Serum Beta‐Trace Protein as a Novel Predictor of Pregnancy‐Induced Hypertension

Duan, Bide; Zhang, Lei; Ding, Xiaoyan; Li, Ling; Li, Yuan; Geng, Hui; Ma, Yuyan

doi:10.1111/jch.12801

Cited by 5 publications

(2 citation statements)

References 30 publications

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“…More recently, it has been reported that serum level of L-PGDS may represent a biomarker of kidney function ( White et al, 2015 ), pregnancy-induced hypertension ( Duan et al, 2016 ), and active lupus nephritis ( Brunner et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

Lipocalin-Like Prostaglandin D Synthase but Not Hemopoietic Prostaglandin D Synthase Deletion Causes Hypertension and Accelerates Thrombogenesis in Mice

Song

Ricciotti

Liang

et al. 2018

J Pharmacol Exp Ther

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Prostaglandin (PG) D2 is formed by two distinct PGD synthases (PGDS): lipocalin-type PGDS (L-PGDS), which acts as a PGD2-producing enzyme and as extracellular lipophilic transporter, and hematopoietic PGDS (H-PGDS), a σ glutathione-S-transferase. PGD2 plays an important role in the maintenance of vascular function; however, the relative contribution of L-PGDS– and H-PGDS–dependent formation of PGD2 in this setting is unknown. To gain insight into the function played by these distinct PGDS, we assessed systemic blood pressure (BP) and thrombogenesis in L-Pgds and H-Pgds knockout (KO) mice. Deletion of L-Pgds depresses urinary PGD2 metabolite (PGDM) by ∼35%, whereas deletion of H-Pgds does so by ∼90%. Deletion of L-Pgds, but not H-Pgds, elevates BP and accelerates the thrombogenic occlusive response to a photochemical injury to the carotid artery. HQL-79, a H-PGDS inhibitor, further depresses PGDM in L-Pgds KO mice, but has no effect on BP or on the thrombogenic response. Gene expression profiling reveals that pathways relevant to vascular function are dysregulated in the aorta of L-Pgds KOs. These results indicate that the functional impact of L-Pgds deletion on vascular homeostasis may result from an autocrine effect of L-PGDS–dependent PGD2 on the vasculature and/or the L-PGDS function as lipophilic carrier protein.

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Section: Introductionmentioning

confidence: 99%

Lipocalin-Like Prostaglandin D Synthase but Not Hemopoietic Prostaglandin D Synthase Deletion Causes Hypertension and Accelerates Thrombogenesis in Mice

Song

Ricciotti

Liang

et al. 2018

J Pharmacol Exp Ther

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show abstract

“…Thus, the kidneys eliminate BTP by glomerular filtration, and renal failure patients have increased serum BTP values 35 50 51 52 53 . Most recently, BTP has emerged as a novel biomarker of cardiovascular risk, and different studies have explored the role of BTP in hypertension 54 55 56 57 . Thus, increased BTP levels might also reflect injuries in the renal tubules and arterioles due to extended hypertension 58 59 .…”

Section: Beta-trace Proteinmentioning

confidence: 99%

Beta-trace Protein as a new non-invasive immunological Marker for Quinolinic Acid-induced impaired Blood-Brain Barrier Integrity

Baranyi

Amouzadeh-Ghadikolai

Lewinski

et al. 2017

Sci Rep

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Quinolinic acid, a macrophage/microglia-derived excitotoxin fulfills a plethora of functions such as neurotoxin, gliotoxin, and proinflammatory mediator, and it alters the integrity and cohesion of the blood-brain barrier in several pathophysiological states. Beta-trace protein (BTP), a monomeric glycoprotein, is known to indicate cerebrospinal fluid leakage. Thus, the prior aim of this study was to investigate whether BTP might non-invasively indicate quinolinic acid-induced impaired blood-brain barrier integrity. The research hypotheses were tested in three subsamples with different states of immune activation (patients with HCV-infection and interferon-α, patients with major depression, and healthy controls). BTP has also been described as a sensitive marker in detecting impaired renal function. Thus, the renal function has been considered. Our study results revealed highest quinolinic acid and highest BTP- levels in the subsample of patients with HCV in comparison with the other subsamples with lower or no immune activation (quinolinic acid: F = 21.027, p < 0.001 [ANOVA]; BTP: F = 6.792, p < 0.01 [ANOVA]). In addition, a two-step hierarchical linear regression model showed that significant predictors of BTP levels are quinolinic acid, glomerular filtration rate and age. The neurotoxin quinolinic acid may impair blood-brain barrier integrity. BTP might be a new non-invasive biomarker to indicate quinolinic acid-induced impaired blood-brain barrier integrity.

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HSPA8 Is Identified as a Novel Regulator of Hypertensive Disorders in Pregnancy by Modulating the β-Arrestin1/A1AR Axis

Zhang

Wang

et al. 2021

Reprod. Sci.

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Serum Beta‐Trace Protein as a Novel Predictor of Pregnancy‐Induced Hypertension

Cited by 5 publications

References 30 publications

Lipocalin-Like Prostaglandin D Synthase but Not Hemopoietic Prostaglandin D Synthase Deletion Causes Hypertension and Accelerates Thrombogenesis in Mice

Lipocalin-Like Prostaglandin D Synthase but Not Hemopoietic Prostaglandin D Synthase Deletion Causes Hypertension and Accelerates Thrombogenesis in Mice

Beta-trace Protein as a new non-invasive immunological Marker for Quinolinic Acid-induced impaired Blood-Brain Barrier Integrity

HSPA8 Is Identified as a Novel Regulator of Hypertensive Disorders in Pregnancy by Modulating the β-Arrestin1/A1AR Axis

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