TY - JOUR
T1 - In vitro simulation of placental transport
T2 - Part II. Glucose transfer across the placental barrier model
AU - Levkovitz, R.
AU - Zaretsky, U.
AU - Jaffa, A. J.
AU - Hod, M.
AU - Elad, D.
N1 - Funding Information:
This research was partially supported by the Australian Friends of Tel Aviv University (Victoria), and the Nicholas and Elizabeth Slezak Super Center for Cardiac Research and Biomedical Engineering in Tel Aviv University. We wish to thank Profs. Yariv Yogev and Nir Melamed from Rabin Medical Center and Prof. Shmuel Einav from Tel Aviv University for valuable discussions and continuous support.
PY - 2013/8
Y1 - 2013/8
N2 - Introduction: In utero fetal development and fetal programming for adulthood life are strongly associated with maternal-to-fetal transfer of nutrient and other substances. Gestational diabetes mellitus (GDM) is a major problem and associated with abnormal fetal development, but the mechanisms underlying glucose transport across the placenta barrier (PB) are not completely understood. Methods: We developed a placenta simulator that can mimic feto-maternal blood circulations along with real transfer across the in vitro biological model of the PB, which is made of a co-culture of endothelial cells (EC) and trophoblast cells (TC) on both sides of a denuded amniotic membrane (AM). Maternal-tofetal transfer of glucose was monitored over 24 h. Results: The AM is highly permeable to glucose compared to the cellular structures and can serve as a substrate for the co-culture model. The transfer characteristics for glucose are independent of its initial concentration in the maternal compartment, but strongly dependent on the cellular components of the PB. The EC are more resistive to glucose transfer than the TC. The in vitro PB model is the most resistive to glucose transfer. Discussion and conclusion: The good correlation between the present in vitro results with existing in vivo data demonstrated the potential of this new approach, which can be extended to study various aspects of transplacental transfer, including medications, relevant to GDM or any problem related to in utero programing.
AB - Introduction: In utero fetal development and fetal programming for adulthood life are strongly associated with maternal-to-fetal transfer of nutrient and other substances. Gestational diabetes mellitus (GDM) is a major problem and associated with abnormal fetal development, but the mechanisms underlying glucose transport across the placenta barrier (PB) are not completely understood. Methods: We developed a placenta simulator that can mimic feto-maternal blood circulations along with real transfer across the in vitro biological model of the PB, which is made of a co-culture of endothelial cells (EC) and trophoblast cells (TC) on both sides of a denuded amniotic membrane (AM). Maternal-tofetal transfer of glucose was monitored over 24 h. Results: The AM is highly permeable to glucose compared to the cellular structures and can serve as a substrate for the co-culture model. The transfer characteristics for glucose are independent of its initial concentration in the maternal compartment, but strongly dependent on the cellular components of the PB. The EC are more resistive to glucose transfer than the TC. The in vitro PB model is the most resistive to glucose transfer. Discussion and conclusion: The good correlation between the present in vitro results with existing in vivo data demonstrated the potential of this new approach, which can be extended to study various aspects of transplacental transfer, including medications, relevant to GDM or any problem related to in utero programing.
KW - Amniotic membrane
KW - Endothelial cells
KW - Feto-maternal transfer
KW - GLUT1
KW - Gestational diabetes mellitus (GDM)
KW - Permeability coefficient
KW - Trophoblast cells
UR - http://www.scopus.com/inward/record.url?scp=84882448888&partnerID=8YFLogxK
U2 - 10.1016/j.placenta.2013.05.006
DO - 10.1016/j.placenta.2013.05.006
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AN - SCOPUS:84882448888
SN - 0143-4004
VL - 34
SP - 708
EP - 715
JO - Placenta
JF - Placenta
IS - 8
ER -