TY - JOUR
T1 - ITE Suppresses Angiogenic Responses in Human Artery and Vein Endothelial Cells
T2 - Differential Roles of AhR
AU - Li, Yan
AU - Wang, Kai
AU - Zou, Qing yun
AU - Jiang, Yi zhou
AU - Zhou, Chi
AU - Zheng, Jing
N1 - Publisher Copyright:
© 2017 Elsevier Inc.
PY - 2017/12
Y1 - 2017/12
N2 - Aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor is involved in regulation of many essential biological processes including vascular development and angiogenesis. 2-(1′H-indole-3′-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE) is an AhR ligand, which regulates immune responses and cancer cell growth. However, the roles of the ITE/AhR pathway in mediating placental angiogenesis remains elusive. Here, we determined if ITE affected placental angiogenic responses via AhR in human umbilical vein (HUVECs) and artery endothelial (HUAECs) cells in vitro. We observed that ITE dose- and time-dependently inhibited proliferation and viability of HUAECs and HUVECs, whereas it inhibited migration of HUAECs, but not HUVECs. While AhR siRNA significantly suppressed AhR protein expression in HUVECs and HUAECs, it attenuated the ITE-inhibited angiogenic responses of HUAECs, but not HUVECs. Collectively, ITE suppressed angiogenic responses of HUAECs and HUVECs, dependent and independent of AhR, respectively. These data suggest that ITE may regulate placental angiogenesis.
AB - Aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor is involved in regulation of many essential biological processes including vascular development and angiogenesis. 2-(1′H-indole-3′-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE) is an AhR ligand, which regulates immune responses and cancer cell growth. However, the roles of the ITE/AhR pathway in mediating placental angiogenesis remains elusive. Here, we determined if ITE affected placental angiogenic responses via AhR in human umbilical vein (HUVECs) and artery endothelial (HUAECs) cells in vitro. We observed that ITE dose- and time-dependently inhibited proliferation and viability of HUAECs and HUVECs, whereas it inhibited migration of HUAECs, but not HUVECs. While AhR siRNA significantly suppressed AhR protein expression in HUVECs and HUAECs, it attenuated the ITE-inhibited angiogenic responses of HUAECs, but not HUVECs. Collectively, ITE suppressed angiogenic responses of HUAECs and HUVECs, dependent and independent of AhR, respectively. These data suggest that ITE may regulate placental angiogenesis.
KW - Angiogenesis
KW - Aryl hydrocarbon receptor
KW - Endothelial cells
KW - ITE
UR - http://www.scopus.com/inward/record.url?scp=85030768397&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85030768397&partnerID=8YFLogxK
U2 - 10.1016/j.reprotox.2017.09.010
DO - 10.1016/j.reprotox.2017.09.010
M3 - Article
C2 - 28986273
AN - SCOPUS:85030768397
SN - 0890-6238
VL - 74
SP - 181
EP - 188
JO - Reproductive Toxicology
JF - Reproductive Toxicology
ER -