SATB2-Nanog axis links age-related intrinsic changes of mesenchymal stem cells from craniofacial bone

Zhou, Peipei; Wu, Geng; Zhang, Ping; Xu, Rongyao; Ge, Jie; Fu, Yu; Zhang, Yuchao; Du, Yifei; Ye, Jinhai; Cheng, Jie; Jiang, Hongbing

doi:10.18632/aging.101041

Cited by 22 publications

(26 citation statements)

References 44 publications

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“…Previous studies also demonstrated that decreased stemness and increased senescence are the primary causes of declines in osteogenic differentiation of BMSCs (Fehrer, & Lepperdinger, 2005; Zhou et al., 2016). In this study, we observed that the stemness and osteogenic differentiation of BMSCs were significantly reduced with increasing age, while the aging phenotype and adipogenic differentiation of aged BMSCs were markedly increased.…”

Section: Discussionmentioning

confidence: 99%

“…SATB2 is a target gene of miR‐31a‐5p, which has been proven by some prior studies (Aprelikova et al., 2010; Deng, Weng et al., 2013; Deng, Zhou et al., 2013). Our previous investigation has demonstrated that SATB2, as a transcriptional regulator, functions broadly (Dong et al., 2015) and is involved in osteogenic differentiation in age‐related BMSCs (Strickland, Wasserman, Giassi, Djordjevic, & Parra‐Herran, 2016; Zhou et al., 2016). Our results from both knockdown and gain‐of‐function approaches showed that miR‐31a‐5p inhibited osteogenic differentiation by negatively regulating SATB2 expression.…”

Section: Discussionmentioning

confidence: 99%

“…Our previous results also demonstrated that SATB2 improves the stemness capacity and osteogenic differentiation of aged human BMSCs (Zhou et al., 2016). In addition, miR‐31a‐5p has been reported to directly target bone relevant markers, such as RUNX2, OSX, and DKK1 (Baglio, Devescovi, Granchi, & Baldini, 2013; Deng, Wu et al., 2013; Gao et al., 2011; Lv et al., 2017).…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA‐31a‐5p from aging BMSCs links bone formation and resorption in the aged bone marrow microenvironment

et al. 2018

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The alteration of age‐related molecules in the bone marrow microenvironment is one of the driving forces in osteoporosis. These molecules inhibit bone formation and promote bone resorption by regulating osteoblastic and osteoclastic activity, contributing to age‐related bone loss. Here, we observed that the level of microRNA‐31a‐5p (miR‐31a‐5p) was significantly increased in bone marrow stromal cells (BMSCs) from aged rats, and these BMSCs demonstrated increased adipogenesis and aging phenotypes as well as decreased osteogenesis and stemness. We used the gain‐of‐function and knockdown approach to delineate the roles of miR‐31a‐5p in osteogenic differentiation by assessing the decrease of special AT‐rich sequence‐binding protein 2 (SATB2) levels and the aging of BMSCs by regulating the decline of E2F2 and recruiting senescence‐associated heterochromatin foci (SAHF). Notably, expression of miR‐31a‐5p, which promotes osteoclastogenesis and bone resorption, was markedly higher in BMSCs‐derived exosomes from aged rats compared to those from young rats, and suppression of exosomal miR‐31a‐5p inhibited the differentiation and function of osteoclasts, as shown by elevated RhoA activity. Moreover, using antagomiR‐31a‐5p, we observed that, in the bone marrow microenvironment, inhibition of miR‐31a‐5p prevented bone loss and decreased the osteoclastic activity of aged rats. Collectively, our results reveal that miR‐31a‐5p acts as a key modulator in the age‐related bone marrow microenvironment by influencing osteoblastic and osteoclastic differentiation and that it may be a potential therapeutic target for age‐related osteoporosis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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MicroRNA‐31a‐5p from aging BMSCs links bone formation and resorption in the aged bone marrow microenvironment

et al. 2018

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“…In vertebrate skeletogenesis, SATB2 has been implicated as a key component of a transcriptional network that regulates skeletal development and osteoblast differentiation (Dobreva et al, ; Zhao et al, ). Our previous results suggested that SATB2 plays a potential role in regulating the stemness, autophagy, and anti‐aging properties of craniofacial BMSCs (Dong et al, ; Zhou et al, ). Besides, estrogen has been reported that it inhibits senescence‐like phenotype in human mammary epithelial cells (Liu et al, ) and enhances osteogenesis in rat bone (Jagger, Chow, & Chambers, ).…”

Section: Introductionmentioning

confidence: 98%

Estrogen regulates stemness and senescence of bone marrow stromal cells to prevent osteoporosis via ERβ‐SATB2 pathway

