

[3] Tottori Univ, Sch Med, Dept Internal Med, Yonago, Tottori 683, Japan

[4] Washington Hosp Ctr NW, Mol Endocrinol Lab, MedStar Res Inst, Washington, DC 20010 USA

[5] Saitama Univ, Cell Biol Lab, Dept Regulat Biol, Urawa, Saitama 338, Japan

[6] Yamanashi Med Univ, Dept Pathol, Tamaho, Yamanashi, Japan

[7] Saga Med Sch, Dept Pathol, Saga, Japan

[8] Ohio Univ, Sch Osteopath Med, Athens, OH 45701 USA

[9] Edison Biotechnol Inst, Athens, OH USA

来源：

JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM | 2002年 / 87卷 / 02期

关键词：

D O I：

10.1210/jc.87.2.938

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Expression of the Pendred syndrome gene (PDS/Pds) is thought to be responsible for the iodide transport in the thyroid as well as the formation and function of the inner ear. Its mRNA is also expressed in the kidney and placenta. We report here that PDS and its encoded protein (pendrin) are also expressed in the endometrium. The RNA levels of rat PDS in the endometrium and kidney were much higher than those of the thyroid, opposite of the pattern of RNA expression in humans. In human endometrium, pendrin localization changed from the basal to apical surfaces of the epithelium during progression of the menstrual cycle. This suggests a possible role for pendrin in cationic ion transport required to maintain the physiological function of the endometrium. Since there is no evidence of endometrial abnormalities in patients with Pendred syndrome, it suggests the existence of a compensatory mechanisms for pendrin's function in the uterus.

引用

页码：938 / 941

页数：4

共 25 条

[1] Expression of Na+/I- symporter and pendred syndrome genes in trophoblast cells [J].