Adenosine A2A receptor regulates expression of vascular endothelial growth factor in feto-placental endothelium from normal and late-onset pre-eclamptic pregnancies

Acurio, Jesenia; Herlitz, Kurt; Troncoso, Felipe; Aguayo, Claudio; Bertoglia, Patricio; Escudero, Carlos

doi:10.1007/s11302-016-9538-z

Cited by 18 publications

(11 citation statements)

References 36 publications

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“…These results support the hypothesis of a crosstalk between A 2A and ERs, although the underlying mechanism is still unknown. Since previous evidence described that estrogen [ 9 ] or A 2A receptor [ 18 , 19 , 20 ] independently upregulated VEGF, we decided to analyze this factor in our experimental setting. Thus, mPEC from female WT mice showed a threefold increase in VEGF levels compared with mPEC from female A 2A KO mice.…”

Section: Discussionmentioning

confidence: 99%

“…After serum deprivation, cells were incubated with 5-bromo-2-deoxyuridine (BrdU) in the presence (24 h) of adenosine deaminase (ADA, 0.1 U/mL) either alone or in combination with the following agonists: 17β-estradiol (ER, non-selective agonist, E2; 10 −7 M), CGS-21680 (A 2A , selective agonist, 10 −5 M), and NECA (adenosine receptor non-selective agonist, 10 −5 M), or with the selective antagonists for ERα (MPP, 10 −6 M) and ERβ (PTHPP, 10 −6 M) as well as for the A 2A adenosine receptors (ZM-241385, 10 −4 M) in parallel experiments. Cells were fixed and measurements were performed according to the manufacturer’s instructions (Roche Diagnostics, IN, USA), as we previously reported [ 20 ].…”

Section: Methodsmentioning

confidence: 99%

“…In particular, A 2A (and A 2B ) receptors increase endothelial cell proliferation and migration in humans [ 13 , 14 , 15 ], pigs [ 16 ], and rats [ 17 ]. Moreover, A 2A also increases the functional expression of VEGF in endothelial cells [ 18 , 19 , 20 ]. Accordingly, the key role of the A 2A receptor in angiogenesis has been confirmed using A 2A -deficient mice (A 2A KO), which showed reduced blood vessel and extracellular matrix formation [ 21 ] and a delayed in vivo wound healing process [ 22 ] compared to wild type mice (WT).…”

Section: Introductionmentioning

confidence: 99%

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Advantages in Wound Healing Process in Female Mice Require Upregulation A2A-Mediated Angiogenesis under the Stimulation of 17β-Estradiol

Troncoso

Herlitz

Acurio

et al. 2020

IJMS

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Estrogenic steroids and adenosine A2A receptors promote the wound healing and angiogenesis processes. However, so far, it is unclear whether estrogen may regulate the expression and pro-angiogenic activity of A2A receptors. Using in vivo analyses, we showed that female wild type (WT) mice have a more rapid wound healing process than female or male A2A-deficient mice (A2AKO) mice. We also found that pulmonary endothelial cells (mPEC) isolated from female WT mice showed higher expression of A2A receptor than mPEC from male WT mice. mPEC from female WT mice were more sensitive to A2A-mediated pro-angiogenic response, suggesting an ER and A2A crosstalk, which was confirmed using cells isolated from A2AKO. In those female cells, 17β-estradiol potentiated A2A-mediated cell proliferation, an effect that was inhibited by selective antagonists of estrogen receptors (ER), ERα, and ERβ. Therefore, estrogen regulates the expression and/or pro-angiogenic activity of A2A adenosine receptors, likely involving activation of ERα and ERβ receptors. Sexual dimorphism in wound healing observed in the A2AKO mice process reinforces the functional crosstalk between ER and A2A receptors.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Advantages in Wound Healing Process in Female Mice Require Upregulation A2A-Mediated Angiogenesis under the Stimulation of 17β-Estradiol

Troncoso

Herlitz

Acurio

et al. 2020

IJMS

Self Cite

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“…NO is produced by vascular endothelial cells, and its functions include the dilation of blood vessels, and regulation of blood vessel tension and of the cardiovascular system during preg-nancy ( 27 , 28 ). Increasing evidence suggested that L-NAME can be used as an inducer of PE symptoms in pregnant rats ( 29 - 31 ). In the present study, it was observed that SBP, DBP, MAP and UP level in the L-NAME group were higher compared with those in the control group.…”

Section: Discussionmentioning

confidence: 99%

Silencing of Annexin A1 suppressed the apoptosis and inflammatory response of preeclampsia rat trophoblasts

