IL-17A regulates autophagy and promotes osteoclast differentiation through the ERK/mTOR/Beclin1 pathway

Tang, Haojun; Zhu, Shida; Chen, Kai; Yuan, Shujie; Hu, Jun-zu; Wang, Hong-Kai

doi:10.1371/journal.pone.0281845

Cited by 8 publications

(10 citation statements)

References 31 publications

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“…128 A low concentration of IL-17A can inhibit the phosphorylation of ERK and mTOR, increase the expression of Beclin1, lead to the increase of autophagy of osteoclast precursors, reduce the apoptosis of osteoclast precursors, and promote osteoclast differentiation. 134 In addition, a low concentration of IL-17A can also promote the autophagy of osteoclast precursors by activating the RANKL-JNK pathway. 135 However, the effect of high concentrations on osteoclasts and osteoclast precursors is controversial.…”

Section: Il Familymentioning

confidence: 99%

“…A low concentration of IL‐17A can promote the differentiation of osteoclast precursors 133 and inhibit the apoptosis of osteoclast precursors derived from raw264.7 128 . A low concentration of IL‐17A can inhibit the phosphorylation of ERK and mTOR, increase the expression of Beclin1, lead to the increase of autophagy of osteoclast precursors, reduce the apoptosis of osteoclast precursors, and promote osteoclast differentiation 134 . In addition, a low concentration of IL‐17A can also promote the autophagy of osteoclast precursors by activating the RANKL‐JNK pathway 135 .…”

Section: Cytokines Of Immunology Play a Crucial Role In Osteoimmunolo...mentioning

confidence: 99%

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Exercise and osteoimmunology in bone remodeling

Zhao,

Du,

Yan

et al. 2024

The FASEB Journal

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Bones can form the scaffolding of the body, support the organism, coordinate somatic movements, and control mineral homeostasis and hematopoiesis. The immune system plays immune supervisory, defensive, and regulatory roles in the organism, which mainly consists of immune organs (spleen, bone marrow, tonsils, lymph nodes, etc.), immune cells (granulocytes, platelets, lymphocytes, etc.), and immune molecules (immune factors, interferons, interleukins, tumor necrosis factors, etc.). Bone and the immune system have long been considered two distinct fields of study, and the bone marrow, as a shared microenvironment between the bone and the immune system, closely links the two. Osteoimmunology organically combines bone and the immune system, elucidates the role of the immune system in bone, and creatively emphasizes its interdisciplinary characteristics and the function of immune cells and factors in maintaining bone homeostasis, providing new perspectives for skeletal‐related field research. In recent years, bone immunology has gradually become a hot spot in the study of bone‐related diseases. As a new branch of immunology, bone immunology emphasizes that the immune system can directly or indirectly affect bones through the RANKL/RANK/OPG signaling pathway, IL family, TNF‐α, TGF‐β, and IFN‐γ. These effects are of great significance for understanding inflammatory bone loss caused by various autoimmune or infectious diseases. In addition, as an external environment that plays an important role in immunity and bone, this study pays attention to the role of exercise‐mediated bone immunity in bone reconstruction.

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Section: Il Familymentioning

confidence: 99%

Section: Cytokines Of Immunology Play a Crucial Role In Osteoimmunolo...mentioning

confidence: 99%

Exercise and osteoimmunology in bone remodeling

Zhao,

Du,

Yan

et al. 2024

The FASEB Journal

View full text Add to dashboard Cite

show abstract

“…The target sequences were as follows: 5 0 -CCTAAGGTTAAGTCGCCCTCG-3 0 (snc) and 5 0 -CCCAAATTCTGAGGACAAGAA-3 0 (si). siRNAs were transfected into A549 cells using Lipofectamine 3000 reagent (Thermo Fisher Scientific, Waltham, MA, USA), following the manufacturer's instructions [11].…”

Section: Rna Interferencementioning

confidence: 99%

“…In addition, many studies showed that IL-17A affects bone remodeling [9,10]. Exogenous IL-17A affects autophagy in osteoclast precursors (OCPs), thus affecting osteoclast differentiation [11]. Apoptosis refers to programmed cell death that occurs during development or under the influence of specific factors [12].…”

