Secreted frizzled-related protein 5 (SFRP5) protects ATDC5 cells against LPS-induced inflammation and apoptosis via inhibiting Wnt5a/JNK pathway

Sun, Ming‐Hui; Min, Lingtian; Chen, Cheng; Li, Qing; Weng, Wenjie

doi:10.1186/s13018-021-02260-5

Cited by 18 publications

(3 citation statements)

References 28 publications

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“…In this study, we showed that TNF-α upregulates the expression of Wnt5a through the MAPK-dependent NF-κB pathway. When Wnt5a is involved in the inflammatory process, it also activates the MAPK pathway (including ERK1/2, P38, JNK) and the NF-κB pathway [10,33]. Both the MAPK and NF-κB pathways are also involved in the upregulation of cytokine and chemokine expression [9,34].…”

Section: Discussionmentioning

confidence: 99%

Wnt5a Regulates Odontoblast Inflammation by Promoting CCL2 Expression

Ge¹,

Huang²,

Zhao³

et al. 2021

Preprint

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Objective Wnt5a is involved inflammation, including pulpitis, by upregulating cytokine/chemokine expression. Odontoblasts are the first layer cells in dental pulp and respond to inflammatory stimuli. However, whether Wnt5a is involved in odontoblast inflammation is unclear. This study aimed to investigate the role of Wnt5a in odontoblast inflammation. Methods We measured and compared Wnt5a- or TNF-α-induced cytokine/chemokine expression in mouse odontoblast-like (17IIA11) cells by real-time PCR and Western blotting. Transwell assays were used to examine the effect of Wnt5a on RAW264.7 macrophage migration. We examined whether the nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways were involved in the molecular mechanism of TNF-α or Wnt5a in 17IIA11 cells by Western blotting. Results TNF-α upregulated Wnt5a in odontoblasts. Wnt5a upregulated CCL2 expression in odontoblasts and enhanced RAW264.7 cell migration. We also found that TNF-α-induced Wnt5a expression was abrogated by inhibiting the MAPK pathway or NF-κB activity and that inhibiting MAPK activity could lead to decreased NF-κB activity. Conclusions Wnt5a is involved in the TNF-α-induced inflammatory response in odontoblasts. TNF-α upregulates Wnt5a expression via MAPK-dependent NF-κB activation in odontoblasts. Wnt5a upregulates CCL2 expression in odontoblasts and enhances RAW264.7 macrophage migration.

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Section: Discussionmentioning

confidence: 99%

Wnt5a Regulates Odontoblast Inflammation by Promoting CCL2 Expression

Ge¹,

Huang²,

Zhao³

et al. 2021

Preprint

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“…Sun et al studied the effect of Secreted frizzled-related protein 5 (SFRP5), an endogenous inhibitor of Wnt5a, on the inflammatory response of OA and found that overexpression of SFRP5 reduced the expression of inflammatory factors such as IL-1β, IL-6, TNF-α and ROS. Additionally, they demonstrated that SFRP5 attenuates LPS-induced OA inflammation and chondrocyte apoptosis through the Wnt5a/JNK pathway ( Sun et al, 2021 ).…”

Section: The Role Of Wnt Signaling In Cartilage Degenerationmentioning

confidence: 99%

Role of Wnt signaling pathway in joint development and cartilage degeneration

Li¹,

Han²,

Li³

et al. 2023

Front. Cell Dev. Biol.

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Osteoarthritis (OA) is a prevalent musculoskeletal disease that affects approximately 500 million people worldwide. Unfortunately, there is currently no effective treatment available to stop or delay the degenerative progression of joint disease. Wnt signaling pathways play fundamental roles in the regulation of growth, development, and homeostasis of articular cartilage. This review aims to summarize the role of Wnt pathways in joint development during embryonic stages and in cartilage maintenance throughout adult life. Specifically, we focus on aberrant mechanical loading and inflammation as major players in OA progression. Excessive mechanical load activates Wnt pathway in chondrocytes, resulting in chondrocyte apoptosis, matrix destruction and other osteoarthritis-related changes. Additionally, we discuss emerging Wnt-related modulators and present an overview of emerging treatments of OA targeting Wnt signaling. Ultimately, this review provides valuable insights towards discovering new drugs or gene therapies targeting Wnt signaling pathway for diagnosing and treating osteoarthritis and other degenerative joint diseases.

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“…The anti-inflammatory function of SFRP5 is exerted by the neutralization of c-Jun N-terminal kinases (JNK) in the downstream of the Wnt signaling pathway, to repress the production of inflammatory cytokines [162,166] (Figure 4). SFRP5 facilitates adipogenic differentiation and adipocyte expansion [167,168].…”

Section: Biological Actionsmentioning

confidence: 99%

The Role of Anti-Inflammatory Adipokines in Cardiometabolic Disorders: Moving beyond Adiponectin

Jung

2021

IJMS

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The global burden of obesity has multiplied owing to its rapidly growing prevalence and obesity-related morbidity and mortality. In addition to the classic role of depositing extra energy, adipose tissue actively interferes with the metabolic balance by means of secreting bioactive compounds called adipokines. While most adipokines give rise to inflammatory conditions, the others with anti-inflammatory properties have been the novel focus of attention for the amelioration of cardiometabolic complications. This review compiles the current evidence on the roles of anti-inflammatory adipokines, namely, adiponectin, vaspin, the C1q/TNF-related protein (CTRP) family, secreted frizzled-related protein 5 (SFRP5), and omentin-1 on cardiometabolic health. Further investigations on the mechanism of action and prospective human trials may pave the way to their clinical application as innovative biomarkers and therapeutic targets for cardiovascular and metabolic disorders.

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Secreted frizzled-related protein 5 (SFRP5) protects ATDC5 cells against LPS-induced inflammation and apoptosis via inhibiting Wnt5a/JNK pathway

Cited by 18 publications

References 28 publications

Wnt5a Regulates Odontoblast Inflammation by Promoting CCL2 Expression

Wnt5a Regulates Odontoblast Inflammation by Promoting CCL2 Expression

Role of Wnt signaling pathway in joint development and cartilage degeneration

The Role of Anti-Inflammatory Adipokines in Cardiometabolic Disorders: Moving beyond Adiponectin

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