Interactions between Intercellular Adhesion Molecule-5 (ICAM-5) and β1 integrins regulate neuronal synapse formation.

Lin Ning, Li Tian, Sergei Smirnov, Helena Vihinen, Olaya Llano Sanchez, Kyle Vick, Ronald L. Davis, Claudio Rivera Baeza, Carl G. Gahmberg

Forskningsoutput: TidskriftsbidragArtikelVetenskapligPeer review

Sammanfattning

ICAM-5 is a dendrite-specific adhesion molecule, which functions in both the immune and nervous systems. ICAM-5 is the only identified negative regulator for spine maturation so far. Shedding of ICAM-5 ectodomain leads to promoted spine maturation and enhanced synaptic activity. However, the mechanism by which ICAM-5 regulates spine development remains poorly understood. In this study, we found that ablation of ICAM5 expression resulted in a significant increase in the formation of synaptic contacts and the frequency of miniature excitatory postsynaptic currents, an indicator of pre-synaptic release probability. Antibodies against ICAM-5 and β1 integrins altered spine maturation. Furthermore we found that β1 integrins serve as binding partners for ICAM-5. β1 integrins were immune precipitated with ICAM-5 from mouse brain and the binding region in ICAM-5 was localized to the two first Ig-domains. β1 integrins were juxtaposed to filopodia tips at the early stage of synaptic formation, but as synapses matured, β1 integrins covered the mushroom spines. Loss of β1 integrins from the pre-synaptic sites affected the morphology of the post-synaptic structures. ICAM-5 ectodomain cleavage decreased or increased respectively, when the interaction between ICAM-5 and β1 integrins was potentiated or weakened using antibodies. These results suggest that the interaction between ICAM-5 and β1 integrins plays an important role in formation of functional synapses.
Originalspråkengelska
TidskriftJournal of Cell Science
Volym126
Utgåva1
Sidor (från-till)77-89
Antal sidor13
ISSN0021-9533
DOI
StatusPublicerad - 2013
MoE-publikationstypA1 Tidskriftsartikel-refererad

Vetenskapsgrenar

  • 1184 Genetik, utvecklingsbiologi, fysiologi

Citera det här

@article{e4612463e17141d5bec85d94db802caa,
title = "Interactions between Intercellular Adhesion Molecule-5 (ICAM-5) and β1 integrins regulate neuronal synapse formation.",
abstract = "ICAM-5 is a dendrite-specific adhesion molecule, which functions in both the immune and nervous systems. ICAM-5 is the only identified negative regulator for spine maturation so far. Shedding of ICAM-5 ectodomain leads to promoted spine maturation and enhanced synaptic activity. However, the mechanism by which ICAM-5 regulates spine development remains poorly understood. In this study, we found that ablation of ICAM5 expression resulted in a significant increase in the formation of synaptic contacts and the frequency of miniature excitatory postsynaptic currents, an indicator of pre-synaptic release probability. Antibodies against ICAM-5 and β1 integrins altered spine maturation. Furthermore we found that β1 integrins serve as binding partners for ICAM-5. β1 integrins were immune precipitated with ICAM-5 from mouse brain and the binding region in ICAM-5 was localized to the two first Ig-domains. β1 integrins were juxtaposed to filopodia tips at the early stage of synaptic formation, but as synapses matured, β1 integrins covered the mushroom spines. Loss of β1 integrins from the pre-synaptic sites affected the morphology of the post-synaptic structures. ICAM-5 ectodomain cleavage decreased or increased respectively, when the interaction between ICAM-5 and β1 integrins was potentiated or weakened using antibodies. These results suggest that the interaction between ICAM-5 and β1 integrins plays an important role in formation of functional synapses.",
keywords = "1184 Genetics, developmental biology, physiology, NEUROBIOLOGY, dendritic spine, synapse formation",
author = "Lin Ning and Li Tian and Sergei Smirnov and Helena Vihinen and {Llano Sanchez}, Olaya and Kyle Vick and Davis, {Ronald L.} and {Rivera Baeza}, Claudio and Gahmberg, {Carl G.}",
year = "2013",
doi = "10.1242/jcs.106674",
language = "English",
volume = "126",
pages = "77--89",
journal = "Journal of Cell Science",
issn = "0021-9533",
publisher = "Company of Biologists Ltd",
number = "1",

}

Interactions between Intercellular Adhesion Molecule-5 (ICAM-5) and β1 integrins regulate neuronal synapse formation. / Ning, Lin; Tian, Li; Smirnov, Sergei; Vihinen, Helena; Llano Sanchez, Olaya; Vick, Kyle; Davis, Ronald L.; Rivera Baeza, Claudio; Gahmberg, Carl G.

