UC-MSCs or UC-MSC-derived CPCs injected into degenerated IVD
Improvement in the histology, cellularity, ECM proteins, water, and GAGs contents and higher expression of NP specific markers SOX9, ACAN, COL2, FOXF1, and KRT19 with CPCs
Improvement in the histology, cellularity, sulfated GAGs, and water contents of the NP. Expression of SOX9, ACAN, COL2, FOXF1, KRT19, PAX6, CA12, and COMP
UC-MSCs or UC-MSC-derived CPCs injected into degenerated IVD
Expression of chondrogenic markers and downregulation of pain and inflammatory genes. Differentiation of transplanted UC-MSCs and CPCs in functional NPCs. Better survival, homing, and distribution in IVD with CPCs.
Intra-articular injection of 50 or 100 μg/μL AM/UC particulate decellularized
Attenuation of cartilage destruction, significant increase in cartilage thickness and volume, significant decrease in total lesion area with high dose at 4 weeks postinjection
Intra-articular injection of UC-MSCs on days 1 and 3
Repair of cartilage and patella, improvement of the healing of the surrounding tissue, reduction of joint effusion and inflammation (reduction of TNF-α, IL-6, and IL-7 blood levels)
Chondrogenesis induction, upregulation of the expression of growth factors, ECM markers, and anti-inflammatory cytokines, and reduced expression of proinflammatory cytokines. Medium dose exerted the best effects
Single (day 1) or three (on days 1, 7 and 14) intra-articular injections of 2.5 x 105 UC-MSCs
Amelioration of cartilage erosion, alleviation of inflammatory cells infiltration and hyperplasia of the synovium by repeated injections. Increase number of SFCs on the articular cartilage surface
Intraperitoneal injection of UC-MSCs each day for 5 days
Reduction of the severity of RA, reduced levels of proinflammatory cytokines and chemokines (TNF-α, IL-6, and MCP-1) and increased levels of the anti-inflammatory cytokine (IL-10), Th1/Th2 type responses shifting and Tregs induction
Improvement arthritis, delay of radiological progression, and inhibition of synovial hyperplasia by downregulation of RORγt and upregulation of Foxp3 expression, inhibition of IL-17 and promotion of TGF-β expression, inhibition of proliferation and promotion of apoptosis in T lymphocytes and increased Tregs ratio
Ameliorate arthritis and inhibit synovial hyperplasia in a dose-dependent manner by inhibiting T lymphocyte proliferation and promoting their apoptosis, decreasing Th17 cell proportion and increasing that of Tregs, decreasing serum IL-17, and enhanced IL-10 and TGF-β expression, decreasing RORγt and increased FOXP3 expression
rabbit chondrocytes seeded in decellularized WJ-ECM scaffold inserted into the cartilage defects
All defects were filled completely with repaired tissue, and most of which were hyaline cartilage compared to WJ-ECM alone in which the defects filled partially with repaired tissue
WJ-MSCs seeded in ACECM-oriented scaffold implanted into the articular cartilage defect
The WJ-MSCs-ACECM scaffold complex achieved better quality repair and regeneration of hyaline cartilage compared to microfracture (predominant clinical treatment strategy for damaged cartilage)
WJ-MSCs and pACs mixed in 3 ratios: 100:0, 0:100 and 50:50 and seeded into ACECM-oriented scaffolds implanted into the articular cartilage defect
50:50 ratio was more similar to native cartilage and better integrated with the surrounding tissue, more abundant cartilage-specific content and significantly higher mechanical strength, no significant joint effusion or bone marrow edema signal. WJ-MSCs possessed low immunogenicity and escaped destruction by the immune system
WJ/CS composite scaffold loaded with UC-MSCs implanted into the articular cartilage defect
The composite scaffold loaded with UC-MSCs repaired cartilage defects better than did the WJ scaffold loaded with UC-MSCs. Both the scaffold and UC-MSCs showed low immunogenicity
undifferentiated or chondrogenically induced WJ-MSCs seeded in ECM of swine cartilage-derived scaffolds
Tissues repair observed over 16 months, with a hyaline-like neocartilage layer and regenerated subchondral bone. No immune rejection. WJ-MSCs were superior to those differentiated
Rat: 25 μg/mL of WJ-MSC exosomes injected in joint cavity (5 times, every 7 days) Rabbit: ACECM scaffold implanted into osteochondral defect with 25 μg/mL of WJ-MSCs exosomes injected in joint cavity, 5 times every 7 days
WJ-MSC exosomes enhance the effect of the ACECM scaffold and promote osteochondral regeneration, regulate the microenvironment of the articular cavity promoting the polarization of macrophages toward the M2 phenotype and inhibiting the inflammatory response. WJ-MSC exosomes contain many miRNAs that can promote the regeneration of hyaline cartilage
