Adiponectin enhances osteogenic differentiation in human adipose-derived stem cells by activating the APPL1-AMPK signaling pathway

Chen, Tong; Wu, Yuwei; Lu, Hui; Guo, Yuan; Tang, Zhihui

doi:10.1016/j.bbrc.2015.03.168

Cited by 49 publications

(43 citation statements)

References 23 publications

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“…ApN and AdipoR1 were discovered to be ubiquitously expressed in bone-forming cells 10 , indicating that ApN not only influences bone metabolism through its endocrine effects but also acts directly on bone-forming cells through its autocrine/paracrine effects 19, 23–26 . Chen et al .…”

Section: Discussionmentioning

confidence: 99%

“…Chen et al . found ApN can activate the APPL1-AMPK pathway to promote osteogenic differentiation in human adipose-derived stem cells 23 . Lee et al .…”

Section: Discussionmentioning

confidence: 99%

“…found that sustained ApN release can promote peri-implant osteogenesis in ovariectomization rabbits by suppressing osteoclasts 18 . ApN can increase bone mass by suppressing osteoclastogenesis and bone resorption 19, 20 , stimulating local angiogenesis 21, 22 , or promoting osteogenic differentiation 19, 23–27 . Several osteogenesis signalling pathways have been found to be activated in the presence of ApN; however, few studies have discussed the relevance of ApN and the Wnt/β-catenin pathway with respect to osteogenesis.…”

Section: Introductionmentioning

confidence: 99%

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Adiponectin regulates BMSC osteogenic differentiation and osteogenesis through the Wnt/β-catenin pathway

Wang

Zhang

Shao

et al. 2017

Sci Rep

101

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Recent studies have demonstrated the stimulatory effects of adiponectin on bone formation, but the mechanism underlying these effects remains unclear. The Wnt/β-catenin pathway, one of the most important pathways in osteogenesis, has rarely been associated with the osteogenic effects of adiponectin in previous studies. The present study was designed to investigate the effects of adiponectin on bone mesenchymal stem cell (BMSC) osteogenic differentiation and bone formation through the Wnt/β-catenin pathway. We detected adiponectin receptor expression in BMSCs, constructed a recombinant adenovirus containing the human adiponectin gene, and then used the adenovirus to transfect BMSCs in vitro or injected the adenovirus into bone defect areas in animal models. Wnt/β-catenin pathway and osteogenesis were detected by real-time PCR, western blotting, immunofluorescence, HE staining and micro-CT. In both our in vivo and in vitro experiments, we detected higher gene and protein expression levels of the Wnt/β-catenin pathway-related factors β-catenin and cyclinD1 in adiponectin transgenic BMSCs and rats. Similar results were noted regarding the gene and protein expression levels of osteogenesis-related genes. In addition, more new bone formation was observed in the adiponectin-treated groups. Our results indicate that adiponectin could facilitate BMSC osteogenic differentiation and osteogenesis, and the Wnt/β-catenin pathway was involved in the osteogenic effect of adiponectin.

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Section: Discussionmentioning

confidence: 99%

“…Chen et al . found ApN can activate the APPL1-AMPK pathway to promote osteogenic differentiation in human adipose-derived stem cells 23 . Lee et al .…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Adiponectin regulates BMSC osteogenic differentiation and osteogenesis through the Wnt/β-catenin pathway

Wang

Zhang

Shao

et al. 2017

Sci Rep

101

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“…AdipoR1 is more tightly linked to the activation of AMPK, p38-MAPK, JNK, peroxisome proliferator-activated receptor- (PPAR-) α , and nuclear factor- (NF-) k B pathways that regulate the inhibition of gluconeogenesis together with increased fatty acid oxidation, while AdipoR2 is more involved in the activation of the PPAR-pathways, which stimulate energy dissipation by increasing fatty acid oxidation and inhibit oxidative stress and inflammation. T-cadherin has also been reported as a receptor for high molecular multimers of adiponectin [63–68]. Adiponectin may attenuate TNF- α , IL-6, MCP-1, vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and endothelial-leukocyte adhesion molecule 1 (ELAM-1) expression, inflammation, oxidation, and fibrosis in AT through the inhibition of NF- k B activation [69–71].…”

Section: Adipokines and Their Receptorsmentioning

confidence: 99%

Adipokine Contribution to the Pathogenesis of Osteoarthritis

Azamar-Llamas

Hernández-Molina

Ramos-Ávalos

et al. 2017

Mediators of Inflammation

134

106

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Recent studies have shown that overweight and obesity play an important role in the development of osteoarthritis (OA). However, joint overload is not the only risk factor in this disease. For instance, the presence of OA in non-weight-bearing joints such as the hand suggests that metabolic factors may also contribute to its pathogenesis. Recently, white adipose tissue (WAT) has been recognized not only as an energy reservoir but also as an important secretory organ of adipokines. In this regard, adipokines have been closely associated with obesity and also play an important role in bone and cartilage homeostasis. Furthermore, drugs such as rosuvastatin or rosiglitazone have demonstrated chondroprotective and anti-inflammatory effects in cartilage explants from patients with OA. Thus, it seems that adipokines are important factors linking obesity, adiposity, and inflammation in OA. In this review, we are focused on establishing the physiological mechanisms of adipokines on cartilage homeostasis and evaluating their role in the pathophysiology of OA based on evidence derived from experimental research as well as from clinical-epidemiological studies.

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“…This is probably associated with the negative effect of adiponectin on the OPG/RANKL axis [37]. Some studies have suggested an effect of adiponectin on adipose-derived stem cells (hASCs) [38].…”

Section: Parametermentioning

confidence: 99%

Association Between Plasma Concentration of Klotho Protein, Osteocalcin, Leptin, Adiponectin, and Bone Mineral Density in Patients with Chronic Kidney Disease

et al. 2018

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Patients with early-stage chronic kidney disease (CKD) are susceptible to changes in metabolic processes. Partial loss of kidney function leads to homoeostatic disturbances in bone and fatty tissue. The aim of this study was to investigate the association between plasma concentrations of Klotho protein, FGF23, leptin, adiponectin, osteocalcin, and bone mineral density (BMD) in patients with CKD in the pre-dialysis period. The study involved 52 patients with CKD and 23 patients with no kidney disease. In both groups, BMD, body mass index and serum or plasma concentrations of lipids, glucose, creatinine, calcium, phosphorus, parathormone, leptin, adiponectin, osteocalcin, Klotho, and FGF23 were measured. The group with CKD had statistically significant higher concentrations of leptin (p<0.001), parathormone (p<0.001), and osteocalcin (p<0.001) in comparison with the control group. Patients with CKD also had statistically significant lower BMD in the femoral neck in comparison with the control group. Osteocalcin correlated negatively with BMD. The results of our study suggest that elevated osteocalcin is the most sensitive marker of decreased bone mass in patients with CKD. Osteocalcin correlated negatively with BMD and GFR. The loss of bone mass in CKD patients was greatest in the femoral neck.

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Adiponectin enhances osteogenic differentiation in human adipose-derived stem cells by activating the APPL1-AMPK signaling pathway

Cited by 49 publications

References 23 publications

Adiponectin regulates BMSC osteogenic differentiation and osteogenesis through the Wnt/β-catenin pathway

Adiponectin regulates BMSC osteogenic differentiation and osteogenesis through the Wnt/β-catenin pathway

Adipokine Contribution to the Pathogenesis of Osteoarthritis

Association Between Plasma Concentration of Klotho Protein, Osteocalcin, Leptin, Adiponectin, and Bone Mineral Density in Patients with Chronic Kidney Disease

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