Research Spotlight | New Mechanism of Regulating Sensory Innervation In Bone

2020-11-21Author:adminpraise:0

The team of Professor Meriem Lamghari from Universidade do Porto recently reported the new mechanism of controlling sensory innervation in bone, indicating that the signaling profile associated with osteoblast phenotype differentiating program can regulate the patterning of sensory innervation, and also highlight osteoblast-derived Shh as an essential player in this cue-induced regulation.

Congratulations to researcher for publishing the latest articles in the top-level journal "Bone Research". It is a great honor for Elabscience's products to contribute to this great scientific research achievement. Elabscience is determined to be strict with itself and be the most loyal partner of scientific research scholars!

Fundamental Information

Title: Osteoblasts are inherently programmed to repel sensory innervation

Journal: Bone Research

IF11.508(2019)

Institution of the first author: Universidade do Porto, Portugal

Institution of the corresponding author: Universidade do Porto, Portugal

Elabscience® Products Cited:

Cat. No

Application

Detection target

Species

Tested sample

E-EL-H1274

ELISA

Human SEMA3A

Human

Cell culture media

ABSTRACT

Tissue innervation is a complex process controlled by the expression profile of signaling molecules secreted by tissue-resident cells that dictate the growth and guidance of axons. Sensory innervation is part of the neuronal network of the bone tissue with a defined spatiotemporal occurrence during bone development. Yet, the current understanding of the mechanisms regulating the map of sensory innervation in the bone tissue is still limited.

Here, we demonstrated that differentiation of human mesenchymal stem cells to osteoblasts leads to a marked impairment of their ability to promote axonal growth, evidenced under sensory neurons and osteoblastic-lineage cells crosstalk. The mechanisms by which osteoblast lineage cells provide this nonpermissive environment for axons include paracrine-induced repulsion and loss of neurotrophic factors expression.

We identified a drastic reduction of NGF and BDNF production and stimulation of Sema3A, Wnt4, and Shh expression culminating at late stage of OB differentiation. We noted a correlation between Shh expression profile, OB differentiation stages, and OB-mediated axonal repulsion. Blockade of Shh activity and signaling reversed the repulsive action of osteoblasts on sensory axons. Finally, to strengthen our model, we localized the expression of Shh by osteoblasts in bone tissue.

Overall, our findings provide evidence that the signaling profile associated with osteoblast phenotype differentiating program can regulate the patterning of sensory innervation, and highlight osteoblast-derived Shh as an essential player in this cue-induced regulation.

Highlights

1. This paper demonstrated that differentiation of human MSC to OB phenotype leads to marked impairment of their ability to promote axonal growth and creates a nonpermissive environment for the sensory nerve fibers through the paracrine-induced repulsion and loss of neurotrophic factors expression.

2. It was found that a drastic reduction of NGF and BDNF production and stimulation of Sema3A, Wnt4, and Shh expression culminating at late stage of OB differentiation

3. Osteoblast-derived Shh plays an essential role in this cue-induced regulation

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