Diverse effects of type II collagen on osteogenic and adipogenic differentiation of mesenchymal stem cells

Chiu, Li Hsuan; Yeh, Tien Shun; Huang, Huei Mei; Leu, Sy Jye; Yang, Charng Bin; Tsai, Yu Hui

doi:10.1002/jcp.22976

Cited by 22 publications

(20 citation statements)

References 33 publications

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“…In turn, many of these characteristics have been shown previously to influence cellular responses to TGF-β3. For example, cellular responses to soluble growth factors can be modulated by insoluble environmental factors such as cell-matrix interactions [52-54] and substrate stiffness [55,56]. In the present study, Day 0 values (data not shown) demonstrated that CDM scaffolds possessed collagen and GAG compositions equivalent to native cartilage [57].…”

Section: Discussionmentioning

confidence: 57%

The effects of crosslinking of scaffolds engineered from cartilage ECM on the chondrogenic differentiation of MSCs

et al. 2013

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Scaffolds fabricated from cartilage extracellular matrix provide a chondroinductive environment that stimulates cartilaginous matrix synthesis in a variety of cell types. A limitation of these cartilage-derived matrix (CDM) scaffolds is that they contract during in vitro culture, which unpredictably alters their shape. The current study examined the hypothesis that collagen crosslinking techniques could inhibit cell-mediated contraction of CDM scaffolds. We analyzed the effects of dehydrothermal (DHT) treatment, ultraviolet light irradiation (UV), and the chemical crosslinker carbodiimide (CAR) on scaffold contraction and chondrogenic differentiation of adult human bone marrow-derived stem cells (MSCs). Both physical and chemical crosslinking treatments retained the original scaffold dimensions. DHT and UV treatments produced significantly higher glycosaminoglycan and collagen contents than CAR crosslinked and non-crosslinked constructs. Crosslinking treatments influenced the composition of newly synthesized matrix, and DHT treatment best matched the composition of native cartilage. DHT, UV, and non-crosslinked CDM films supported cell attachment, while CAR crosslinking inhibited cell adhesion. These results affirm that collagen crosslinking treatments can prevent cell-mediated contraction of CDM scaffolds. Interestingly, crosslinking treatments influence chondrogenic differentiation. These effects seem to be mediated by modifications to cell-matrix interactions between MSCs and the CDM; however, further work is necessary to elucidate a specific mechanism.

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Section: Discussionmentioning

confidence: 57%

The effects of crosslinking of scaffolds engineered from cartilage ECM on the chondrogenic differentiation of MSCs

et al. 2013

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“…Several studies have reported that human MSCs can be induced to enter the osteogenic differentiation pathway in the presence of type I extracellular matrix (ECM) proteins (Salasznyk et al, 2004;Kihara et al, 2006) and type II collagen stimulates (Chiu et al, 2012). COL4A4 was also up-regulated during osteogenic differentiation from rat bone marrow stromal cells (Kaur et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Identification of long non-coding RNA involved in osteogenic differentiation from mesenchymal stem cells using RNA-Seq data

Song¹,

Gu²,

Qian³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. The aim of this study was to identify long non-coding RNA (lncRNA) associated with osteogenic differentiation from mesenchymal stem cells (MSCs) using high-throughput RNA sequencing (RNA-Seq) data. RNA-Seq dataset was obtained from the European Bioinformatics Institute (accession No. PRJEB4496), including two replicates each for immortalized mesenchymal stem cells iMSC#3 cultured in growth medium (GM) and differentiation medium (DM) for 28 days. The clean reads were aligned to a hg19 reference genome by Tophat and assembled by Cufflinks to identify the known and novel transcripts. RPKM values were calculated to screen for differentially expressed RNA. Novel lncRNA were screened based on various filter criteria. Subsequently, the underlying function of novel lncRNAs were predicted by functional annotation by ERPIN, a coexpression network was constructed by WGCNA and the KEGG pathway enriched by KOBAS. A total of 3171 RNA differentially expressed between the DM and GM groups (2597 mRNA and 574 lncRNA) were identified. Among the 574 differentially expressed lncRNA, 357 were known and 217 were novel lncRNA. Furthermore, 32 novel lncRNA were found to be miRNA precursors (including miR-689, miR-640, miR-601, and miR-544). A total of 18269 ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (4): 18268-18279 (2015) Identifying lncRNA affecting osteogenic differentiation 14,275 co-expression relationships and 217 co-expression networks were obtained between novel lncRNA and mRNA. The differentially expressed lncRNA and mRNA were enriched into 6 significant pathways, including those for cancer, ECM-receptor interaction, and focal adhesion. Therefore, novel lncRNAwere identified and their underlying function predicted, which may provide the basis for future analyses of the role of lncRNA in osteoblastic differentiation.

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“…However, we are investigating this different phenotype in future work. What’s more, collagen type II is not the only structural material for the cartilage matrix; it can modulate chondrogenesis and osteogenesis as an extracellular signal molecule [39], [40], [41]. Therefore, alterations of signaling pathways regulating endochondral ossification in the growth plate caused by the ERS-UPR-apoptosis cascade and/or a lack of normal collagen may be a promising research direction.…”

Section: Discussionmentioning

confidence: 99%

Endoplasmic Reticulum Stress-Unfolding Protein Response-Apoptosis Cascade Causes Chondrodysplasia in a col2a1 p.Gly1170Ser Mutated Mouse Model

et al. 2014

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The collagen type II alpha 1 (COL2A1) mutation causes severe skeletal malformations, but the pathogenic mechanisms of how this occurs are unclear. To understand how this may happen, a col2a1 p.Gly1170Ser mutated mouse model was constructed and in homozygotes, the chondrodysplasia phenotype was observed. Misfolded procollagen was largely synthesized and retained in dilated endoplasmic reticulum and the endoplasmic reticulum stress (ERS)-unfolded protein response (UPR)-apoptosis cascade was activated. Apoptosis occurred prior to hypertrophy, prevented the formation of a hypertrophic zone, disrupted normal chondrogenic signaling pathways, and eventually caused chondrodysplasia. Heterozygotes had normal phenotypes and endoplasmic reticulum stress intensity was limited with no abnormal apoptosis detected. Our results suggest that earlier chondrocyte death was related to the ERS-UPR-apoptosis cascade and that this was the chief cause of chondrodysplaia. The col2a1 p.Gly1170Ser mutated mouse model offered a novel connection between misfolded collagen and skeletal malformation. Further investigation of this mouse mutant model can help us understand mechanisms of type II collagenopathies.

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Diverse effects of type II collagen on osteogenic and adipogenic differentiation of mesenchymal stem cells

Cited by 22 publications

References 33 publications

The effects of crosslinking of scaffolds engineered from cartilage ECM on the chondrogenic differentiation of MSCs

The effects of crosslinking of scaffolds engineered from cartilage ECM on the chondrogenic differentiation of MSCs

Identification of long non-coding RNA involved in osteogenic differentiation from mesenchymal stem cells using RNA-Seq data

Endoplasmic Reticulum Stress-Unfolding Protein Response-Apoptosis Cascade Causes Chondrodysplasia in a col2a1 p.Gly1170Ser Mutated Mouse Model

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