Zhang

et al. 2017

Journal Cellular Physiology

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Decline of pluripotency in bone marrow stromal cells (BMSCs) associated with estrogen deficiency leads to a bone formation defect in osteoporosis. Special AT-rich sequence binding protein 2 (SATB2) is crucial for maintaining stemness and osteogenic differentiation of BMSCs. However, whether SATB2 is involved in estrogen-deficiency associated-osteoporosis is largely unknown. In this study, we found that estrogen mediated pluripotency and senescence of BMSCs, primarily through estrogen receptor beta (ERβ). BMSCs from the OVX rats displayed increased senescence and weaker SATB2 expression, stemness, and osteogenic differentiation, while estrogen could rescue these phenotypes. Inhibition of ERβ or ERα confirmed that SATB2 was associated with ERβ in estrogen-mediated pluripotency and senescence of BMSCs. Furthermore, estrogen mediated the upregulation of SATB2 through the induction of ERβ binding to estrogen response elements (ERE) located at -488 of the SATB2 gene. SATB2 overexpression alleviated senescence and enhanced stemness and osteogenic differentiation of OVX-BMSCs. SATB2-modified BMSCs transplantation could prevent trabecular bone loss in an ovariectomized rat model. Collectively, our study revealed the role of SATB2 in stemness, senescence, and osteogenesis of OVX-BMSCs. These results indicate that estrogen prevents osteoporosis by promoting stemness and osteogenesis, and inhibiting senescence of BMSCs through an ERβ-SATB2 pathway. Therefore, SATB2 is a novel anti-osteoporosis target gene.

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“…Because of this, iPSCs have a stronger ability to proliferate than differentiated cells and were predicted to be transferred into adult cells via parallel mathematical modeling and numerical simulation [26]. Studies have shown that in successfully induced stem cells with a differentiation potential, a number of embryonic stem cell protein markers such as NANOG, SSEA-3, SSEA-4, TRA-1-60 and TRA-1-81 are expressed [27-29], wherein SSEA-3 and SSEA-4 are cell membrane proteins, TRA-1-60 and TRA-1-81 are cytoplasmic proteins, and NANOG is a cell nuclear protein [30-32]. The iPSCs obtained in this study also expressed the above proteins, indicating that the iPSCs obtained in this study were similar to embryonic stem cells.…”

Section: Discussionmentioning

confidence: 99%

The Construction and Identification of Induced Pluripotent Stem Cells Derived from Acute Myelogenous Leukemia Cells

Zhu¹,

Chen²,

Chen³

et al. 2017

Cell Physiol Biochem

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Objective: The present study aimed to establish an induced pluripotent stem cell (iPSC) line from acute myelogenous leukemia (AML) cells in vitro and identify their biological characteristics. Methods: Cells from the AML-infiltrated skin from an M6 patient were infected with a lentivirus carrying OCT4, SOX2, KLF4 and C-MYC to induce iPSCs. The characteristics of the iPSCs were confirmed by alkaline phosphatase (ALP) staining. The proliferation ability of iPSCs was detected with a CCK-8 assay. The expression of pluripotency markers was measured by immunostaining, and the expression of stem cell-related genes was detected by qRT-PCR; distortion during the induction process was detected by karyotype analysis; the differentiation potential of iPSCs was determined by embryoid body-formation and teratoma-formation assays. ALP staining confirmed that these cells exhibited positive staining and had the characteristics of iPSCs. Results: The CCK-8 assay showed that the iPSCs had the ability to proliferate. Immunostaining demonstrated that iPSC clones showed positive expression of NANOG, SSEA-3, SSEA-4, TRA-1-60 and TRA-1-81. qRT-PCR results revealed that the mRNA expression of Nanog, Lin28, Cripto, FOX3, DNMT3b, DPPA2, and DPPA4 significantly increased in iPSCs. Karyotype analysis found no chromosome aberration in the iPSCs. The results of the embryoid body-formation and teratoma-formation assays indicated that the iPSCs had the potential to differentiate into all three germ layers. Conclusion: Our study provided evidence that an iPSC line derived from AML cells was successfully established.

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SATB2-Nanog axis links age-related intrinsic changes of mesenchymal stem cells from craniofacial bone

Cited by 22 publications

References 44 publications

MicroRNA‐31a‐5p from aging BMSCs links bone formation and resorption in the aged bone marrow microenvironment

MicroRNA‐31a‐5p from aging BMSCs links bone formation and resorption in the aged bone marrow microenvironment

Estrogen regulates stemness and senescence of bone marrow stromal cells to prevent osteoporosis via ERβ‐SATB2 pathway

The Construction and Identification of Induced Pluripotent Stem Cells Derived from Acute Myelogenous Leukemia Cells

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