Visfatin alters the cytokine and matrix-degrading enzyme profile during osteogenic and adipogenic MSC differentiation

Tsiklauri, Lali; Werner, J.; Kampschulte, Marian; Frommer, Klaus; Berninger, L.; Irrgang, M.; Glenske, Kristina; Hose, Dirk; Khassawna, Thaqif El; Pons-Kühnemann, Jörn; Rehart, Stefan; Wenisch, Sabine; Müller‐Ladner, Ulf; Neumann, Elena

doi:10.1016/j.joca.2018.06.001

Cited by 33 publications

(23 citation statements)

References 47 publications

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“…Leptin enhanced bone growth and maturation by increasing osteoblast number and activity through the peripheral pathways (Turner et al, 2013). Visfatin impaired bone remodeling via both inducing the pro‐inflammatory factors and dysregulating the MMP/TIMP balance during MSCs differentiation (Tsiklauri et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Chemerin located in bone marrow promotes osteogenic differentiation and bone formation via Akt/Gsk3β/β‐catenin axis in mice

Zhang

Huang

et al. 2021

Journal Cellular Physiology

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Chemerin, a secreted protein mainly produced by adipocytes and hepatocytes, plays a variety of roles in endocrine or paracrine signaling. As reported in human epidemiology, chemerin was correlated with osteoporosis. And the previous in vitro study found that chemerin knockdown promoted osteogenesis and inhibited adipogenesis. However, the function of chemerin in bone metabolism and the underlying mechanism remains unclear. In this study, we uncovered the in vivo function of chemerin in bone homeostasis. We discovered that in obese mice, chemerin was increased in serum, while decreased in the bone marrow; and the chemerin expression in bone tissue was positively correlated with osteogenic genes. To further investigate the function of chemerin in bone metabolism, we generated chemerin deficiency and overexpression mice. We found bone mass and osteogenesis were decreased in chemerin deficiency mice, while were increased in chemerin overexpression mice. Furthermore, we observed that the chemerin expression increased during osteogenic differentiation of MSCs. Besides, we verified that chemerin promoted osteogenic differentiation in C3H10T1/2 cells and BMSCs through Akt/Gsk3β/β‐catenin axis. Treatment with Akt inhibitor (MK2206) abolished the promoting effect of chemerin on osteogenic differentiation and active β‐catenin. Together, our results suggest chemerin in bone marrow, not in serum, promotes osteogenic differentiation and bone formation via Akt/Gsk3β/β‐catenin axis. Chemerin may serve as a therapeutic strategy for osteoporosis.

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Section: Introductionmentioning

confidence: 99%

Chemerin located in bone marrow promotes osteogenic differentiation and bone formation via Akt/Gsk3β/β‐catenin axis in mice

Zhang

Huang

et al. 2021

Journal Cellular Physiology

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“…Li et al found that MSC lineage fate determination is affected by cell energy metabolism and revealed a possible mechanism for senile osteoporosis, indicating that visfatin may affect MSC differentiation into adipocytes or osteoblasts [ 30 ]. Furthermore, Lali et al found that IL-8 levels are significantly increased by visfatin during MSC differentiation, and these elevated levels induce the differentiation of human bone marrow cells into osteoclasts [ 31 ]. Apart from the effects on osteoblast proliferation and collagen synthesis, visfatin also plays a crucial role in osteoclast formation by inhibiting osteoclastogenesis, which indicates its role in osteophyte formation in the context of inflammatory diseases [ 20 , 32 ].…”

Section: Roles Of Visfatin In Oamentioning

confidence: 99%

An Update on the Emerging Role of Visfatin in the Pathogenesis of Osteoarthritis and Pharmacological Intervention

