Differential Receptor for Advanced Glycation End Products Expression in Preeclamptic, Intrauterine Growth Restricted, and Gestational Diabetic Placentas

Alexander, Kristen; Mejía, Camilo A.; Jordan, Clinton; Nelson, Michael B.; Howell, Brian M.; Jones, Carissa P; Reynolds, Paul; Arroyo, Juan A.

doi:10.1111/aji.12462

Cited by 33 publications

(30 citation statements)

References 40 publications

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“…Microarray analysis indicated a number of genes that were up- or down-regulated by the miR-518b mimic. Among the 124 target genes down-regulated more than 2-fold (Supplementary Table S1), two genes (tyrosine hydroxylase: TH and hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1: HSD3B1 ) were previously demonstrated to be involved in the pathogenesis of preeclampsia202122, and five genes (endothelin receptor type A: EDNRA , advanced glycosylation end product-specific receptor: AGER , wingless-type MMTV integration site family member 2: WNT2 , complement component 9: C9 , and transient receptor potential cation channel, subfamily M, member 2: TRPM2 ) play roles in preeclampsia with foetal growth restriction23242526272829303132 (Table 1). Likewise, among the 112 target genes up-regulated over 2-fold by the miR-518b mimic (Supplementary Table S2), four genes [hemopexin: HPX , serpin peptidase inhibitor, clade B (ovalbumin), member 2: SERPINB2 , lipoprotein, Lp(a): LPA , and tumour necrosis factor superfamily, member 10: TNFSF10 ] show involvement in preeclampsia35363738, and two genes (CD69 molecule: CD69 and stanniocalcin 1: STC1 ) are involved in preeclampsia with foetal growth restriction333439 (Table 1).…”

Section: Resultsmentioning

confidence: 99%

“…miR-518b seems to control multiple target genes located on various chromosomes. Interestingly, some miR-518b target genes were previously demonstrated to associate with preeclampsia (e.g., TH and HSD3B1 for down-regulated genes, and HPX, SERPINB2, LPA and TNFSF10 for up-regulated genes)20212235363738 and with preeclampsia with foetal growth restriction (e.g., EDNRA, AGER, WNT2, C9 , and TRPM2 for down-regulated genes, and CD69 and STC1 for up-regulated genes)23242526272829303132333439. However, further experiments are needed to demonstrate a causal relationship between the expression of pregnancy-associated miRNAs and pregnancy-related disorders.…”

Section: Discussionmentioning

confidence: 99%

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Feasibility of placenta-derived mesenchymal stem cells as a tool for studying pregnancy-related disorders

Fuchi

Miura

Doi

et al. 2017

Sci Rep

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The cellular and molecular mechanisms responsible for pregnancy-related disorders remain unclear. We investigated the feasibility of using placenta-derived mesenchymal stem cells (MSCs) as a tool to study such pregnancy-related disorders. We isolated and expanded adequate numbers of cells with characteristic features of MSCs from the chorionic plate (CP-MSCs), chorionic villi (CV-MSCs), and decidua basalis (DB-MSCs) of human term placental tissues. All placenta-derived MSCs expressed pregnancy-associated C14MC microRNA (miRNA) (miR-323-3p). Interestingly, the placenta-specific C19MC miRNAs (miR-518b and miR517a) were clearly expressed in CP-MSCs and CV-MSCs of foetal origin, but were barely expressed in DB-MSCs of maternal origin. Furthermore, expression levels of placenta-specific C19MC miRNAs in CV-MSCs remained stable during the ex vivo expansion process and across different pregnancy phases (first trimester versus third trimester). High-efficiency siRNA transfection was confirmed in twice-passaged CV-MSCs with little toxicity, and microarray analysis was used to screen for miR-518b target genes. Placenta-derived MSCs, especially CV-MSCs, are a potential tool for investigating the role of placental miRNAs in pregnancy-related disorders.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Feasibility of placenta-derived mesenchymal stem cells as a tool for studying pregnancy-related disorders

Fuchi

Miura

Doi

et al. 2017

Sci Rep

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“…An underlying mechanistic theme of the smoke-related disease states outlined in this review is chronic inflammation, in which RAGE is a key modulator. Essential to understanding the clear link between RAGE and disease progression is the key concept that RAGE expression is increased by exposure to tobacco smoke [5,209,210,211,212] and the induction of RAGE causes inflammatory disease symptoms similar or identical to the ones described herein [23,195,213,214,215,216,217]. …”

Section: Rage: a Plausible Unifying Mechanismmentioning

confidence: 92%

“…Such tobacco-derived AGEs are formed by Malliard chemical pathways and are the key ligand that perpetuates pro-inflammatory RAGE signaling [16]. AGEs that bind RAGE have been implicated in a large and diverse group of diseases including respiratory inflammatory diseases [17], cardiovascular disease [18], cancer [19], diabetes [20], neurodegenerative disorders [21], placental dysfunction [22,23], osteoarthritis [24], and general inflammation [25]. In mechanistic terms, AGE-RAGE interaction initiates a cascade of events that results in the induction of chronic inflammation and impaired cell survival [26,27].…”

