Asymmetric Syncytial Expression of GLUT9 Splice Variants in Human Term Placenta and Alterations in Diabetic Pregnancies

被引:40
作者
Bibee, Kristin P. [1 ]
Illsley, Nicholas P. [2 ]
Moley, Kelle H. [1 ,3 ]
机构
[1] Washington Univ, Sch Med, Dept Obstet & Gynecol, St Louis, MO 63110 USA
[2] UMDNJ New Jersey Med Sch, Dept Obstet Gynecol & Womens Hlth, Newark, NJ USA
[3] Washington Univ, Sch Med, Dept Cell Biol & Physiol, St Louis, MO 63110 USA
关键词
glucose transport; syncytiotrophoblast; microvillus membrane; basal membrane; maternal diabetes; INSULIN-RESISTANCE; GLUCOSE TRANSPORTERS; FRUCTOSE; BLOOD; COMPLICATIONS; ASSOCIATION; ALTERS;
D O I
10.1177/1933719110380276
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Glucose transport from the maternal to fetal side of the placenta is critical for fetal growth and development due to the absence of fetal gluconeogenesis. Human GLUT9, existing as 2 isoforms, is a novel member of the transporter family. This study investigated the localization and relative expression levels of these isoforms in the human term placenta from both control and diabetic patients. Placenta samples were collected from normal pregnancies and those complicated by maternal diabetes (White classifications A1, A2, and B). Antibodies specific for the different isoforms were used to detect expression. Both forms of the protein are expressed in syncytiotrophoblast cells. Subcellular fractionation revealed an asymmetrical expression pattern with GLUT9a on basal membranes, whereas GLUT9b localizes to microvillus membranes. Expression of both isoforms is significantly increased in placental tissue from diabetic pregnancies. Altered expression of GLUT9 in the placenta may play a role in the fetal pathophysiology associated with diabetes-complicated pregnancies.
引用
收藏
页码:20 / 27
页数:8
相关论文
共 35 条
  • [1] Identification and characterization of human glucose transporter-like protein-9 (GLUT9) - Alternative splicing alters trafficking
    Augustin, R
    Carayannopoulos, MO
    Dowd, LO
    Phay, JE
    Moley, JF
    Moley, KH
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (16) : 16229 - 16236
  • [2] QUANTITATION AND IMMUNOLOCALIZATION OF GLUCOSE TRANSPORTERS IN THE HUMAN PLACENTA
    BARROS, LF
    YUDILEVICH, DL
    JARVIS, SM
    BEAUMONT, N
    BALDWIN, SA
    [J]. PLACENTA, 1995, 16 (07) : 623 - 633
  • [3] Placental glucose transfer and fetal growth
    Baumann, MU
    Deborde, S
    Illsley, NP
    [J]. ENDOCRINE, 2002, 19 (01) : 13 - 22
  • [4] Epidemiology of gestational diabetes mellitus and its association with Type 2 diabetes
    Ben-Haroush, A
    Yogev, Y
    Hod, M
    [J]. DIABETIC MEDICINE, 2004, 21 (02) : 103 - 113
  • [5] Expression profile and protein levels of placental products as indirect measures of placental function in in vitro-derived bovine pregnancies
    Bertolini, M
    Wallace, CR
    Anderson, GB
    [J]. REPRODUCTION, 2006, 131 (01) : 163 - 173
  • [6] The pathobiology of diabetic complications - A unifying mechanism
    Brownlee, M
    [J]. DIABETES, 2005, 54 (06) : 1615 - 1625
  • [7] GLUT9 is differentially expressed and targeted in the preimplantation embryo
    Carayannopoulos, MO
    Schlein, A
    Wyman, A
    Chi, M
    Keembiyehetty, C
    Moley, KH
    [J]. ENDOCRINOLOGY, 2004, 145 (03) : 1435 - 1443
  • [8] Involvement of oxidative stress and NADPH oxidase activation in the development of cardiovascular complications in a model of insulin resistance, the fructose-fed rat
    Delbosc, S
    Paizanis, E
    Magous, R
    Araiz, C
    Dimo, T
    Cristol, JP
    Cros, G
    Azay, J
    [J]. ATHEROSCLEROSIS, 2005, 179 (01) : 43 - 49
  • [9] Facilitative Glucose Transporter 9 Expression Affects Glucose Sensing in Pancreatic β-Cells
    Evans, Sarah A.
    Doblado, Manuel
    Chi, Maggie M.
    Corbett, John A.
    Moley, Kelle H.
    [J]. ENDOCRINOLOGY, 2009, 150 (12) : 5302 - 5310
  • [10] Diabetes alters the expression and activity of the human placental GLUT1 glucose transporter
    Gaither, K
    Quraishi, AN
    Illsley, NP
    [J]. JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1999, 84 (02) : 695 - 701