ICAM-5 affects spine maturation by regulation of NMDA receptor binding to α-actinin

Lin, Ning; Paetau, Sonja; Nyman-Huttunen, Henrietta; Tian, Li; Gahmberg, Carl G.

doi:10.1242/bio.201410439

Cited by 8 publications

(6 citation statements)

References 44 publications

(67 reference statements)

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“…Once the ectodomain is cleaved, the cytoplasmic tail is released from the actin-linking protein α-actinin. The interaction with α-actinin is important for neurite sprouting and elongation and spine maturation ( Nyman-Huttunen et al, 2006 ; Ning et al, 2015 ).…”

Section: Introductionmentioning

confidence: 99%

Neuronal ICAM-5 Inhibits Microglia Adhesion and Phagocytosis and Promotes an Anti-inflammatory Response in LPS Stimulated Microglia

Paetau

Rõlova

Lin

et al. 2017

Front. Mol. Neurosci.

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The intercellular adhesion molecule-5 (ICAM-5) regulates neurite outgrowth and synaptic maturation. ICAM-5 overexpression in the hippocampal neurons induces filopodia formation in vitro. Since microglia are known to prune supernumerous synapses during development, we characterized the regulatory effect of ICAM-5 on microglia. ICAM-5 was released as a soluble protein from N-methyl-D-aspartic acid (NMDA)-treated neurons and bound by microglia. ICAM-5 promoted down-regulation of adhesion and phagocytosis in vitro. Microglia formed large cell clusters on ICAM-5-coated surfaces whereas they adhered and spread on the related molecule ICAM-1. ICAM-5 further reduced the secretion of the proinflammatory cytokines tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β), but on the contrary induced the secretion of the anti-inflammatory IL-10 from lipopolysaccharide (LPS) stimulated microglia. Thus, ICAM-5 might be involved in the regulation of microglia in both health and disease, playing an important neuroprotective role when the brain is under immune challenges and as a “don’t-eat-me” signal when it is solubilized from active synapses.

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Section: Introductionmentioning

confidence: 99%

Neuronal ICAM-5 Inhibits Microglia Adhesion and Phagocytosis and Promotes an Anti-inflammatory Response in LPS Stimulated Microglia

Paetau

Rõlova

Lin

et al. 2017

Front. Mol. Neurosci.

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“…ImageJ (version 1.8.0) was used to quantitatively analyze the results of immunofluorescence images. Manders' coefficients M1 and M2 were used to evaluate the overlap of two proteins (Ning, Paetau, Nyman‐Huttunen, Tian & Gahmberg, 2015), plugin Coloc 2 was selected. Subsequently, the staining results from testin RNAi and scramble RNAi groups were compared.…”

Section: Methodsmentioning

confidence: 99%

Testin regulates the blood‐testis barrier via disturbing occludin/ZO‐1 association and actin organization

Wang

Xie

et al. 2020

Journal Cellular Physiology

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The blood-testis barrier (BTB) separates the seminiferous epithelium into the apical and basal compartments. The BTB has to operate timely and accurately to ensure the correct migration of germ cells, meanwhile maintaining the immunological barrier.Testin was first characterized from primary Sertoli cells, it is a secretory protein and a sensitive biomarker to monitor junctions between Sertoli and germ cells. Till now, the functions of testin on BTB dynamics and the involving mechanisms are unknown.Herein, testin acts as a regulatory protein on BTB integrity. In vitro testin knockdown by RNAi caused significant damage to the Sertoli cell barrier with no apparent changes in the protein levels of several major tight junction (TJ), adhesion junction, and gap junction proteins. Also, testin RNAi caused the diffusion of two TJ structural proteins, occludin and ZO-1, diffusing away from the Sertoli cell surface into the cytoplasm. Association and colocalization between ZO-1 and occludin were decreased after testin RNAi, examined by Co-IP and coimmunofluorescent staining, respectively. Furthermore, testin RNAi induced a dramatic disruption on the arrangement of actin filament bundles and a reduced F-actin/G-actin ratio. The actin regulatory protein ARP3 appeared at the Sertoli cell interface after testin RNAi without its protein level change, whereas overexpressing testin in Sertoli cells showed no effect on TJ barrier integrity. The above findings suggest that besides as a monitor for Sertoli-germ cell junction integrity, testin is also an essential molecule to

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“…The colocalization of galectin-3 and CD147 was determined by measuring the Manders' coefficients M1 and M2. 17 Values of these coefficients range from 0 to 1 and express the fraction of intensity in a channel that is located in pixels where there is above threshold intensity in the other color channel. For that purpose, the plugin Coloc 2 was applied to the red and green channels of the images.…”

Section: Methodsmentioning

confidence: 99%

Colocalization of Galectin-3 With CD147 Is Associated With Increased Gelatinolytic Activity in Ulcerating Human Corneas

Cruzat

González‐Andrades

Mauris

et al. 2018

Invest. Ophthalmol. Vis. Sci.

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PurposeGalectin-3 is a carbohydrate-binding protein known to promote expression of matrix metalloproteinases, a hallmark of ulceration, through interaction with the extracellular matrix metalloproteinase inducer CD147. The aim of this study was to investigate the distribution of galectin-3 in corneas of patients with ulcerative keratitis and to determine its relationship to CD147 and the presence of gelatinolytic activity.MethodsThis was an observational case series involving donor tissue from 13 patients with active corneal ulceration and 6 control corneas. Fixed-frozen sections of the corneas were processed to localize galectin-3 and CD147 by immunofluorescence microscopy. Gelatinolytic activity was detected by in situ zymography.ResultsTissue from patients with active corneal ulceration showed a greater galectin-3 immunoreactivity in basal epithelia and stroma compared with controls. Immunofluorescence grading scores revealed increased colocalization of galectin-3 and CD147 in corneal ulcers at the epithelial–stromal junction and within fibroblasts. Quantitative analysis using the Manders' colocalization coefficient demonstrated significant overlap in corneas from patients with ulcerative keratitis (M1 = 0.29; M2 = 0.22) as opposed to control corneas (M1 = 0.01, P < 0.01; M2 = 0.02, P < 0.05). In these experiments, there was a significant positive correlation between the degree of galectin-3 and CD147 colocalization and the presence of gelatinolytic activity.ConclusionsOur results indicate that concomitant stimulation and colocalization of galectin-3 with CD147 are associated with increased gelatinolytic activity in the actively ulcerating human cornea and suggest a mechanism by which galectin-3 may contribute to the degradation of extracellular matrix proteins during ulceration.

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ICAM-5 affects spine maturation by regulation of NMDA receptor binding to α-actinin

Cited by 8 publications

References 44 publications

Neuronal ICAM-5 Inhibits Microglia Adhesion and Phagocytosis and Promotes an Anti-inflammatory Response in LPS Stimulated Microglia

Neuronal ICAM-5 Inhibits Microglia Adhesion and Phagocytosis and Promotes an Anti-inflammatory Response in LPS Stimulated Microglia

Testin regulates the blood‐testis barrier via disturbing occludin/ZO‐1 association and actin organization

Colocalization of Galectin-3 With CD147 Is Associated With Increased Gelatinolytic Activity in Ulcerating Human Corneas

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