Feng

Wang

et al. 2018

Int J Mol Med

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Preeclampsia (PE) is a disorder that is characterized by pregnancy-induced hypertension. It has been reported that Annexin A1 (ANXA1) is highly expressed in the plasma of women diagnosed with PE. Therefore, the present study aimed to examine the effect of ANXA1 on PE rats. The PE animal model was constructed in rats using Nω-nitro-L-arginine methyl ester (L-NAME), and the blood pressure and urine protein levels of rats were detected. The pathological features of placental tissue, and the levels of inflammatory factors and ANXA1 were respectively measured by hematoxylin-eosin staining, enzyme-linked immunosorbent assay and immunohistochemical assay. The activity of trophoblasts obtained from PE placental tissue was measured using immunofluorescence staining, while cell apoptosis was assessed using flow cytometry. The levels of associated factors were determined by reverse transcription-quantitative polymerase chain reaction and western blot analysis. The results identified that systolic blood pressure, diastolic blood pressure, mean arterial pressure and urine protein levels were enhanced, and that the contents of ANXA1, tumor necrosis factor alpha (TNF-α), interleukin (IL)-1β, IL-6 and IL-8 were increased in the L-NAME group. Transfection with small interfering RNA (siRNA)-ANXA1 markedly decreased the apoptosis and inflammatory response of trophoblasts. In addition, siRNA-ANXA1 upregulated the levels of B-cell lymphoma-2 (Bcl-2) and pro-caspase-3, and downregulated the levels of Bcl-2-associated X protein, cleaved-caspase-3, TNF-α, IL-1β, IL-6 and IL-8. Furthermore, siRNA-ANXA1 repressed the phosphorylation of Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3); however, siRNA-ANXA1 did not alter the levels of JAK2 and STAT3. Therefore, silencing of ANXA1 suppressed the apoptosis and inflammatory response of PE rat trophoblasts, and downregulated JAK2/STAK3 pathway.

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“…reported that altered expressions of VEGF and its receptors in the umbilical cord played a crucial role in disrupting the umbilical cord vascular endothelium, which might contribute to preeclampsia . In human umbilical vein endothelial cells (HUVECs) and human placental microvascular endothelial cells isolated from preeclampsia patients, levels of VEGF mRNA seemed to be regulated by adenosine A2A receptor . In a mouse model of preeclampsia, which mimicked human preeclampsia with renal injury, VEGF was reported to protect against preeclampsia .…”

Section: Introductionmentioning

confidence: 99%

Ferulic acid alleviates symptoms of preeclampsia in rats by upregulating vascular endothelial growth factor

Gong

Wan

Yuan

et al. 2017

Clin Exp Pharma Physio

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Preeclampsia is a complication affecting pregnant women worldwide, which leads to maternal and fetal morbidity and mortality. In this study, we evaluated the efficacy of ferulic acid (FA) on an N -nitro-L-arginine methyl ester hydrochloride (L-NAME) induced rat model of preeclampsia. L-NAME was administered to pregnant rats to induce preeclampsia. 48 rats were divided into three experimental groups (n=16 each): control group, preeclampsia group and preeclampsia with FA treatment (preeclampsia+FA). Physiological characteristics such as urine volume, total urine protein and blood pressure were assessed. Expressions levels of urinary nephrin and podocin mRNAs were analyzed by RT-PCR. Levels of renal vascular endothelial growth factor (VEGF), renal soluble fms-like tyrosine kinase-1 (sFlt-1) and serum placenta growth factor (PlGF) were also examined. Urine volume, total urine protein and blood pressure were markedly increased in preeclampsia group rats compared to control (P<.05), which were then significantly reduced in preeclampsia+FA group (P<.05). Expressions of urinary nephrin and podocin mRNAs, levels of VEGF, sFlt-1 and PlGF were also reversed in preeclampsia+FA group compared to preeclampsia rats (P<.05). We hereby report for the first time, FA alleviates preeclampsia symptoms in a rat preeclampsia model, supporting its potential value in treating preeclampsia.

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Adenosine A2A receptor regulates expression of vascular endothelial growth factor in feto-placental endothelium from normal and late-onset pre-eclamptic pregnancies

Abstract: We aim to investigate whether A 2A

Cited by 18 publications

References 36 publications

Advantages in Wound Healing Process in Female Mice Require Upregulation A2A-Mediated Angiogenesis under the Stimulation of 17β-Estradiol

Advantages in Wound Healing Process in Female Mice Require Upregulation A2A-Mediated Angiogenesis under the Stimulation of 17β-Estradiol

Silencing of Annexin A1 suppressed the apoptosis and inflammatory response of preeclampsia rat trophoblasts

Ferulic acid alleviates symptoms of preeclampsia in rats by upregulating vascular endothelial growth factor

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