Nogo-A in the visual system development and in ocular diseases

Pernet, Vincent

doi:10.1016/j.bbadis.2017.04.008

Cited by 19 publications

(17 citation statements)

References 134 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Much of the myelin-related brakes on plasticity have been attributed to signaling through the Nogo receptor, NgR (58). The neurite outgrowth inhibitor Nogo-A (Rtn4), which signals through NgR, was up-regulated by oligodendrocytes at P20 (SI Appendix, Fig.…”

Section: Mapping Cell Type-specific Transcriptional Responses To Tonementioning

confidence: 99%

Single-nucleus RNA sequencing of mouse auditory cortex reveals critical period triggers and brakes

Kalish

Barkat

Diel

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Auditory experience drives neural circuit refinement during windows of heightened brain plasticity, but little is known about the genetic regulation of this developmental process. The primary auditory cortex (A1) of mice exhibits a critical period for thalamocortical connectivity between postnatal days P12 and P15, during which tone exposure alters the tonotopic topography of A1. We hypothesized that a coordinated, multicellular transcriptional program governs this window for patterning of the auditory cortex. To generate a robust multicellular map of gene expression, we performed droplet-based, single-nucleus RNA sequencing (snRNA-seq) of A1 across three developmental time points (P10, P15, and P20) spanning the tonotopic critical period. We also tone-reared mice (7 kHz pips) during the 3-d critical period and collected A1 at P15 and P20. We identified and profiled both neuronal (glutamatergic and GABAergic) and nonneuronal (oligodendrocytes, microglia, astrocytes, and endothelial) cell types. By comparing normal- and tone-reared mice, we found hundreds of genes across cell types showing altered expression as a result of sensory manipulation during the critical period. Functional voltage-sensitive dye imaging confirmed GABA circuit function determines critical period onset, while Nogo receptor signaling is required for its closure. We further uncovered previously unknown effects of developmental tone exposure on trajectories of gene expression in interneurons, as well as candidate genes that might execute tonotopic plasticity. Our single-nucleus transcriptomic resource of developing auditory cortex is thus a powerful discovery platform with which to identify mediators of tonotopic plasticity.

show abstract

Section: Mapping Cell Type-specific Transcriptional Responses To Tonementioning

confidence: 99%

Single-nucleus RNA sequencing of mouse auditory cortex reveals critical period triggers and brakes

Kalish

Barkat

Diel

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

show abstract

“…Nogo-A protein, most widely examined as a potent neurite growth inhibitor, has never been studied in patients with liver cirrhosis or PH. Studies have examined the expression of Nogo-A in cardiomyocytes[21], enteric nervous system[22], in ocular diseases[23] and hepatocellular carcinoma[24]. Nogo-A has also been reported to be a negative regulator of retinal and CNS[25,26] angiogenesis, but the effects on an-giogenesis in liver diseases remains unknown.…”

Section: Introductionmentioning

confidence: 99%

Plasma Nogo-A and placental growth factor levels are associated with portal hypertension in patients with liver cirrhosis

