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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Titanium-enriched medium drives low profile of ECM remodeling as a pre-requisite to pre-osteoblast viability and proliferative phenotype

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Author(s):
da Costa Fernandes, Celio J. [1] ; Bezerra, Fabio J. B. [1] ; Souza, Bruno de Campos [1] ; Campos, Monica Aparecida [1] ; Zambuzzi, Willian Fernando [1, 2]
Total Authors: 5
Affiliation:
[1] Sao Paulo State Univ, UNESP, Biosci Inst, Dept Chem & Biochem, Campus Botucatu, Botucatu, SP - Brazil
[2] UNESP, IBB, Elect Microscopy, Botucatu, SP - Brazil
Total Affiliations: 2
Document type: Journal article
Source: JOURNAL OF TRACE ELEMENTS IN MEDICINE AND BIOLOGY; v. 50, p. 339-346, 2018.
Web of Science Citations: 4
Abstract

Titanium is widely used for biomedical applications, but little information is being delivered regarding the cellular/molecular mechanisms explaining their efficacy, mainly considering the effects of the Ti-released trace elements on pre-osteoblasts. We addressed this issue by investigating decisive intracellular signal transduction able to modulate cytoskeleton rearrangement, proliferative phenotype and extracellular matrix (ECM) remodeling. We considered titanium grades N and V, submitted or not to dual acid-etching (w/DAE or wo/DAE, respectively). Our results showed there is no cytotoxicity, preserving AKT involvement. Additionally, Ti-enriched medium promoted a diminution of the downstream signaling upon integrin activation (phosphorylating Rac1 and cofilin), guaranteeing a dynamic cytoskeleton rearrangement. Moreover, the low profile of ECM remodeling obtained in response to trace molecules released by Ti-based devices seems contributing to the osteoblast performance in mediating extracellular support to cell anchorage. This hypothesis was validated by the up-expression of beta 1-integrin, src and Focal adhesion kinase (fak) genes, mainly in response to titanium grade V. Proliferative phenotype showed an unbalance between cyclin-dependent kinases (CDKs) and p15(INK4b)/p21(CiP1). In conjunction, we showed for the first time that trace elements from Ti-based biomedical devices provoke important modulation of the osteoblast biology, driving cell anchoring, viability, and proliferative phenotype. Certainly, these biological outcomes compromise implant osseointegration. (AU)

FAPESP's process: 14/22689-3 - Microvesicle/proteins-mediated paracrine signaling among bone and endothelial cells during bone development and regeneration
Grantee:Willian Fernando Zambuzzi
Support Opportunities: Research Grants - Young Investigators Grants