Contribution of atypical chemokine receptor 2/ACKR2 in bone remodeling

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dc.creatorIzabella Lucas de Abreu Lima
dc.creatorTarcília Aparecida da Silva
dc.creatorJanine Mayra da Silva
dc.creatorLetícia Fernanda Duffles Rodrigues
dc.creatorDavidson Frois Madureira
dc.creatorAngélica Cristina Fonseca
dc.creatorGustavo Pompermaier Garlet
dc.creatorMauro Martins Teixeira
dc.creatorRemo Castro Russo
dc.creatorSandra Yasuyo Fukada
dc.date.accessioned2025-04-17T15:24:35Z
dc.date.accessioned2025-09-09T01:34:09Z
dc.date.available2025-04-17T15:24:35Z
dc.date.issued2017-08
dc.description.sponsorshipCNPq - Conselho Nacional de Desenvolvimento Científico e Tecnológico
dc.description.sponsorshipFAPEMIG - Fundação de Amparo à Pesquisa do Estado de Minas Gerais
dc.format.mimetypepdf
dc.identifier.doihttps://doi.org/10.1016/j.bone.2017.05.003
dc.identifier.issn1873-2763
dc.identifier.urihttps://hdl.handle.net/1843/81699
dc.languageeng
dc.publisherUniversidade Federal de Minas Gerais
dc.relation.ispartofBone
dc.rightsAcesso Restrito
dc.subjectChemokines
dc.subjectOrthodontics
dc.subjectBone Remodeling
dc.subjectProteins
dc.subjectOsteoblasts
dc.subjectCell count
dc.subjectReceptors, chemokine
dc.subjectTooth movement techniques
dc.subjectPeriodontium
dc.subject.otherBone remodeling
dc.subject.otherChemokines
dc.subject.otherOrthodontics
dc.titleContribution of atypical chemokine receptor 2/ACKR2 in bone remodeling
dc.typeArtigo de periódico
local.citation.epage122
local.citation.spage113
local.citation.volume101
local.description.resumoIntroduction: Bone remodeling is a tightly regulated process influenced by chemokines. ACKR2 is a decoy receptor for CC chemokines functioning as regulator of inflammatory response. In this study we investigated whether the absence of ACKR2 would affect bone phenotype and remodeling induced by mechanical loading. Methods: An orthodontic appliance was placed between incisors and first molar of ACKR2 deficient (ACKR2-/-) and C57BL6/J (wild-type/WT) mice. Microtomography, histology and qPCR were performed to evaluate bone parameters, orthodontic tooth movement (OTM), bone cells counts and the expression of ACKR2, bone remodeling markers, CC chemokines and chemokines receptors. Bone marrow cells (BMC) from WT and ACKR2-/- mice were differentiated in osteoclasts and osteoblasts for analysis of activity and expression of specific markers. Results: Mechanical stimulus induced ACKR2 production in periodontium. The expression of ACKR2 in vitro was mostly detected in mature osteoclasts and early-differentiated osteoblasts. Although ACKR2-/- mice exhibited regular phenotype in maxillary bone, the amount of OTM, osteoclasts counts and the expression of pro-resorptive markers were increased in this group. In contrast, the number of osteoblasts and related markers were decreased. OTM resulted in augmented expression of CC chemokines and receptors CCR5 and CCR1 in periodontium, which was higher in ACKR2-/- than WT mice. In vitro experiments demonstrated an augmented formation of osteoclasts and diminished differentiation of osteoblasts in ACKR2-/- mice. Conclusions: These data suggests that ACKR2 functions as a regulator of mechanically-induced bone remodeling by affecting the differentiation and activity of bone cells and the availability of CC chemokines at periodontal microenvironment. Therapeutic strategies based on increase of ACKR2 might be useful to hinder bone loss in inflammatory conditions.
local.identifier.orcidhttps://orcid.org/0000-0003-3870-8621
local.identifier.orcidhttps://orcid.org/0000-0001-9623-7835
local.identifier.orcidhttps://orcid.org/0000-0002-1473-7455
local.identifier.orcidhttps://orcid.org/0000-0002-2781-9986
local.identifier.orcidhttps://orcid.org/0000-0003-0938-9043
local.identifier.orcidhttps://orcid.org/0000-0002-5071-8382
local.identifier.orcidhttps://orcid.org/0000-0002-6944-3008
local.identifier.orcidhttps://orcid.org/0000-0002-1715-3834
local.identifier.orcidhttps://orcid.org/0000-0002-6589-4784
local.publisher.countryBrasil
local.publisher.departmentFAO - DEPARTAMENTO DE CLÍNICA
local.publisher.departmentICB - DEPARTAMENTO DE BIOQUÍMICA E IMUNOLOGIA
local.publisher.departmentICB - DEPARTAMENTO DE FARMACOLOGIA
local.publisher.departmentICB - DEPARTAMENTO DE FISIOLOGIA E BIOFÍSICA
local.publisher.departmentICB - DEPARTAMENTO DE MORFOLOGIA
local.publisher.initialsUFMG
local.url.externahttps://www.sciencedirect.com/science/article/abs/pii/S8756328217301618?via%3Dihub

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