Ghrelin protects against nucleus pulposus degeneration through inhibition of NF-κB signaling pathway and activation of Akt signaling pathway

Li, Weiwei; Wu, Xiaonan; Qu, Ruize; Wang, Wenhan; Chen, Xiaomin; Cheng, Lei; Liu, Yaoge; Guo, Linlin; Zhao, Yunpeng; Liu, Chao

doi:10.18632/oncotarget.19695

Cited by 15 publications

(31 citation statements)

References 59 publications

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“…It has been reported that ghrelin can affect many inflammatory diseases 31,32,46 , but it remains unknown whether ghrelin expression is associated with the development of contact dermatitis and psoriasis. In this study, we established mouse models of contact dermatitis and psoriasis using OXA and IMQ, respectively.…”

Section: Resultsmentioning

confidence: 99%

Ghrelin protects against contact dermatitis and psoriasiform skin inflammation by antagonizing TNF-α/NF-κB signaling pathways

Chen

et al. 2019

Sci Rep

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Contact dermatitis and psoriasis are skin disorders caused by immune dysregulation, yet much remains unknown about their underlying mechanisms. Ghrelin, a recently discovered novel peptide and potential endogenous anti-inflammatory factor expressed in the epidermis, is involved in skin repair and disease. In this study, we investigated the expression pattern and therapeutic effect of ghrelin in both contact dermatitis and psoriasis mouse models induced by oxazolone (OXA) and imiquimod (IMQ), respectively, and in TNF-α-stimulated RAW264.7 macrophages, NHEKs and skin fibroblasts. Ghrelin expression was reduced in both the OXA-induced contact dermatitis and IMQ-induced psoriasis mouse models. Furthermore, treatment with ghrelin attenuated skin inflammation in both the contact dermatitis and psoriasis mouse models. Mice administered PBS after OXA- or IMQ-induced model generation exhibited typical skin inflammation, whereas ghrelin treatment in these mouse models substantially decreased the dermatitis phenotype. In addition, exogenous ghrelin attenuated the inflammatory reaction induced by TNF-α in RAW264.7 cells. Moreover, ghrelin administration limited activation of NF-κB signaling. In summary, ghrelin may represent a potential molecular target for the prevention and treatment of inflammatory skin diseases, including contact dermatitis and psoriasis.

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Section: Resultsmentioning

confidence: 99%

Ghrelin protects against contact dermatitis and psoriasiform skin inflammation by antagonizing TNF-α/NF-κB signaling pathways

Chen

et al. 2019

Sci Rep

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“…Total RNA was extracted from the from knee joint articular cartilage or cultured primary chondrocytes of each experimental group using the RNeasy kit (Qiagen, Valencia, CA, USA) as previously reported [81], and first-strand cDNA was generated using the ImProm-II reverse transcription system (Qiagen, Valencia, CA). Real-time PCR was performed, with SYBR Green I dye used to monitor DNA synthesis.…”

Section: Methodsmentioning

confidence: 99%

Cortistatin binds to TNF-α receptors and protects against osteoarthritis

Zhao

et al. 2019

EBioMedicine

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Background Osteoarthritis (OA) is a common degenerative disease, and tumor necrosis factor (TNF-α) is known to play a critical role in OA. Cortistatin (CST) is a neuropeptide discovered over 20  years ago, which plays a vital role in inflammatory reactions. However, it is unknown whether CST is involved in cartilage degeneration and OA development. Methods The interaction between CST and TNF-α receptors was investigated through Coimmunoprecipitation and Biotin-based solid-phase binding assay. Western blot, Real-time PCR, ELISA, immunofluorescence staining, nitrite production assay and DMMB assay of GAG were performed for the primary chondrocyte experiments. Surgically induced and spontaneous OA models were established and western blot, flow cytometry, Real-time PCR, ELISA, immunohistochemistry and fluorescence in vivo imaging were performed for in vivo experiments. Findings CST competitively bound to TNFR1 as well as TNFR2. CST suppressed proinflammatory function of TNF-α. Both spontaneous and surgically induced OA models indicated that deficiency of CST led to an accelerated OA-like phenotype, while exogenous CST attenuated OA development in vivo. Additionally, TNFR1- and TNFR2-knockout mice were used for analysis and indicated that TNFRs might be involved in the protective role of CST in OA. CST inhibited activation of the NF-κB signaling pathway in OA. Interpretation This study provides new insight into the pathogenesis and therapeutic strategy of cartilage degenerative diseases, including OA. Fund The , the , .

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“…Insulin resistance, diabetes & obesity [11][12][13], rheumatoid arthritis [70], psoriasis [95], SLE [87], atherosclerosis [147] Systemic sclerosis with PAH [82], increased appetite [126] PAI- Alzheimer's [120] Insulin resistance &diabetes [11,12], hyperlipidemia [25], kidney failure [27,28], gestational diabetes [40], IVDD [48], rheumatoid arthritis& osteoarthritis [47,58], systemic sclerosis complications: PAH, DVT, PE, digital ulcers [76,77], SLE with renal involvement [87], psoriasis [92], Alzheimer's [118], major depression & bipolar [122,123], NAFLD&NASH [125], diabetic microvascular complications [154], atherosclerosis and cardiovascular disease [155], sepsis [162], acute pancreatitis [163]…”

Section: • Preeclampsiamentioning

confidence: 99%

“…Shi et al reported increased levels of visfatin in nucleus pulposus tissue in more severe IVDD grades than less severe grades [46]. Finally, ghrelin similarly is proved to have a role in nuclear pulposus degeneration [47]. Another study by Li and colleagues showed that resistin binds to toll-like receptor 4 (TLR4) that leads to an increase in chemokine ligands 4 (CCL4) expression in nucleus pulposus cells, causing macrophage infiltration [48].…”

Section: Adipocytokines and Rheumatologymentioning

confidence: 99%

Adipocytokines: Are they the Theory of Everything?

et al. 2020

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Introduction: Adipose tissue secretes various bioactive peptides/proteins, immune molecules and inflammatory mediators which are known as adipokines or adipocytokines. Adipokines play important roles in the maintenance of energy homeostasis, appetite, glucose and lipid metabolism, insulin sensitivity, angiogenesis, immunity and inflammation. Enormous number of studies from all over the world proved that adipocytokines are involved in the pathogenesis of diseases affecting nearly all body systems, which raises the question whether we can always blame adipocytokines as the triggering factor of every disease that may hit the body. Objective: Our review targeted the role played by adipocytokines in the pathogenesis of different diseases affecting different body systems including diabetes mellitus, kidney diseases, gynecological diseases, rheumatologic disorders, cancers, Alzheimer's, depression, muscle disorders, liver diseases, cardiovascular and lung diseases. Methodology: We cited more than 33 recent literature reviews that discussed the role played by adipocytokines in the pathogenesis of different diseases affecting different body systems. Conclusion: More evidence is being discovered to date about the role played by adipocytokines in more diseases and extra research is needed to explore hidden roles played by adipokine imbalance on disease pathogenesis.

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Ghrelin protects against nucleus pulposus degeneration through inhibition of NF-κB signaling pathway and activation of Akt signaling pathway

Cited by 15 publications

References 59 publications

Ghrelin protects against contact dermatitis and psoriasiform skin inflammation by antagonizing TNF-α/NF-κB signaling pathways

Ghrelin protects against contact dermatitis and psoriasiform skin inflammation by antagonizing TNF-α/NF-κB signaling pathways

Cortistatin binds to TNF-α receptors and protects against osteoarthritis

Adipocytokines: Are they the Theory of Everything?

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