I: Journal of Cell Science, Vol. 126, Nr. 1, 2013, s. 77-89.

Forskningsoutput: TidskriftsbidragArtikelVetenskapligPeer review

TY - JOUR

T1 - Interactions between Intercellular Adhesion Molecule-5 (ICAM-5) and β1 integrins regulate neuronal synapse formation.

AU - Ning, Lin

AU - Tian, Li

AU - Smirnov, Sergei

AU - Vihinen, Helena

AU - Llano Sanchez, Olaya

AU - Vick, Kyle

AU - Davis, Ronald L.

AU - Rivera Baeza, Claudio

AU - Gahmberg, Carl G.

PY - 2013

Y1 - 2013

N2 - ICAM-5 is a dendrite-specific adhesion molecule, which functions in both the immune and nervous systems. ICAM-5 is the only identified negative regulator for spine maturation so far. Shedding of ICAM-5 ectodomain leads to promoted spine maturation and enhanced synaptic activity. However, the mechanism by which ICAM-5 regulates spine development remains poorly understood. In this study, we found that ablation of ICAM5 expression resulted in a significant increase in the formation of synaptic contacts and the frequency of miniature excitatory postsynaptic currents, an indicator of pre-synaptic release probability. Antibodies against ICAM-5 and β1 integrins altered spine maturation. Furthermore we found that β1 integrins serve as binding partners for ICAM-5. β1 integrins were immune precipitated with ICAM-5 from mouse brain and the binding region in ICAM-5 was localized to the two first Ig-domains. β1 integrins were juxtaposed to filopodia tips at the early stage of synaptic formation, but as synapses matured, β1 integrins covered the mushroom spines. Loss of β1 integrins from the pre-synaptic sites affected the morphology of the post-synaptic structures. ICAM-5 ectodomain cleavage decreased or increased respectively, when the interaction between ICAM-5 and β1 integrins was potentiated or weakened using antibodies. These results suggest that the interaction between ICAM-5 and β1 integrins plays an important role in formation of functional synapses.

AB - ICAM-5 is a dendrite-specific adhesion molecule, which functions in both the immune and nervous systems. ICAM-5 is the only identified negative regulator for spine maturation so far. Shedding of ICAM-5 ectodomain leads to promoted spine maturation and enhanced synaptic activity. However, the mechanism by which ICAM-5 regulates spine development remains poorly understood. In this study, we found that ablation of ICAM5 expression resulted in a significant increase in the formation of synaptic contacts and the frequency of miniature excitatory postsynaptic currents, an indicator of pre-synaptic release probability. Antibodies against ICAM-5 and β1 integrins altered spine maturation. Furthermore we found that β1 integrins serve as binding partners for ICAM-5. β1 integrins were immune precipitated with ICAM-5 from mouse brain and the binding region in ICAM-5 was localized to the two first Ig-domains. β1 integrins were juxtaposed to filopodia tips at the early stage of synaptic formation, but as synapses matured, β1 integrins covered the mushroom spines. Loss of β1 integrins from the pre-synaptic sites affected the morphology of the post-synaptic structures. ICAM-5 ectodomain cleavage decreased or increased respectively, when the interaction between ICAM-5 and β1 integrins was potentiated or weakened using antibodies. These results suggest that the interaction between ICAM-5 and β1 integrins plays an important role in formation of functional synapses.

KW - 1184 Genetics, developmental biology, physiology

KW - NEUROBIOLOGY

KW - dendritic spine

KW - synapse formation

U2 - 10.1242/jcs.106674

DO - 10.1242/jcs.106674

M3 - Article

VL - 126

SP - 77

EP - 89

JO - Journal of Cell Science

JF - Journal of Cell Science

SN - 0021-9533

IS - 1

ER -