Gelman

Šaltenienė

Pranculis

et al. 2019

WJG

View full text Add to dashboard Cite

BACKGROUND Clinically significant portal hypertension (CSPH) and severe portal hypertension (SPH) increase the risk for decompensation and life-threatening complications in liver cirrhosis. Pathologic angiogenesis might contribute to the formation of these conditions. Placental growth factor (PlGF) and Nogo-A protein are biomarkers of pathological angiogenesis, but data on their role in liver cirrhosis and portal hypertension is scarce. AIM To determine plasma levels of PlGF and Nogo-A in patients with liver cirrhosis, CSPH, SPH and potential to predict portal hypertension. METHODS A cohort of 122 patients with hepatitis C virus and/or alcohol-induced liver cirrhosis with characterized hepatic venous pressure gradient (HVPG) were included in the study. Demographic data, medical history, Child-Turcotte-Pugh and Model of End Stage liver disease score, clinical chemistry, liver stiffness values were recorded on the day of the procedure prior HVPG measurement. The degree of portal hypertension was determined by the invasive HVPG measurement. Nogo-A and PlGF plasma levels were evaluated using enzyme linked immunosorbent assay. The control group consisted of 30 healthy age- and sex- matched individuals. RESULTS Peripheral PlGF levels were higher and Nogo-A levels were lower in patients with liver cirrhosis (23.20 vs 9.85; P < 0.0001 and 2.19 vs 3.12; P = 0.004 respectively). There was a positive linear correlation between peripheral levels of PlGF and HVPG ( r = 0.338, P = 0.001) and negative linear correlation between the peripheral Nogo-A levels and HVPG ( r = -0.267, P = 0.007). PlGF levels were higher in CSPH and SPH ( P = 0.006; P < 0.0001) whereas Nogo-A levels were lower ( P = 0.01; P < 0.033). Area under the curve for the diagnosis of CSPH for PlGF was 0.68 ( P = 0.003) and for Nogo-A - 0.67 ( P = 0.01); for SPH 0.714 ( P < 0.0001) and 0.65 ( P = 0.014) respectively. PlGF levels were higher and Nogo-A levels were lower in patients with esophageal varices ( P < 0.05). PlGF cut-off value of 25 pg/mL distinguished patients with CSPH at 55.7% sensitivity and 76.7% specificity; whereas Nogo-A cut-off value of 1.12 ng/mL was highly specific (93.1%) for the diagnosis of CSPH. CONCLUSION Plasma PlGF levels were higher while Nogo-A levels were lower in patients with liver cirrhosis and portal hypertension. Biomarkers showed moderate predictive value in determining CSPH and SPH.

show abstract

“…Functional impairments in surviving neurons may thus account to a large extent for visual deficits after retinal injury. Moreover, the fact that retinal neurons have a very weak ability to regenerate after injury is likely to participate in the vision deterioration caused by ocular diseases 3 – 5 . Molecular mechanisms restricting visual neuron plasticity have been described in the injured retina.…”

Section: Introductionmentioning

confidence: 99%

Nogo-A inactivation improves visual plasticity and recovery after retinal injury

et al. 2018

Self Cite

View full text Add to dashboard Cite

Myelin-associated proteins such as Nogo-A are major inhibitors of neuronal plasticity that contribute to permanent neurological impairments in the injured CNS. In the present study, we investigated the influence of Nogo-A on visual recovery after retinal injuries in mice. Different doses of N-methyl-d-aspartate (NMDA) were injected in the vitreous of the left eye to induce retinal neuron death. The visual function was monitored using the optokinetic response (OKR) as a behavior test, and electroretinogram (ERG) and local field potential (LFP) recordings allowed to assess changes in retinal and cortical neuron activity, respectively. Longitudinal OKR follow-ups revealed reversible visual deficits after injection of NMDA ≤ 1 nmole in the left eye and concomitant functional improvement in the contralateral visual pathway of the right eye that was let intact. Irreversible OKR loss observed with NMDA ≥ 2 nmol was correlated with massive retinal cell death and important ERG response decline. Strikingly, the OKR mediated by injured and intact eye stimulation was markedly improved in Nogo-A KO mice compared with WT animals, suggesting that the inactivation of Nogo-A promotes visual recovery and plasticity. Moreover, OKR improvement was associated with shorter latency of the N2 wave of Nogo-A KO LFPs relative to WT animals. Strikingly, intravitreal injection of anti-Nogo-A antibody (11C7) in the injured eye exerted positive effects on cortical LFPs. This study presents the intrinsic ability of the visual system to recover from NMDA-induced retinal injury and its limitations. Nogo-A neutralization may promote visual recovery in retinal diseases such as glaucoma.

show abstract

Nogo-A in the visual system development and in ocular diseases

Cited by 19 publications

References 134 publications

Single-nucleus RNA sequencing of mouse auditory cortex reveals critical period triggers and brakes

Single-nucleus RNA sequencing of mouse auditory cortex reveals critical period triggers and brakes

Plasma Nogo-A and placental growth factor levels are associated with portal hypertension in patients with liver cirrhosis

Nogo-A inactivation improves visual plasticity and recovery after retinal injury

Contact Info

Product

Resources

About