SMAD7 prevents heterotopic ossification in a rat Achilles tendon injury model via regulation of endothelial-mesenchymal transition

The FEBS Journal
Chi ZhangCong-feng Luo

Abstract

The endothelial-mesenchymal transition (EndMT) is known to play a central role in the pathological process of heterotopic ossification (HO). Based on the ability of SMAD7 (mothers against decapentaplegic homolog 7) to block EndMT-related processes such as myofibroblast transformation, we hypothesized that SMAD7 may be a potential therapeutic target for HO. We constructed a lentivirus overexpressing SMAD7 and tested on rat aortic endothelial cells for optimal titre and transduction efficiency. The lentivirus was then injected into a surgical rat model of Achilles tendon injury. Expression of endothelial markers and mesenchymal markers at the injury sites was subsequently quantified by qPCR and western analysis. Lentiviral delivery of SMAD7 in vivo resulted in an upregulation of endothelial markers (CD31, VE-cadherin) and a downregulation of mesenchymal markers (N-cadherin and vimentin), suggesting that EndMT is blocked due to local SMAD7 overexpression. The difference is more apparent at 10 weeks than at 6 weeks after surgery. X-ray imaging and histological staining further confirmed the absence of ossified structure in the tendon tissue injected with SMAD7-delivering lentivirus, as opposed to the control groups. Post-surgical H...Continue Reading

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Jan 17, 2017·Tissue Engineering. Part B, Reviews·Sushmitha Durgam, Matthew Stewart
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Jul 1, 2021·Journal of Cellular and Molecular Medicine·Bing TuCunyi Fan

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