ABSTRACT
BACKGROUND: In recent years, researchers discovered that menstrual blood-derived stem cells (MenSCs) have the potential to differentiate into a wide range of tissues including the chondrogenic lineage. In this study, we aimed to investigate the effect of MenSCs encapsulated in fibrin glue (FG) on healing of osteochondral defect in rabbit model. METHODS: We examined the effectiveness of MenSCs encapsulated in FG in comparison with FG alone in the repair of osteochondral defect (OCD) lesions of rabbit knees after 12 and 24 weeks. RESULTS: Macroscopical evaluation revealed that the effectiveness of MenSCs incorporation with FG is much higher than FG alone in repair of OCD defects. Indeed, histopathological evaluation of FG + MenSCs group at 12 weeks post-transplantation demonstrated that defects were filled with hyaline cartilage-like tissue with proper integration, high content of glycosaminoglycan and the existence of collagen fibers especially collagen type II, as well as by passing time (24 weeks post-transplantation), the most regenerated tissue in FG + MenSCs group was similar to hyaline cartilage with relatively good infill and integration. As the same with the result of 12 weeks post-implantation, the total point of microscopical examination in FG + MenSCs group was higher than other experimental groups, however, no significant difference was detected between groups at 24 weeks (p>0.05). CONCLUSION: In summary, MenSCs as unique stem cell population, is suitable for in vivo repair of OCD defects and promising for the future clinical application.
Subject(s)
Collagen , Collagen Type II , Fibrin Tissue Adhesive , Fibrin , Hyalin , Hyaline Cartilage , Knee , Stem CellsABSTRACT
Cartilage is an avascular, aneural, and alymphatic connective tissue with a limited capacity caused by low mitotic activity of its resident cells, chondrocytes. Natural repair of full thickness cartilage defects usually leads to the formation of fibrocartilage with lower function and mechanical force compared with the original hyaline cartilage and further deterioration can occur. Tissue engineering and regenerative medicine is a promising strategy to repair bone and articular cartilage defects and rehabilitate joint functions by focusing on the optimal combination of cells, material scaffolds, and signaling molecules. The unique physical and topographical properties of nano?brous structures allow them to mimic the extracellular matrix of native cartilage, making an appropriate resemblance to induce cartilage tissue regeneration and reconstruction. To improve simulation of native cartilage, the incorporation of nanofibrous scaffolds with suitable corresponsive cells could be effective. In this review article, an attempt was made to present the current state of cartilage tissue engineering using nanofibrous scaffolds and stem cells as high proliferative immune privilege cells with chondrogenic differentiation ability. The comprehensive information was retrieved by search of relevant subject headings in Medline/Pubmed and Elsevier databases
ABSTRACT
Background: It has been reported that secreted frizzled-related protein-4 known as an antagonist of Wnt signaling pathway plays a role in luteinization process of rodent granulosa cells. The purpose of this study was twofold: 1] to determine whether recombinant human secreted frizzled-related protein-4 [rhSFRP-4] could directly induce terminal differentiation of rat Granulosa Cells [GCs] and 2] to understand how the modulation of beta-catenin and Protein Kinase B [PKB]/AKT activity by exogenous SFRP-4 could be involved in steroidogenesis
Methods: GCs were firstly stimulated with Follicle-Stimulating Hormone [FSH] named as FSH-primed cells then were treated with luteinizing hormone [LH]. Then estradiol [E[2]] and progesterone [P[4]] production levels were assessed in the absence or presence of rhSFRP-4 treatment. The expression levels of activated beta-catenin, pAKTser[473], pGSK3 beta ser[9] were assessed by western blot or immuno-fluoresence
Results: In the presence of rhSFRP-4, there was 38% decreased E[2] levels compared to untreated FSH-primed cells [p<0.05], and P[4] production subsequently decreased. However, in GCs pre-treated with rhSFRP-4 prior to addition of FSH, P[4] levels increased 2-fold compared with untreated cells [p<0.05]. Unexpectedly, treatment with rhSFRP-4 prior to LH stimulation inhibited LH-induced P[4] secretion. Treatment with low [0.5 ng/ml] but not high [50 ng/ml] concentrations of rhSFRP-4 led to significantly increased levels of pGSK3 beta ser[9] [1.6-fold] and nuclear active beta-catenin [2.8-fold] in GCs compared with untreated cells. Interestingly, pre-treating GCs with rhsFPR4 prior to LH stimulation resulted in a 38% decrease in pAKTser[473] levels compared with those in LH-treated cells [p<0.05]
Conclusion: Taken together, our results showed that rhSFRP-4 could directly induce terminal differentiation in GCs via the modulation of beta-catenin and PKB/AKT pathways and that it does so in a dose-dependent manner