ITE Suppresses Angiogenic Responses in Human Artery and Vein Endothelial Cells: Differential Roles of AhR

Li, Yan; Wang, Kai; Zou, Qingyun; Jiang, Yi‐Zhou; Zhou, Chi; Zheng, Jing

doi:10.1016/j.reprotox.2017.09.010

Cited by 22 publications

(32 citation statements)

References 43 publications

(95 reference statements)

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“…2013a, b, ; Li et al . , ). FGF2 or VEGFA was added into the bottom wells (final concentration of 100 ng mL −1 ; catalog number 10014‐HNAE and catalog number 80006‐RNAB, respectively; Sino Biologic Inc., Beijing, China).…”

Section: Methodsmentioning

confidence: 99%

“…; Li et al . , ). Briefly, after 2 days of transfection, cells were inoculated into 96‐well plates (5 ‐ 8000 cells per well) and cultured overnight.…”

Section: Methodsmentioning

confidence: 99%

“…For cell migration assays, after 2 days of transfection with the vehicle, ssiRNA and GNA11 siRNA, cells were serum-starved and placed (30,000 per insert) into each insert using a transwell system (catalog number 351158, Corning, Corning, NY, USA) as described previously (Jiang et al 2013a(Jiang et al , b, 2014Li et al 2015Li et al , 2017. FGF2 or VEGFA was added into the bottom wells (final concentration of 100 ng mL −1 ; catalog number 10014-HNAE and catalog number 80006-RNAB, respectively; Sino Biologic Inc., Beijing, China).…”

Section: Cell Migrationmentioning

confidence: 99%

“…Cell proliferation was evaluated using the crystal violet method as described previously (Wang et al 2008;Song et al 2009;Li et al 2015Li et al , 2017. Briefly, after 2 days of transfection, cells were inoculated into 96-well plates (5 -8000 cells per well) and cultured overnight.…”

Section: Cell Proliferationmentioning

confidence: 99%

“…Western blot analysis was conducted as described (Dai et al 2011;Jiang et al 2013a, b;Li et al 2015Li et al , 2017. Cells were lysed in the lysis buffer [50 mM Hepes, 0.1 M NaCl, 10 mM EDTA, 4 mM sodium pyrophosphate, 10 mM sodium fluoride, 2 mM sodium orthovanadate (pH 7.5), 1 mM phenylmethylsulphonylfluoride, 1% Triton X-100, 5 μg mL −1 leupeptin, 5 μg mL −1 aprotinin].…”

Section: Western Blottingmentioning

confidence: 99%

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GNA11 differentially mediates fibroblast growth factor 2‐ and vascular endothelial growth factor A‐induced cellular responses in human fetoplacental endothelial cells

Zou

Zhao

et al. 2018

The Journal of Physiology

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During pregnancy, fetoplacental angiogenesis is dramatically increased in association with rapidly elevated blood flow. Any disruption of fetoplacental angiogenesis may lead to pregnancy complications such as intrauterine growth restriction. Fibroblast growth factor 2 (FGF2) and vascular endothelial growth factor A (VEGFA) are crucial regulators of fetoplacental angiogenesis. G protein α subunits q (GNAq) and 11 (GNA11) are two members of the Gα subfamily involved in mediating vascular growth and basal blood pressure. However, little is known about the roles of GNA11 alone with respect to mediating the FGF2- and VEGFA-induced fetoplacental endothelial function. Using a cell model of human umbilical cord vein endothelial cells cultured under physiological chronic low O (3% O ), we showed that GNA11 small interfering RNA (siRNA) dramatically inhibited (P < 0.05) FGF2- and VEGFA-stimulated fetoplacental endothelial migration (by ∼36% and ∼50%, respectively) but not proliferation and permeability. GNA11 siRNA also elevated (P < 0.05) FGF2- and VEGFA-induced phosphorylation of phospholipase C-β3 (PLCβ3) at S537 in a time-dependent fashion but not mitogen-activated protein kinase 3/1 (ERK1/2) and v-akt murine thymoma viral oncogene homologue 1 (AKT1). These data suggest that GNA11 mediates FGF2- and VEGFA-stimulated fetoplacental endothelial cell migration partially via altering the activation of PLCβ3.

