Identification and characterization of human LYPD6, a new member of the Ly-6 superfamily

Zhang, Yifeng; Lang, Qingyu; Li, Jie; Xie, Fang; Wan, Bo; Liu, Yu

doi:10.1007/s11033-009-9663-7

Cited by 29 publications

(26 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This observation was significant also when confounding effects were considered (ANCOVA, FDR P <0.05; Table 3 ). Significantly higher placental mRNA level of the transcription regulator LYPD6 [24] was identified in all patient groups: GDM (t-test: P = 1.3×10 −5 ; FDR P <0.05; fc = 1.79), PE ( P = 0.0024; FDR P <0.05; fc = 1.38), LGA ( P = 0.0095; fc = 1.5) and SGA ( P = 0.014; fc = 1.57). In the SGA group, differential placental expression of LYPD6 maintained statistical significance after correcting for confounding effects (ANCOVA, FDR P <0.05; Table 3 ).…”

Section: Resultsmentioning

confidence: 95%

See 1 more Smart Citation

Mid-Gestational Gene Expression Profile in Placenta and Link to Pregnancy Complications

et al. 2012

View full text Add to dashboard Cite

Despite the importance of placenta in mediating rapid physiological changes in pregnancy, data on temporal dynamics of placental gene expression are limited. We completed the first transcriptome profiling of human placental gene expression dynamics (GeneChips, Affymetrix®; ∼47,000 transcripts) from early to mid-gestation (n = 10; gestational weeks 5–18) and report 154 genes with significant transcriptional changes (ANOVA, FDR P<0.1). TaqMan RT-qPCR analysis (n = 43; gestational weeks 5–41) confirmed a significant (ANOVA and t-test, FDR P<0.05) mid-gestational peak of placental gene expression for BMP5, CCNG2, CDH11, FST, GATM, GPR183, ITGBL1, PLAGL1, SLC16A10 and STC1, followed by sharp decrease in mRNA levels at term (t-test, FDR P<0.05). We hypothesized that normal course of late pregnancy may be affected when genes characteristic to mid-gestation placenta remain highly expressed until term, and analyzed their expression in term placentas from normal and complicated pregnancies [preeclampsia (PE), n = 12; gestational diabetes mellitus (GDM), n = 12; small- and large-for-gestational-age newborns (SGA, LGA), n = 12+12]. STC1 (stanniocalcin 1) exhibited increased mRNA levels in all studied complications, with the most significant effect in PE- and SGA-groups (t-test, FDR P<0.05). In post-partum maternal plasma, the highest STC1 hormone levels (ELISA, n = 129) were found in women who had developed PE and delivered a SGA newborn (median 731 vs 418 pg/ml in controls; ANCOVA, P = 0.00048). Significantly higher expression (t-test, FDR P<0.05) of CCNG2 and LYPD6 accompanied with enhanced immunostaining of the protein was detected in placental sections of PE and GDM cases (n = 15). Our study demonstrates the importance of temporal dynamics of placental transcriptional regulation across three trimesters of gestation. Interestingly, many genes with high expression in mid-gestation placenta have also been implicated in adult complex disease, promoting the discussion on the role of placenta in developmental programming. The discovery of elevated maternal plasma STC1 in pregnancy complications warrants further investigations of its potential as a biomarker.

show abstract

Section: Resultsmentioning

confidence: 95%

“…To determine protein expression levels of cytoplasmic molecules of LYPD6 [24] and CCNG2 [30], immunohistochemical (IHC) staining was performed in placental sections from control ( n = 5), GDM ( n = 5) and PE ( n = 5) pregnancies. Characteristics of the IHC study groups are provided in Table S1 .…”

Section: Resultsmentioning

confidence: 99%

Mid-Gestational Gene Expression Profile in Placenta and Link to Pregnancy Complications

et al. 2012

View full text Add to dashboard Cite

show abstract

“…Recently, LYPD6 was found to recruit to the WNT receptor complex to positively regulate WNT signaling (27,28). Interestingly, MDP-induced membrane recruitment of NOD2 to activate downstream signaling is well established (29,30).…”

Section: Lypd6 Is Essential To Activate Wnt Signaling By Nod2mentioning

confidence: 99%

WNT-Inflammasome Signaling Mediates NOD2-Induced Development of Acute Arthritis in Mice

Singh

Holla

Ramachandra

et al. 2015

The Journal of Immunology

View full text Add to dashboard Cite

In addition to its role in innate immunity, the intracellular pathogen sensor nucleotide-binding oligomerization domain 2 (NOD2) has been implicated in various inflammatory disorders, including the development of acute arthritis. However, the molecular mechanisms involved in the development of NOD2-responsive acute arthritis are not clear. In this study, we demonstrate that NOD2 signals to a cellular protein, Ly6/PLAUR domain–containing protein 6, in a receptor-interacting protein kinase 2–TGF-β–activated kinase 1–independent manner to activate the WNT signaling cascade. Gain- or loss-of-function of the WNT signaling pathway in an in vivo experimental mouse arthritis model or in vitro systems established the role for WNT-responsive X-linked inhibitor of apoptosis during the development of acute arthritis. Importantly, WNT-stimulated X-linked inhibitor of apoptosis mediates the activation of inflammasomes. The subsequent caspase-1 activation and IL-1β secretion together contribute to the phenotypic character of the inflammatory condition of acute arthritis. Thus, identification of a role for WNT-mediated inflammasome activation during NOD2 stimulation serves as a paradigm to understand NOD2-associated inflammatory disorders and develop novel therapeutics.

show abstract

“…[36] LYPD6 can inhibit transcriptional activity of the AP-1 transcription factor complex, a key activated mediator of inflammation in endothelial cells subject to atherogenic blood flow conditions. [37,38] The variant rs113816216 at 5q31.3 is located in the intron of FSTL4, a poorly characterized gene. [36] However, the FSTL4 paralog FSTL1 encodes a protein that induces innate immunity by acting as a toll-like receptor-4 (TLR-4) agonist.…”

Section: Mediators Of Inflammationmentioning

confidence: 99%

Inflammation in human cerebral aneurysms: pathogenesis, diagnostic imaging, genetics, and therapeutics

Dooley¹,

Hudson²,

Hasan³

2015

Neuroimmunol Neuroinflammation

View full text Add to dashboard Cite

Intracranial aneurysms are a life-threatening cerebrovascular pathology with a probability of spontaneous rupture. Current intervention techniques carry inherent risk. Recent investigation has reinforced inflammation's role in the pathophysiological process of cerebral aneurysms. These data suggest alternative diagnostic and noninvasive therapeutic strategies. Furthermore, novel characteristics of the underlying disease have been elucidated through distinct bioinformatic and gene expression profile analyses. This article will emphasize the most recent investigation, highlighting findings of clinical significance and etiological relevance.

show abstract

Identification and characterization of human LYPD6, a new member of the Ly-6 superfamily

Cited by 29 publications

References 30 publications

Mid-Gestational Gene Expression Profile in Placenta and Link to Pregnancy Complications

Mid-Gestational Gene Expression Profile in Placenta and Link to Pregnancy Complications

WNT-Inflammasome Signaling Mediates NOD2-Induced Development of Acute Arthritis in Mice

Inflammation in human cerebral aneurysms: pathogenesis, diagnostic imaging, genetics, and therapeutics

Contact Info

Product

Resources

About