Spinal cord injury (SCI) remains among the most challenging pathologies worldwide and has limited therapeutic possibilities and a very bleak prognosis. Biomaterials and stem cell transplantation are promising treatments for functional recovery in SCI. Seven patients with acute complete SCI diagnosed by a combination of methods were included in the study, and different lengths (2.0–6.0 cm) of necrotic spinal cord tissue were surgically cleaned under intraoperative neurophysiological monitoring. Subsequently, NeuroRegen scaffolds loaded with autologous bone marrow mononuclear cells (BMMCs) were implanted into the cleaned site. All patients participated in 6 months of rehabilitation and at least 3 years of clinical follow-up. No adverse symptoms associated with stem cell or functional scaffold implantation were observed during the 3-year follow-up period. Additionally, partial shallow sensory and autonomic nervous functional improvements were observed in some patients, but no motor function recovery was observed. Magnetic resonance imaging suggested that NeuroRegen scaffold implantation supported injured spinal cord continuity after treatment. These findings indicate that implantation of NeuroRegen scaffolds combined with stem cells may serve as a safe and promising clinical treatment for patients with acute complete SCI. However, determining the therapeutic effects and exact application methods still requires further study.

No abstract

Spinal supraspinous ligament (SL) osteogenesis is the key risk of ankylosing spondylitis (AS), with an unclear pathogenesis. We previously found that transforming growth factor β1 (TGF‐β1), bone morphogenetic proteins (eg BMP2) and type III TGF‐β1 receptor (TβRIII) expression were markedly up‐regulated in AS‐SLs. However, the roles of these closely related molecules in AS are unknown. Here, we showed that BMP2, TGF‐β1, TβRIII and S100A4 (a fibroblast marker) were abundant in active osteogenic AS‐SL tissues. In vitro, AS‐SL fibroblasts (AS‐SLFs) showed high BMP2, TGF‐β1 and TβRIII expression and auto‐osteogenic capacity. We further evaluated the role of TβRIII in the osteogenesis of normal SLFs. BMP2 combined with TGF‐β1 induced the osteogenesis of TβRIII‐overexpressing SLFs, but the activity was lost in SLFs upon TβRIII knockdown. Moreover, our data suggested that BMP2 combined with TGF‐β1 significantly activated both TGF‐β1/Smad signalling and BMP2/Smad/RUNX2 signalling to induce osteogenesis of SLFs with TβRIII up‐regulation. Furthermore, our multi‐strategy molecular interaction analysis approach indicated that TGF‐β1 presented BMP2 to TβRIII, sequentially facilitating BMP2 recognition by BMPR1A and promoting the osteogenesis of TβRIII‐overexpressing SLFs. Collectively, our results indicate that TGF‐β1 combined with BMP2 may participate in the osteogenic differentiation of AS‐SLF by acting on up‐regulated TβRIII, resulting in excessive activation of both TGF‐β1/Smad and BMP2/BMPR1A/Smad/RUNX2 signalling.