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Abstract
The incidence of tendon re-tears post-surgery is an ever present complication. It is suggested that the application of biological factors, such as bone morphogenetic protein 7 (BMP-7), can reduce complication rates by promoting tenogenic characteristics in in vitro studies. However, there remains a dearth of information in regards to the mechanisms of BMP-7 signalling in tenocytes. Using primary human tenocyte-like cells (hTLCs) from the supraspinatus tendon the BMP-7 signalling pathway was investigated: induction of the BMP associated Smad pathway and non-Smad pathways (AKT, p38, ERK1/2 and JNK); alterations in gene expression of BMP-7 associated receptors, Smad pathway components, Smad target gene (ID1) and tenogenic marker scleraxis. BMP-7 increases the expression of specific BMP associated receptors, BMPR-Ib and BMPR-II, and Smad8. Additionally, BMP-7 activates significantly Smad1/5/8 and slightly p38 pathways as indicated by an increase in phosphorylation and proven by inhibition experiments, where p-ERK1/2 and p-JNK pathways remain mainly unresponsive. Furthermore, BMP-7 increases the expression of the Smad target gene ID1, and the tendon specific transcription factor scleraxis. The study shows that tenocyte-like cells undergo primarily Smad8 and p38 signalling after BMP-7 stimulation. The up-regulation of tendon related marker genes and matrix proteins such as Smad8/9, scleraxis and collagen I might lead to positive effects of BMP-7 treatment for rotator cuff repair, without significant induction of osteogenic and chondrogenic markers.
Highlights
High rates of re-tears or non-healing represent the common complications after surgical intervention to repair the rotator cuff tendons
Gene expression was evaluated by quantitative real time polymerase chain reaction
The present study shows for the first time that bone morphogenetic protein-7 (BMP-7) leads to an increase in phosphorylation of rSmads in human tenocyte-like cells (hTLCs)
Summary
High rates of re-tears or non-healing represent the common complications after surgical intervention to repair the rotator cuff tendons. There is a point of view that the investigation and optimisation of biological treatment strategies will reduce future rates of re-tears and non-healing post-surgery. One such biological strategy would be the application of growth factors, such as bone morphogenetic protein-7 (BMP-7), to improve the healing outcome after tendon surgery. The Smad pathway is initiated by binding of a BMP molecule to the receptor complex resulting in a phosphorylation of the receptor regulated Smad1/5/8 (rSmads). On the other hand the Smad-independent pathways are activated by phosphorylated BMP bound receptor complex[12] and act via Akt[16,17], Erk1/218,19, p3820,21, JNK18,22 and Rho/ROCK23 pathways
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