Determinants of stem cell lineage differentiation toward chondrogenesis versus adipogenesis

Abstract

Adult stem cells, also termed as somatic stem cells, are undifferentiated cells, detected among differentiated cells in a tissue or an organ. Adult stem cells can differentiate toward lineage specific cell types of the tissue or organ in which they reside. They also have the ability to differentiate into mature cells of mesenchymal tissues, such as cartilage, fat and bone. Despite the fact that the balance has been comprehensively scrutinized between adipogenesis and osteogenesis and between chondrogenesis and osteogenesis, few reviews discuss the relationship between chondrogenesis and adipogenesis. In this review, the developmental and transcriptional crosstalk of chondrogenic and adipogenic lineages are briefly explored, followed by elucidation of signaling pathways and external factors guiding lineage determination between chondrogenic and adipogenic differentiation. An in-depth understanding of overlap and discrepancy between these two mesenchymal tissues in lineage differentiation would benefit regeneration of high-quality cartilage tissues and adipose tissues for clinical applications.

Liver Kinase B1 Fine‐Tunes Lineage Commitment of Human Fetal Synovium‐Derived Stem Cells

“…In accordance with a recent hypothesis that there is crosstalk between chondrogenesis and adipogenesis, in this study, we found that the mRNA level of LKB1 decreased during chondrogenic or adipogenic differentiation of human fetal SDSCs, indicating that LKB1 might be involved in the determination of these two lineages. To confirm the role of LKB1 in the differentiation of MSCs, human fetal SDSCs were cultured in various differentiation media following the KO or OE of LKB1 .…”

Molecular and Lifestyle Factors Modulating Obesity Disease

“…Moreover, TGFβ and Hedgehog pathways can induce chondrogenesis and impair adipogenesis. Bone morphogenetic proteins signaling can promote either chondrogenesis or adipogenesis through the activation of Smad1/5/8 and p38 pathways [22]. Importantly, several chemical factors exert various effects on stem cells differentiation by affecting different pathways.…”

“…Importantly, several chemical factors exert various effects on stem cells differentiation by affecting different pathways. In fact, dexamethasone induces adipogenesis by means of C/EBPα factors whereas it can inhibit adipogenesis by upregulating RUNX2 expression [22]. Also biochemical and biophysical factors affect the crosstalk between chondrogenesis and adipogenesis through the activation of different signaling pathways.…”

“…Also biochemical and biophysical factors affect the crosstalk between chondrogenesis and adipogenesis through the activation of different signaling pathways. Specifically, these signals act by regulating master trascription factors such as SOX9 for chondrogenesis or C/EBPs and PPARγ for adipogenesis [22].…”

UHRF1 Promotes Proliferation of Human Adipose-Derived Stem Cells and Suppresses Adipogenesis via Inhibiting Peroxisome Proliferator-Activated Receptorγ

“…Adipose tissue-derived stem cells (ADSCs) possess two significant features, involving multipotential differentiation and self-renewal, and proliferation of ADSCs is complex, while that can be precisely controlled by a variety of physiological processes and regulatory molecules [3–7]. The process of adipogenesis is also regulated by several signaling pathways, such as transforming growth factor beta (TGF β ), Wnt, glycogen synthase kinase-3 β (GSK3 β ), and Notch signaling pathway [8, 9]. In addition, it has been reported that the peroxisome proliferator-activated receptor γ (PPAR γ ), cytidine-cytidine-adenosine-adenosine-thymidine (CCAAT)-enhancer-binding protein α (C/EBP α ), and sterol regulatory element-binding proteins (SREBPs) are important nucleus transcription factors, participating in adipogenesis [10].…”