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Section: Methodsmentioning

confidence: 99%

“…; Li et al . , ). Briefly, after 2 days of transfection, cells were inoculated into 96‐well plates (5 ‐ 8000 cells per well) and cultured overnight.…”

Section: Methodsmentioning

confidence: 99%

Section: Cell Migrationmentioning

confidence: 99%

Section: Cell Proliferationmentioning

confidence: 99%

Section: Western Blottingmentioning

confidence: 99%

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GNA11 differentially mediates fibroblast growth factor 2‐ and vascular endothelial growth factor A‐induced cellular responses in human fetoplacental endothelial cells

Zou

Zhao

et al. 2018

The Journal of Physiology

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G Protein α Subunit 14 Mediates Fibroblast Growth Factor 2‐Induced Cellular Responses in Human Endothelial Cells

Zou

Zhao

Zhou

et al. 2018

Journal Cellular Physiology

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During pregnancy, a tremendous increase in fetoplacental angiogenesis is associated with elevated blood flow. Aberrant fetoplacental vascular function may lead to pregnancy complications including pre‐eclampsia. Fibroblast growth factor 2 (FGF2) and vascular endothelial growth factor A (VEGFA) are crucial regulators of fetoplacental endothelial function. G protein α subunit 14 (GNA14), a member of Gαq/11 subfamily is involved in mediating hypertensive diseases and tumor vascularization. However, little is known about roles of GNA14 in mediating the FGF2‐ and VEGFA‐induced fetoplacental endothelial function. Using human umbilical vein endothelial cells (HUVECs) cultured under physiological chronic low oxygen (3% O2) as a cell model, we show that transfecting cells with adenovirus carrying GNA14 complementary DNA (cDNA; Ad‐GNA14) increases (p < 0.05) protein expression of GNA14. GNA14 overexpression blocks (p < 0.05) FGF2‐stimulated endothelial migration, whereas it enhances (p < 0.05) endothelial monolayer integrity (maximum increase of ~35% over the control at 24 hr) in response to FGF2. In contrast, GNA14 overexpression does not significantly alter VEGFA‐stimulated cell migration, VEGFA‐weakened cell monolayer integrity, and intracellular Ca++ mobilization in response to adenosine triphosphate (ATP), FGF2, and VEGFA. GNA14 overexpression does not alter either FGF2‐ or VEGFA‐induced phosphorylation of ERK1/2. However, GNA14 overexpression time‐dependently elevates (p < 0.05) phosphorylation of phospholipase C‐β3 (PLCβ3) at S1105 in response to FGF2, but not VEGFA. These data suggest that GNA14 distinctively mediates fetoplacental endothelial cell migration and permeability in response to FGF2 and VEGFA, possibly in part by altering activation of PLCβ3 under physiological chronic low oxygen.

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Aryl hydrocarbon receptor (AhR) reveals evidence of antagonistic pleiotropy in the regulation of the aging process

Salminen

2022

Cell. Mol. Life Sci.

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The antagonistic pleiotropy hypothesis is a well-known evolutionary theory to explain the aging process. It proposes that while a particular gene may possess beneficial effects during development, it can exert deleterious properties in the aging process. The aryl hydrocarbon receptor (AhR) has a significant role during embryogenesis, but later in life, it promotes several age-related degenerative processes. For instance, AhR factor (i) controls the pluripotency of stem cells and the stemness of cancer stem cells, (ii) it enhances the differentiation of embryonal stem cells, especially AhR signaling modulates the differentiation of hematopoietic stem cells and progenitor cells, (iii) it also stimulates the differentiation of immunosuppressive Tregs, Bregs, and M2 macrophages, and finally, (iv) AhR signaling participates in the differentiation of many peripheral tissues. On the other hand, AhR signaling is involved in many processes promoting cellular senescence and pathological processes, e.g., osteoporosis, vascular dysfunction, and the age-related remodeling of the immune system. Moreover, it inhibits autophagy and aggravates extracellular matrix degeneration. AhR signaling also stimulates oxidative stress, promotes excessive sphingolipid synthesis, and disturbs energy metabolism by catabolizing NAD+ degradation. The antagonistic pleiotropy of AhR signaling is based on the complex and diverse connections with major signaling pathways in a context-dependent manner. The major regulatory steps include, (i) a specific ligand-dependent activation, (ii) modulation of both genetic and non-genetic responses, (iii) a competition and crosstalk with several transcription factors, such as ARNT, HIF-1α, E2F1, and NF-κB, and (iv) the epigenetic regulation of target genes with binding partners. Thus, not only mTOR signaling but also the AhR factor demonstrates antagonistic pleiotropy in the regulation of the aging process.

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ITE Suppresses Angiogenic Responses in Human Artery and Vein Endothelial Cells: Differential Roles of AhR

Cited by 22 publications

References 43 publications

GNA11 differentially mediates fibroblast growth factor 2‐ and vascular endothelial growth factor A‐induced cellular responses in human fetoplacental endothelial cells

GNA11 differentially mediates fibroblast growth factor 2‐ and vascular endothelial growth factor A‐induced cellular responses in human fetoplacental endothelial cells

G Protein α Subunit 14 Mediates Fibroblast Growth Factor 2‐Induced Cellular Responses in Human Endothelial Cells

Aryl hydrocarbon receptor (AhR) reveals evidence of antagonistic pleiotropy in the regulation of the aging process

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