Acta histochemica · 2022
TGFβ1-modified MSC-derived exosome attenuates osteoarthritis by inhibiting PDGF-BB secretion and H-type vessel activity in the subchondral bone.
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Wang Rui, Xu Bin
Аннотация
BACKGROUND: Greater bone resorption increases TGF-β1 release and nestin-positive BMSC recruitment to the subchondral bone marrow, leading to excessive subchondral osteophyte formation and severe wear to articular cartilage. Our previous research demonstrated that BMSCs-ExoTGF-β1 attenuated cartilage damage in osteoarthritis (OA) rats through carrying highly expressed miR-135b.
METHODS: The bone marrow mesenchymal stem cells (BMSCs) were isolated from mouse bone marrow, and BMSC-derived exosomes (BMSCs-Exo) were isolated from BMSCs. OA mouse models were established by anterior cruciate ligament transection (ACLT) surgery on the left knee of mice. Then we explored the therapeutic effect of BMSCs-ExoTGF-β1 on ACLT mice.
RESULTS: BMSCs-ExoTGF-β1 attenuated cartilage damage in OA mice in vivo by ameliorating articular cartilage degeneration and suppressing calcification of the cartilage zone. BMSCs-ExoTGF-β1 also inhibited osteoclastogenesis by suppressing the MAPK pathway in vitro. Micro-computed tomography indicated that BMSCs-ExoTGF-β1 impeded uncoupled subchondral bone remodeling. BMSCs-ExoTGF-β1 also reduced CD31hiEmcnhi vessel activity in the subchondral bone and attenuated OA pain behaviors.
CONCLUSIONS: In conclusion, BMSCs-ExoTGF-β1 maintains the microarchitecture, inhibits abnormal angiogenesis in subchondral bone and exerts protective effect against OA-induced pain and bone resorption on ACLT mice.
DATA AVAILABILITY: The datasets are available from the corresponding author on reasonable request.
METHODS: The bone marrow mesenchymal stem cells (BMSCs) were isolated from mouse bone marrow, and BMSC-derived exosomes (BMSCs-Exo) were isolated from BMSCs. OA mouse models were established by anterior cruciate ligament transection (ACLT) surgery on the left knee of mice. Then we explored the therapeutic effect of BMSCs-ExoTGF-β1 on ACLT mice.
RESULTS: BMSCs-ExoTGF-β1 attenuated cartilage damage in OA mice in vivo by ameliorating articular cartilage degeneration and suppressing calcification of the cartilage zone. BMSCs-ExoTGF-β1 also inhibited osteoclastogenesis by suppressing the MAPK pathway in vitro. Micro-computed tomography indicated that BMSCs-ExoTGF-β1 impeded uncoupled subchondral bone remodeling. BMSCs-ExoTGF-β1 also reduced CD31hiEmcnhi vessel activity in the subchondral bone and attenuated OA pain behaviors.
CONCLUSIONS: In conclusion, BMSCs-ExoTGF-β1 maintains the microarchitecture, inhibits abnormal angiogenesis in subchondral bone and exerts protective effect against OA-induced pain and bone resorption on ACLT mice.
DATA AVAILABILITY: The datasets are available from the corresponding author on reasonable request.