Preparation and characterization of amnion hydrogel and its synergistic effect with adipose derived stem cells towards IL1β activated chondrocytes

Abstract Inflammation leads to chondrocyte senescence and cartilage degeneration, resulting in osteoarthritis (OA). Adipose‐derived stem cells (ADSCs) exert paracrine effects protecting chondrocytes from degenerative changes. However, the lack of optimum delivery systems for ADSCs limits its use in the clinic. The use of extracellular matrix based injectable hydrogels has gained increased attention due to their unique properties. In the present study, we developed hydrogels from amnion tissue as a delivery system for ADSCs. We investigated the potential of amnion hydrogel to maintain ADSC functions, the synergistic effect of AM with ADSC in preventing the catabolic responses of inflammation in stimulated chondrocytes. We also investigated the role of Wnt/β-catenin signaling pathway in IL-1β induced inflammation in chondrocytes and the ability of AM-ADSC to inhibit Wnt/β-catenin signaling. Our results showed that AM hydrogels supported cell viability, proliferation, and stemness. ADSCs, AM hydrogels and AM-ADSCs inhibited the catabolic responses of IL-1β and inhibited the Wnt/β-catenin signaling pathway, indicating possible involvement of Wnt/β-catenin signaling pathways in IL-1β induced inflammation. The results also showed that the synergistic effect of AM-ADSCs was more pronounced in preventing catabolic responses in activated chondrocytes. In conclusion, we showed that AM hydrogels can be used as a potential carrier for ADSCs, and can be developed as a potential therapeutic agent for treating OA.

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The Role of the Extracellular Signal-Related Kinase Signaling Pathway in Osteogenic Differentiation of Human Adipose-Derived Stem Cells and in Adipogenic Transition Initiated by Dexamethasone

Tissue Engineering Part A ◽

10.1089/ten.tea.2009.0175 ◽

2009 ◽

Vol 15 (11) ◽

pp. 3487-3497 ◽

Cited By ~ 43

Author(s):

Qihai Liu ◽

Lian Cen ◽

Heng Zhou ◽

Shuo Yin ◽

Guangpeng Liu ◽

...

Keyword(s):

Stem Cells ◽

Osteogenic Differentiation ◽

Signaling Pathway ◽

Adipose Derived Stem Cells ◽

Kinase Signaling ◽

Extracellular Signal ◽

Kinase Signaling Pathway

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The Role of the Wnt Signaling Pathway in the Osteogenic Differentiation of Human Adipose-derived Stem Cells under Mechanical Stimulation

Journal of Hard Tissue Biology ◽

10.2485/jhtb.24.169 ◽

2015 ◽

Vol 24 (2) ◽

pp. 169-180

Author(s):

Hong-ming Du ◽

Li-ya Wang ◽

Xiao-hui Zheng ◽

Wei Tang ◽

Lei Liu ◽

...

Keyword(s):

Stem Cells ◽

Wnt Signaling ◽

Osteogenic Differentiation ◽

Signaling Pathway ◽

Mechanical Stimulation ◽

Wnt Signaling Pathway ◽

Adipose Derived Stem Cells

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Autophagy regulates the therapeutic potential of adipose-derived stem cells in LPS-induced pulmonary microvascular barrier damage

Cell Death and Disease ◽

10.1038/s41419-019-2037-8 ◽

2019 ◽

Vol 10 (11) ◽

Cited By ~ 3

Author(s):

Chichi Li ◽

Jingye Pan ◽

Lechi Ye ◽

Honglei Xu ◽

Beibei Wang ◽

...

Keyword(s):

Stem Cells ◽

Lung Injury ◽

Therapeutic Potential ◽

Microvascular Endothelial Cell ◽

Adipose Derived Stem Cells ◽

Protective Effects ◽

Paracrine Effects ◽

Autophagy Inhibition ◽

Lps Treatment

Abstract Adipose-derived stem cells (ADSCs) have been shown to be beneficial in some pulmonary diseases, and the paracrine effect is the major mechanism underlying ADSC-based therapy. Autophagy plays a crucial role in maintaining stem cell homeostasis and survival. However, the role of autophagy in mediating ADSC paracrine effects has not been thoroughly elucidated. We examined whether ADSCs participate in lipopolysaccharide (LPS)-induced pulmonary microvascular endothelial cell (PMVEC) barrier damage in a paracrine manner and illuminated the role of autophagy in regulating ADSC paracrine effects. PMVECs and ADSCs with or without autophagy inhibition were cocultured without intercellular contact, and the microvascular barrier function was assessed after LPS treatment. ADSC paracrine function was evaluated by detecting essential growth factors for endothelial cells. For in vivo experiments, ADSCs with or without autophagy inhibition were transplanted into LPS-induced lung-injury mice, and lung injury was assessed. ADSCs significantly alleviated LPS-induced microvascular barrier injury. In addition, ADSC paracrine levels of VEGF, FGF, and EGF were induced by LPS treatment, especially in the coculture condition. Inhibiting autophagy weakened the paracrine function and the protective effects of ADSCs on microvascular barrier injury. Moreover, ADSC transplantation alleviated LPS-induced lung injury, and inhibiting autophagy markedly weakened the therapeutic effect of ADSCs on lung injury. Together, these findings show that ADSC paracrine effects play a vital protective role in LPS-induced pulmonary microvascular barrier injury. Autophagy is a positive mediating factor in the paracrine process. These results are helpful for illuminating the role and mechanism of ADSC paracrine effects and developing effective therapies in acute lung injury.

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