Han

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Osteoarthritis (OA) is one of the most common degenerative joint diseases that affects millions of people worldwide, mainly the aging population. Despite numerous published reports, little is known about the pathology of this disease, and no feasible treatment plan exists to stop OA progression. Recently, extensive basic and clinical studies have shown that adipokines play a key role in OA development. Moreover, some drugs associated with adipokines have shown chondroprotective and anti-inflammatory effects on OA. Visfatin has been shown to play a detrimental role in the progression of OA. It increases the production of matrix metalloproteinases and a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS), induces the production of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α, affects the differentiation of mesenchymal stem cells to adipocytes, and induces osteophyte formation by inhibiting osteoclastogenesis. Although some side effects of chemical visfatin inhibitors have been reported, they were shown to be successful in the treatment of diabetes, cancer, and other diseases that can utilize Chinese herbs, further suggesting that similar therapeutic strategies could be used in OA prevention and treatment. Here, we describe the pathophysiological mechanism of visfatin in OA and discuss some potential pharmacological interventions using Chinese herbs.

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“…Exogenous administration of visfatin can stimulate human leukocytes to produce IL-1β, TNF-α, and IL-6 [37], or induce the secretion of IL-6, IL-8, and MCP-1 during osteogenic and adipogenic differentiation of MSCs [38]. Visfatin may also activate HUVEC to up-regulate the expression of VEGF and MMPs [39].…”

Section: Visfatin-primed Adscs Promote Tumor Stemness and Emt Throughmentioning

confidence: 99%

Visfatin Mediates Malignant Behaviors through Adipose-Derived Stem Cells Intermediary in Breast Cancer

Huang

et al. 2019

Cancers

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Adipose-derived stem cells (ADSCs) have been implicated in tumor growth and metastasis in breast cancer. ADSCs exhibit tumor tropism, and are of increasing clinical relevance due to the autologous fat grafting for breast reconstruction. Although we have previously shown that a high level of the adipocytokine visfatin in human breast cancer tissues correlated with tumor progression mediated by cAbl and STAT3, the effects of visfatin in the tumor microenvironment are unclear. To understand how visfatin modulates breast cancer within the tumor-stromal environment, we examined determinants of breast cancer progression using a visfatin-primed ADSCs-tumor co-culture model. ADSCs were isolated from tumor-free adipose tissue adjacent to breast tumors. ADSCs were treated with or without visfatin for 48 h and then collected for co-culture with breast cancer cell line MDA-MB-231 for 72 h in a transwell system. We found that the MDA-MB-231 cells co-cultured with visfatin-treated ADSCs (vADSCs) had higher levels of cell viability, anchorage independent growth, migration, invasion, and tumorsphere formation than that co-cultured with untreated ADSCs (uADSCs). Growth differentiation factor 15 (GDF15) upregulation was found in the co-culture conditioned medium, with GDF15 neutralizing antibody blocking the promoting effect on MDA-MB-231 in co-culture. In addition, a GDF15-induced AKT pathway was found in MDA-MB-231Cancers 2020, 12, 29 2 of 18 and treatment with PI3K/AKT inhibitor also reversed the promoting effect. In an orthotopic xenograft mouse model, MDA-MB-231 co-injected with vADSCs formed a larger tumor mass than with uADSCs. Positive correlations were noted between visfatin, GDF15, and phosphor-AKT expressions in human breast cancer specimens. In conclusion, visfatin activated GDF15-AKT pathway mediated via ADSCs to facilitate breast cancer progression.

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Visfatin alters the cytokine and matrix-degrading enzyme profile during osteogenic and adipogenic MSC differentiation

Cited by 33 publications

References 47 publications

Chemerin located in bone marrow promotes osteogenic differentiation and bone formation via Akt/Gsk3β/β‐catenin axis in mice

Chemerin located in bone marrow promotes osteogenic differentiation and bone formation via Akt/Gsk3β/β‐catenin axis in mice

An Update on the Emerging Role of Visfatin in the Pathogenesis of Osteoarthritis and Pharmacological Intervention

Visfatin Mediates Malignant Behaviors through Adipose-Derived Stem Cells Intermediary in Breast Cancer

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