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Hypertension in response to placental ischemia during pregnancy: role of B lymphocytes.

Hypertension in response to placental ischemia during pregnancy: role of B lymphocytes.

http://www.wikidata.org/entity/Q35029700

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Elucidating immune mechanisms causing hypertension during pregnancy A leading role for the immune system in the pathophysiology of preeclampsia The renal circulation in normal pregnancy and preeclampsia: is there a place for relaxin?Angiotensin receptor agonistic autoantibodies and hypertension: preeclampsia and beyond Neutrophil Depletion Attenuates Placental Ischemia-Induced Hypertension in the Rat B cells: the old new players in reproductive immunology.The role of inflammation in the pathology of preeclampsia The immune system in hypertension Hypertension, inflammation and T lymphocytes are increased in a rat model of HELLP syndrome Enodthelin 1 is elevated in plasma and explants from patients having uterine leiomyomas.CD4(+) T Cells Play a Critical Role in Mediating Hypertension in Response to Placental Ischemia.Endothelin-1 is not a Mechanism of IL-17 Induced Hypertension during Pregnancy.Vitamin D Supplementation Suppresses Hypoxia-Stimulated Placental Cytokine Secretion, Hypertension and CD4(+) T Cell Stimulation in Response to Placental Ischemia.CD4+ T cells are important mediators of oxidative stress that cause hypertension in response to placental ischemia.Preventing autoimmunity protects against the development of hypertension and renal injury.Receptor-activating autoantibodies and disease: preeclampsia and beyond.Activating autoantibodies to the angiotensin II type I receptor play an important role in mediating hypertension in response to adoptive transfer of CD4+ T lymphocytes from placental ischemic rats Hypertension in response to CD4(+) T cells from reduced uterine perfusion pregnant rats is associated with activation of the endothelin-1 system.A model of preeclampsia in rats: the reduced uterine perfusion pressure (RUPP) model.IL-17-mediated oxidative stress is an important stimulator of AT1-AA and hypertension during pregnancy.Blockade of CD40 ligand for intercellular communication reduces hypertension, placental oxidative stress, and AT1-AA in response to adoptive transfer of CD4+ T lymphocytes from RUPP rats An increased population of regulatory T cells improves the pathophysiology of placental ischemia in a rat model of preeclampsia.Four Pathways Involving Innate Immunity in the Pathogenesis of Preeclampsia.Agonistic autoantibodies to the angiotensin II type I receptor cause pathophysiologic characteristics of preeclampsia.Glycogen phosphorylase isoenzyme BB plasma concentration is elevated in pregnancy and preterm preeclampsia.GPCRs as potential therapeutic targets in preeclampsia.Immune Mechanisms Linking Obesity and Preeclampsia.Increased risk for the development of preeclampsia in obese pregnancies: weighing in on the mechanisms.Vitamin D supplementation improves pathophysiology in a rat model of preeclampsia The Role of PPARs in Placental Immunology: A Systematic Review of the Literature.IL-10 supplementation increases Tregs and decreases hypertension in the RUPP rat model of preeclampsia.Identifying immune mechanisms mediating the hypertension during preeclampsia Endothelial dysfunction. An important mediator in the pathophysiology of hypertension during pre-eclampsia.Angiotensin II type 1 receptor autoantibody (AT1-AA)-mediated pregnancy hypertension.Recent advances in the understanding of the pathophysiology of preeclampsia.Administration of interleukin-17 soluble receptor C suppresses TH17 cells, oxidative stress, and hypertension in response to placental ischemia during pregnancy.The pathophysiology of preeclampsia involves altered levels of angiogenic factors promoted by hypoxia and autoantibody-mediated mechanisms.The role of B cells in pregnancy: the good and the bad.Adaptive immune responses during pregnancy.Vascular dysfunction in preeclampsia.

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P2860

Hypertension in response to placental ischemia during pregnancy: role of B lymphocytes.

http://www.wikidata.org/entity/Q35029700

description

2011 nî lūn-bûn

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2011 թուականի Փետրուարին հրատարակուած գիտական յօդուած

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2011 թվականի փետրվարին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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name

Hypertension in response to placental ischemia during pregnancy: role of B lymphocytes.

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Hypertension in response to placental ischemia during pregnancy: role of B lymphocytes.

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Hypertension in response to placental ischemia during pregnancy: role of B lymphocytes.

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Hypertension in response to placental ischemia during pregnancy: role of B lymphocytes.

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Hypertension in response to placental ischemia during pregnancy: role of B lymphocytes.

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Hypertension in response to placental ischemia during pregnancy: role of B lymphocytes.

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Abram Weimer

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Babbette LaMarca

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James N Martin

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Kedra Wallace

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P2860

What we have learned about preeclampsia

Preeclampsia: linking placental ischemia with cardiovascular-renal dysfunction.

Recent Insights into the pathogenesis of pre-eclampsia.

Pathophysiology of preeclampsia: linking placental ischemia/hypoxia with microvascular dysfunction.

Autoantibody from women with preeclampsia induces soluble Fms-like tyrosine kinase-1 production via angiotensin type 1 receptor and calcineurin/nuclear factor of activated T-cells signaling.

Angiotensin II induces soluble fms-Like tyrosine kinase-1 release via calcineurin signaling pathway in pregnancy.

Angiotensin receptor agonistic autoantibodies induce pre-eclampsia in pregnant mice.

Activating auto-antibodies against the AT1 receptor in preeclampsia.

Autoantibody-mediated angiotensin receptor activation contributes to preeclampsia through tumor necrosis factor-alpha signaling.

Role of the renin-angiotensin system in the pathogenesis of preeclampsia.

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865-871

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