Reduced l-Arginine Transport and Nitric Oxide Synthesis in Human Umbilical Vein Endothelial Cells from Intrauterine Growth Restriction Pregnancies is Not Further Altered by Hypoxia

Casanello, Paola; Krause, Bernardo J.; Torres, E.; Gallardo, Victoria; González, Marcelo; Prieto, Carolina; Escudero, Carlos; Farías, Marcelo; Sobrevía, Luis

doi:10.1016/j.placenta.2009.04.010

Cited by 37 publications

(36 citation statements)

References 42 publications

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“…Alterations in the synthesis and/or biological actions of NO have been related to abnormal blood flow in disorders of pregnancy that present as different entities but appear to share a common origin: the presence of placental endothelial dysfunction. This is the case of gestational diabetes [8,13], intrauterine growth retardation [14,15] and preeclampsia [10], which is the focus of this article.…”

Section: Endothelial Dysfunction In the Placenta And Its Consequencesmentioning

confidence: 99%

New therapeutic approaches to treating hypertension in pregnancy

Mate¹,

Vázquez²,

Leiva³

et al. 2012

Drug Discovery Today

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Section: Endothelial Dysfunction In the Placenta And Its Consequencesmentioning

confidence: 99%

New therapeutic approaches to treating hypertension in pregnancy

Mate¹,

Vázquez²,

Leiva³

et al. 2012

Drug Discovery Today

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“…Contrarily, we did not find an A 2B AR-mediated VEGF expression in preeclampsia, whereas it was evidenced in cell from normal pregnancy. Apparent discrepancy may be related to experimental condition, since in the Feokstitov's report [22] they use a HUVEC cell line, rather than primary culture as we reported; and hypoxia was defined as 4.6% oxygen, which is considered normoxia for primary culture of HUVEC [58]. …”

Section: Discussionmentioning

confidence: 99%

Potential Role of A_2BAdenosine Receptors on Proliferation/Migration of Fetal Endothelium Derived from Preeclamptic Pregnancies

Acurio

Troncoso

Bertoglia

et al. 2014

BioMed Research International

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To investigate the functionality of A2B adenosine receptor (A2BAR) and the nitric oxide (NO) and vascular endothelial growth factor (VEGF) signaling pathway in the endothelial cell proliferation/migration during preeclampsia, we used human umbilical vein endothelial cells (HUVECs) isolated from normal pregnancies (n = 15) or pregnancies with preeclampsia (n = 15). Experiments were performed in presence or absence of the nonselective adenosine receptor agonist NECA, the A2BAR selective antagonist MRS-1754, and the nitric oxide synthase (NOS) inhibitor L-NAME. Results indicated that cells from preeclampsia exhibited a significant higher protein level of A2BAR and logEC50 for NECA-mediated proliferation than normotensive pregnancies. The stimulatory effect of NECA (10 μM, 24 h) on cell proliferation was prevented by MRS-1754 (5 nM) coincubation only in cells from normotensive pregnancies. Nevertheless, L-NAME (100 μM, 24 h) reduced the NECA-induced cell proliferation/migration in HUVEC from normal pregnancy; however in preeclampsia only NECA-induced cell proliferation was reduced by L-NAME. Moreover, NECA increased protein nitration and abundance of VEGF in cells from normal pregnancy and effect prevented by MRS-1754 coincubation. Nevertheless, in preeclampsia NECA did not affect the protein level of VEGF. In conclusion HUVECs from preeclampsia exhibit elevated protein level of A2BAR and impairment of A2BAR-mediated NO/VEGF signaling pathway.

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“…RNA Interference-Small interfering RNA (siRNA) from Sigma was synthesized using previously published and validated sequences for eNOS (30), MEK1 (31), MEK2 (31), and JNK1/2 (32). Sequences (sense) are as follows: eNOS, 5Ј-GGU-CUGCACAGGAAAUGUU(dT)(dT)-3Ј; MEK1, 5Ј-AAGUC-CUGAAGAAAGCUGGAA(dT)(dT)-3Ј; MEK2, 5Ј-AAGGU-CGGCGAACUCAAAGAC(dT)(dT)-3Ј; and JNK1/2, 5Ј-TGA-AAGAATGTCCTACCTT(dT)(dT)-3Ј.…”

Section: Methodsmentioning

confidence: 99%

Endothelial Nitric-oxide Synthase Activation Generates an Inducible Nitric-oxide Synthase-like Output of Nitric Oxide in Inflamed Endothelium

Lowry

Brovkovych

Zhang

et al. 2013

Journal of Biological Chemistry

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Background:In healthy endothelium, agonist-induced eNOS activation results in transient, calcium-dependent NO production. Results: In inflamed endothelium, bradykinin stimulates prolonged eNOS-derived NO that depends on G␣ i , MEK1/2, and JNK, resulting in reduced migration. Conclusion: eNOS activation is mediated differently in normal and inflamed endothelium, resulting in divergent NO production and effects. Significance: High eNOS-derived NO may impair angiogenesis and wound healing in inflammation.

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Reduced l-Arginine Transport and Nitric Oxide Synthesis in Human Umbilical Vein Endothelial Cells from Intrauterine Growth Restriction Pregnancies is Not Further Altered by Hypoxia

Cited by 37 publications

References 42 publications

New therapeutic approaches to treating hypertension in pregnancy

New therapeutic approaches to treating hypertension in pregnancy

Potential Role of A_2BAdenosine Receptors on Proliferation/Migration of Fetal Endothelium Derived from Preeclamptic Pregnancies

Endothelial Nitric-oxide Synthase Activation Generates an Inducible Nitric-oxide Synthase-like Output of Nitric Oxide in Inflamed Endothelium

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Reduced l-Arginine Transport and Nitric Oxide Synthesis in Human Umbilical Vein Endothelial Cells from Intrauterine Growth Restriction Pregnancies is Not Further Altered by Hypoxia

Cited by 37 publications

References 42 publications

New therapeutic approaches to treating hypertension in pregnancy

New therapeutic approaches to treating hypertension in pregnancy

Potential Role of A2BAdenosine Receptors on Proliferation/Migration of Fetal Endothelium Derived from Preeclamptic Pregnancies

Endothelial Nitric-oxide Synthase Activation Generates an Inducible Nitric-oxide Synthase-like Output of Nitric Oxide in Inflamed Endothelium

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Potential Role of A_2BAdenosine Receptors on Proliferation/Migration of Fetal Endothelium Derived from Preeclamptic Pregnancies