Cells must alter their expression profiles and morphological characteristics but also reshape the extracellular matrix (ECM) to fulfill their functions throughout their lifespan. Matrix metalloproteinase 3 (MMP-3) is a member of the matrix metalloproteinase (MMP) family, which can degrade multiple ECM components. MMP-3 can activate multiple pro-MMPs and thus initiates the MMP-mediated degradation reactions. In this review, we summarized the function of MMP-3 and discussed its effects on biological activities. From this point of view, we emphasized the positive and negative roles of MMP-3 in the pathogenesis of disease and cell differentiation, highlighting that MMP-3 is especially closely involved in the occurrence and development of osteoarthritis. Then, we discussed some pathways that were shown to regulate MMP-3. By writing this review, we hope to provide new topics of interest for researchers and attract more researchers to investigate MMP-3.

Regenerative medicine represented by stem cell technology has become one of the pillar medical technologies for human disease treatment. Cytoskeleton plays important roles in maintaining cell morphology, bearing external forces, and maintaining the effectiveness of cell internal structure, among which cytoskeleton related proteins are involved in and play an indispensable role in the changes of cytoskeleton. PDLIM5 is a cytoskeleton-related protein that, like other cytoskeletal proteins, acts as a binding protein. PDZ and LIM domain 5 (PDLIM5), also known as ENH (Enigma homolog), is a cytoplasmic protein with a molecular mass of about 63 KDa that consists of a PDZ domain at the N-terminus and three LIM domains at the C-terminus. PDLIM5 binds to the cytoskeleton and membrane proteins through its PDZ domain and interacts with various signaling molecules, including protein kinases and transcription factors, through its LIM domain. As a cytoskeleton-related protein, PDLIM5 plays an important role in regulating cell proliferation, differentiation and cell fate decision in multiple tissues and cell types. In this review, we briefly summarize the state of knowledge on the PDLIM5 gene, structural properties, and molecular functional mechanisms of the PDLIM5 protein, and its role in cells, tissues, and organ systems, and describe the possible underlying molecular signaling pathways. In the last part of this review, we will focus on discussing the limitations of existing research and the future prospects of PDLIM5 research in turn.

BackgroundAdipose-derived stem cells (ASCs) that show multidifferentiation and anti-immune rejection capacities have been widely used in plastic and reconstructive surgery. Previous studies have indicated that mechanical and biophysical interactions between cells and their surrounding environment regulate essential processes, such as growth, survival, and differentiation, and the cytoskeleton system plays an important role in the mechanotransduction. However, the role of mechanical force in the determination of lineage fate is still unclear.MethodsHuman ASCs (hASCs) were obtained from three different donors by liposuction. Adipogenesis and osteogenesis were determined by Oil Red O and Alizarin Red staining, respectively. The mRNA levels of the cytoskeleton system, PPARγ, and C/EBPα were determined by real-time polymerase chain reaction (RT-PCR). The level of cytoskeleton, PPARγ, and C/EBPα protein levels were measured by Western blotting. The morphology of the cytoskeleton system during adipogenesis was observed with confocal microscopy. hASCs were transfected with a SUN2-specific shRNA to knockdown sun2, and a nontargeting shRNA was used as a control.ResultsWe found that disrupting the physiological balance between the cytoskeleton and the linker of the nucleoskeleton and cytoskeleton (LINC) complex (especially SUN2) could impact the adipogenesis of hASCs in vitro. Microtubule (MT) depolymerization with nocodazole (which interferes with the polymerization of MTs) increased the expression of SUN2 and PPARγ, while taxol (an inhibitor of MT disassembly) showed the opposite results. Meanwhile, hASCs with sun2 knockdown overexpressed MTs and decreased PPARγ expression, thereby inhibiting the adipogenesis. Furthermore, knockdown of sun2 changed the structure of perinuclear MTs.ConclusionsWe demonstrated the presence of cross-talk between MT and SUN2, and this cross-talk plays a critical role in the rebalance of the mechanical environment and is involved in the regulation of PPARγ transport during adipogenic differentiation of hASCs.Electronic supplementary materialThe online version of this article (10.1186/s13287-018-0836-y) contains supplementary material, which is available to authorized users.

The mechanisms underlying the osteogenic differentiation of human bone marrow mesenchymal stem cells (hBMSCs) remain unclear. In the present study, we aimed to identify the key biological processes during osteogenic differentiation. To this end, we downloaded three microarray data sets from the Gene Expression Omnibus (GEO) database: GSE12266, GSE18043 and GSE37558. Differentially expressed genes (DEGs) were screened using the limma package, and enrichment analysis was performed. Protein‐protein interaction network (PPI) analysis and visualization analysis were performed with STRING and Cytoscape. A total of 240 DEGs were identified, including 147 up‐regulated genes and 93 down‐regulated genes. Functional enrichment and pathways of the present DEGs include extracellular matrix organization, ossification, cell division, spindle and microtubule. Functional enrichment analysis of 10 hub genes showed that these genes are mainly enriched in microtubule‐related biological changes, that is sister chromatid segregation, microtubule cytoskeleton organization involved in mitosis, and spindle microtubule. Moreover, immunofluorescence and Western blotting revealed dramatic quantitative and morphological changes in the microtubules during the osteogenic differentiation of human adipose‐derived stem cells. In summary, the present results provide novel insights into the microtubule‐ and cytoskeleton‐related biological process changes, identifying candidates for the further study of osteogenic differentiation of the mesenchymal stem cells.

External volume expansion (EVE) is an effective method of adipose tissue regeneration. However, it remains unclear how EVE induces adipose tissue regeneration. In this study, we developed EVE devices to generate expanded prefabricated adipose tissue (EPAT) in rats and investigated cell proliferation, adipogenesis, and the expression of extracellular matrix (ECM) proteins during the 12 weeks suction. In addition, EPAT-generated decellularized adipose tissue (DAT) was used to assess the role of ECM proteins in cell proliferation and differentiation. Matrix deposition was significantly increased after EVE suction, with fibronectin and laminin showing the most dramatic changes. Fibronectin expression peaked during weeks 1-4, when Ki67 cells in EPAT peaked. Laminin expression peaked during weeks 8-12, when peroxisome proliferator-activated receptor-g expression also peaked. In vitro, adipose-derived stem cells (ASCs) displayed a higher proliferation rate in week 1 DAT, when fibronectin expression was highest, whereas ASC adipogenesis was significantly higher on week 12 DAT, when laminin expression was abundant. These results showed that EVE device enhanced ECM deposition, which is closely related to cell proliferation and differentiation.