Section: Introductionmentioning

confidence: 99%

IL-17A deficiency inhibits lung cancer-induced osteoclastogenesis by promoting apoptosis of osteoclast precursor cells

Wang,

Tang,

Yuan

et al. 2024

PLoS ONE

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Osteoclasts are crucial in the events leading to bone metastasis of lung cancer. Interleukin-17A (IL-17A) affects osteogenesis by regulating the survival of osteoclast precursors (OCPs) and is enriched in lung cancer cells. However, how factors derived from tumor cells that metastasize to bone affect osteoclastogenesis remains poorly understood. We examined whether IL-17A derived from lung cancer cells affects osteoclast differentiation by regulating OCP apoptosis. IL-17A expression was inhibited in A549 non-small cell lung cancer cells using RNA interference. Compared with conditioned medium (CM) from A549 cells (A549-CM), CM from IL-17A-deficient A549 cells (A549-si-CM) suppressed osteoclastogenesis. The mRNA expression of osteoclast-specific genes was downregulated following A549-si-CM treatment. Furthermore, A549-si-CM promoted osteoclast precursor apoptosis at an early stage of osteoclastogenesis, which was related to the promotion of caspase-3 expression by A549-si-CM during osteoclast differentiation. In vivo experiments also showed that inhibition of IL-17A expression in A549 cells reduced osteoclast activation and bone tissue destruction. Collectively, our results indicate that IL-17A deficiency inhibits lung cancer-induced osteoclast differentiation by promoting apoptosis of osteoclast precursors in the early stage of osteoclast formation and that IL-17A is a potential therapeutic target for cancer-associated bone resorption in patients with lung cancer.

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“…Interleukin-17A (IL-17A) can promote the differentiation of OCs precursors into OCs, inhibit the phosphorylation of extracellular regulated kinase (ERK) to increase the expression of Beclin-1, enhance the autophagy activity of OCs precursors through the ERK/mTOR/Beclin1 pathway, and promote OCs differentiation. 107 Chung et al found that knockout of Beclin-1 inhibited RANKL-mediated activation of JNK and p38, thereby inhibiting the expression of OCs-specific gene NFATc1. 108 In vitro, autophagy is activated during RANKL-induced OCs differentiation and requires TRAF6-mediated Beclin-1 ubiquitination, and Beclin-1 knockout mice exhibit impaired OCs bone resorption and thickened bone cortex.…”

Section: Signaling Pathways Involved In Autophagy In Obs and Ocsmentioning

confidence: 99%

The Potential of Natural Compounds Regulating Autophagy in the Treatment of Osteoporosis

Zhao,

Qu,

Zhao

et al. 2023

JIR

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The maintenance of bone homeostasis is dynamically regulated by osteoblast-mediated bone formation and osteoclast-mediated bone resorption. Abnormal differentiation of osteoclast and insufficient osteoblast production can cause bone diseases such as osteoporosis. As one of the highly conserved catabolic pathways in eukaryotic cells, autophagy plays an important role in maintaining cell homeostasis, stress injury repair, proliferation and differentiation. Numerous studies have found that autophagy activity is essential for the survival, differentiation and function of bone cells, and that regulation of autophagy can affect the metabolism of osteoblasts and osteoclasts, thus affecting bone homeostasis. Therefore, using autophagy as a theme, this review outlines the basic process of autophagy, the relationship between autophagy and osteoblasts and osteoclasts, and summarizes the latest research progress of common autophagic signaling pathways in osteoblasts and osteoclasts. The regulatory effects of protein molecules and natural compounds on the autophagy pathway of osteoblasts and osteoclasts discovered in current research are summarized and discussed. This will help to further clarify the mechanism of osteoporosis, understand the relationship between autophagy and osteoporosis, and propose new therapeutic strategies and new ideas for anti-osteoporosis.

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IL-17A regulates autophagy and promotes osteoclast differentiation through the ERK/mTOR/Beclin1 pathway

Cited by 8 publications

References 31 publications

Exercise and osteoimmunology in bone remodeling

Exercise and osteoimmunology in bone remodeling

IL-17A deficiency inhibits lung cancer-induced osteoclastogenesis by promoting apoptosis of osteoclast precursor cells

The Potential of Natural Compounds Regulating Autophagy in the Treatment of Osteoporosis

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