Section: Introductionmentioning

confidence: 99%

Plausible Roles for RAGE in Conditions Exacerbated by Direct and Indirect (Secondhand) Smoke Exposure

Lewis

Hirschi

Arroyo

et al. 2017

IJMS

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Approximately 1 billion people smoke worldwide, and the burden placed on society by primary and secondhand smokers is expected to increase. Smoking is the leading risk factor for myriad health complications stemming from diverse pathogenic programs. First-and second-hand cigarette smoke contains thousands of constituents, including several carcinogens and cytotoxic chemicals that orchestrate chronic inflammatory responses and destructive remodeling events. In the current review, we outline details related to compromised pulmonary and systemic conditions related to smoke exposure. Specifically, data are discussed relative to impaired lung physiology, cancer mechanisms, maternal-fetal complications, cardiometabolic, and joint disorders in the context of smoke exposure exacerbations. As a general unifying mechanism, the receptor for advanced glycation end-products (RAGE) and its signaling axis is increasingly considered central to smoke-related pathogenesis. RAGE is a multi-ligand cell surface receptor whose expression increases following cigarette smoke exposure. RAGE signaling participates in the underpinning of inflammatory mechanisms mediated by requisite cytokines, chemokines, and remodeling enzymes. Understanding the biological contributions of RAGE during cigarette smoke-induced inflammation may provide critically important insight into the pathology of lung disease and systemic complications that combine during the demise of those exposed.

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“…This receptor is capable of binding a host of ligands, such as advanced glycation end‐products (AGEs), high‐mobility group box 1, S100/calgranulins, in addition to other substances . Receptor for advanced glycation end‐products signaling is implicated in the pathogenesis of many inflammatory diseases, such as Alzheimer's disease , diabetes atherosclerosis , chronic obstructive pulmonary disease , and diverse rheumatological disorders . Tobacco smoke induces epithelium to increase the expression of RAGE, its ligands, pro‐inflammatory signaling intermediates, and various cytokines .…”

mentioning

confidence: 99%

Cigarette smoke extract induces oral squamous cell carcinoma cell invasion in a receptor for advanced glycation end‐products‐dependent manner

Chapman

Mick

Hall

et al. 2017

European J Oral Sciences

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. Cigarette smoke extract induces oral squamous cell carcinoma cell invasion in a receptor for advanced glycation end-products-dependent manner. Eur J Oral Sci 2018; 126: 33-40. © 2017 Eur J Oral SciOral squamous cell carcinoma (OSCC) affects approximately 30,000 people and is associated with tobacco use. Little is known about the mechanistic effects of second-hand smoke in the development of OSSC. The receptor for advanced glycation end-products (RAGE) is a surface receptor that is upregulated by second-hand smoke and inhibited by semi-synthetic glycosaminoglycan ethers (SAGEs). Our objective was to determine the role of RAGE during cigarette smoke extractinduced cellular responses and to use SAGEs as a modulating factor of Ca9-22 OSCC cell invasion. Ca9-22 cells were cultured in the presence or absence of cigarette smoke extract and SAGEs. Cell invasion was determined and cells were lysed for western blot analysis. Ras and nuclear factor of kappa light polypeptide gene enhancer in B-cells (NF-jB) activation were determined. Treatment of cells with cigarette smoke extract resulted in: (i) increased invasion of OSCC; (ii) increased RAGE expression; (iii) inhibition of cigarette smoke extract-induced OSCC cell invasion by SAGEs; (iv) increased Ras, increased AKT and NF-jB activation, and downregulation by SAGEs; and (v) increased expression of matrix metalloproteinases (MMPs) 2, 9, and 14, and downregulation by SAGEs. We conclude that cigarette smoke extract increases invasion of OSCC cells in a RAGE-dependent manner. Inhibition of RAGE decreases the levels of its signaling molecules, which results in blocking the cigarette smoke extract-induced invasion.

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Differential Receptor for Advanced Glycation End Products Expression in Preeclamptic, Intrauterine Growth Restricted, and Gestational Diabetic Placentas

Abstract: We conclude that placental RAGE is activated during PE and that RAGE-mediated inflammation in the trophoblast involves increased pro-inflammatory cytokine secretion.

Cited by 33 publications

References 40 publications

Feasibility of placenta-derived mesenchymal stem cells as a tool for studying pregnancy-related disorders

Feasibility of placenta-derived mesenchymal stem cells as a tool for studying pregnancy-related disorders

Plausible Roles for RAGE in Conditions Exacerbated by Direct and Indirect (Secondhand) Smoke Exposure

Cigarette smoke extract induces oral squamous cell carcinoma cell invasion in a receptor for advanced glycation end‐products‐dependent manner

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