Human amnion‐derived mesenchymal stem cells enhance the osteogenic differentiation of human adipose‐derived stem cells by promoting adiponectin excretion via the APPL1‐ERK1/2 signaling pathway. Issue 2 (11th September 2019)

• Record Type: Journal Article
• Authors: Wang, Yuli; Du, Yifei; Yuan, Hua; Pan, Yongchu; Wu, Jun; Du, Xin; Hao, Shushu; Yan, Zixin; Li, Xuan; Liu, Keyue; Xu, Fan
• Is Part Of: IUBMB life. Volume 72:Issue 2(2020)
• Page Start: 296
• Page End: 304
• Publication Date: 2019-09-11
• Subjects: adiponectin -- APPL1‐ERK1/2 signaling pathway -- human adipose‐derived stem cells -- human amnion‐derived mesenchymal stem cell -- osteogenic differentiation; Biochemistry -- Periodicals; Molecular biology -- Periodicals; 572.8
• DOI: 10.1002/iub.2165
• Languages: English
• ISSNs: 1521-6543

Abstract

Abstract: Human adipose‐derived stem cells (HASCs) represent pluripotent cells capable of differentiating into the bone tissue. Meanwhile, human amnion‐derived mesenchymal stem cells (HAMSCs) could cause mesenchymal stem cells to differentiate into the bone tissue. This work assessed the osteogenic effects exerted by HAMSCs on the potential of HASCs to form bone cells. Cell growth was evaluated flow‐cytometrically. Differentiation into osteoblasts and mineral formation were assessed by chromogenic alkaline phosphatase activity substrate assay and Alizarin red S staining. Adiponectin (APN), the adipocytokine secreted by adipocytes, was evaluated by enzyme‐linked immunosorbent assay. In this study, HAMSCs concentration‐dependently induced growth, osteoblastic differentiation, and APN excretion in HASCs. Mechanistically, immunofluorescence and immunoblot revealed HAMSCs promoted cytosolic translocation of leucine zipper motif (APPL1) from the nucleus and induced extracellular signaling‐regulated kinase 1/2 (ERK1/2) phosphorylation in HASCs. Furthermore, HAMSC effects were markedly blunted by pretreatment with APPL1 siRNA and U0126, an ERK1/2 signaling inhibitor with high selectivity. These results suggested that APN excretion is not suppressed by APPL1 knockdown in HASCs, but by ERK1/2 inhibition. These findings collectively indicate that HAMSCs induce the osteogenesis of HASCs by promoting APN excretion through APPL1‐ERK1/2 activation.