Effects of interleukin‐7/interleukin‐7 receptor on RANKL‐mediated osteoclast differentiation and ovariectomy‐induced bone loss by regulating c‐Fos/c‐Jun pathway

Zhao, Jijun; Zhaofeng, Wu; Yu, Yinghao; Cheng, Li

doi:10.1002/jcp.26548

Cited by 19 publications

(17 citation statements)

References 52 publications

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“…IL-7 is a cytokine important for B and T cell development, playing a central role in the homeostasis of the immune system. Its action is required, for example, for successful aging; however, the augmentation of IL-7 above normal levels may disrupt the immune balance [40]. Moreover, while IL-7 deficiency results in lymphopenia, overexpression of IL-7 can cause neoplasia in experimental models [41].…”

Section: Discussionmentioning

confidence: 99%

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Lanthionine, a Novel Uremic Toxin, in the Vascular Calcification of Chronic Kidney Disease: The Role of Proinflammatory Cytokines

Perna

Russo

D’Esposito

et al. 2021

IJMS

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Vascular calcification (VC) is a risk factor for cardiovascular events and mortality in chronic kidney disease (CKD). Several components influence the occurrence of VC, among which inflammation. A novel uremic toxin, lanthionine, was shown to increase intracellular calcium in endothelial cells and may have a role in VC. A group of CKD patients was selected and divided into patients with a glomerular filtration rate (GFR) of <45 mL/min/1.73 m2 and ≥45 mL/min/1.73 m2. Total Calcium Score (TCS), based on the Agatston score, was assessed as circulating lanthionine and a panel of different cytokines. A hemodialysis patient group was also considered. Lanthionine was elevated in CKD patients, and levels increased significantly in hemodialysis patients with respect to the two CKD groups; in addition, lanthionine increased along with the increase in TCS, starting from one up to three. Interleukin IL-6, IL-8, and Eotaxin were significantly increased in patients with GFR < 45 mL/min/1.73 m2 with respect to those with GFR ≥ 45 mL/min/1.73 m2. IL-1b, IL-7, IL-8, IL-12, Eotaxin, and VEGF increased in calcified patients with respect to the non-calcified. IL-8 and Eotaxin were elevated both in the low GFR group and in the calcified group. We propose that lanthionine, but also IL-8 and Eotaxin, in particular, are a key feature of VC of CKD, with possible marker significance.

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Section: Discussionmentioning

confidence: 99%

“…A vast amount of evidence is available on the interconnections between inflammation and alterations of calcium homeostasis in CKD [26,27,[31][32][33]37,40]. These alterations can be both adequately monitored and are indeed determinant of clinical symptoms and organ dysfunction [50,51].…”

Section: Discussionmentioning

confidence: 99%

Lanthionine, a Novel Uremic Toxin, in the Vascular Calcification of Chronic Kidney Disease: The Role of Proinflammatory Cytokines

Perna

Russo

D’Esposito

et al. 2021

IJMS

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“…A role for this cytokine as vaccine adjuvant has also been proposed [ 16 ]. Nevertheless, the augmentation of IL-7 above physiological levels may have a detrimental role disrupting the immunobalance [ 17 ]. Thus, the evidence in our population is that impaired renal clearance correlated with accumulation; whether this accumulation is detrimental or advantageous for the recovery of the disease needs deeper investigation.…”

Section: Discussionmentioning

confidence: 99%

Cytokine and Chemokine Retention Profile in COVID-19 Patients with Chronic Kidney Disease

Ciceri

Bono

Magagnoli

et al. 2022

Toxins

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Chronic kidney disease (CKD) patients are more susceptible to infections compared to the general population. SARS-CoV-2 virus pathology is characterized by a cytokine storm responsible for the systemic inflammation typical of the COVID-19 disease. Since CKD patients have a reduced renal clearance, we decided to investigate whether they accumulate harmful mediators during the COVID-19 disease. We conducted a retrospective study on 77 COVID-19 hospitalized subjects in the acute phase of the illness. Thirteen different cytokines were assessed in plasma collected upon hospitalization. The patients were divided into three groups according to their estimated glomerular filtration rate, eGFR < 30 (n = 23), 30 < eGFR < 60 (n = 33), eGFR > 60 mL/min (n = 21). We found that Tumor Necrosis Factor α and its receptors I and II, Interleukin-7, Leukemia Inhibitory Factor, FAS receptor, Chitinase 3-like I, and the Vascular Endothelial Growth Factor showed an increased accumulation that negatively correlate with eGFR. Moreover, non-survivor patients with an impaired kidney function have significantly more elevated levels of the same mediators. In conclusion, there is a tendency in COVID-19 ESRD patients to accumulate harmful cytokines. The accumulation seems to associate with mortality outcomes and may be due to reduced clearance but also to increased biosynthesis in most severe cases.

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“…In this study, we discovered that c-Fos expression at the mRNA and protein levels was distinctly downregulated following siMEF2C or SB239063 treatment. In addition to the role of p38/MEF2C in c-Fos expression, IL-7/IL-7R promotes RANKL-mediated osteoclast formation through c-Fos/c-Jun pathway (Zhao et al, 2018), while IL-6 affects the transforming rate from zygotes to blastocysts by impacting IL-6st, c-Fos, and c-Jun expression mainly through JAK-STAT signaling pathway (Yu et al, 2018). The investigation about IL-6 or JAK-STAT signaling pathway was not proceeded due to a limitation.…”

Section: Discussionmentioning

confidence: 99%

Administration of SB239063 Ameliorates Ovariectomy-Induced Bone Loss via Suppressing Osteoclastogenesis in Mice

et al. 2019

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Activation of osteoclast formation and function is crucial for the development of osteolytic diseases such as osteoporosis. RANKL (receptor activator of nuclear factor-κB ligand) activates NF-κB (nuclear factor κB), MAPK (mitogen-activated protein kinase), and NFATc1 (nuclear factor of activated T-cells, cytoplasmic 1) signaling pathways to induce osteoclastogenesis. In this study, we demonstrated that SB239063, a p38-specific inhibitor, suppressed osteoclastogenesis and bone resorption via inhibiting phosphorylation of MEF2C (myocyte enhancer factor 2C) and subsequently leading to MEF2C degradation by ubiquitination. Knockdown of MEF2C impaired osteoclast formation due to decreased c-Fos expression. Furthermore, MEF2C can directly bind to the promoter region of c-Fos to initiate its transcription. Interestingly, overexpression of either MEF2C or c-Fos can partially rescue the inhibitory effect of SB239063 on osteoclastogenesis. In addition, in vivo data proved that SB239063 also played a preventive role in both LPS (lipopolysaccharide)- and OVX (ovariectomy)-induced bone loss in mice. In conclusion, our results show that SB239063 can be a potential therapy for osteolytic diseases, and a novel p38/MEF2C/c-Fos axis is essential for osteoclastogenesis.

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Effects of interleukin‐7/interleukin‐7 receptor on RANKL‐mediated osteoclast differentiation and ovariectomy‐induced bone loss by regulating c‐Fos/c‐Jun pathway

Cited by 19 publications

References 52 publications

Lanthionine, a Novel Uremic Toxin, in the Vascular Calcification of Chronic Kidney Disease: The Role of Proinflammatory Cytokines

Lanthionine, a Novel Uremic Toxin, in the Vascular Calcification of Chronic Kidney Disease: The Role of Proinflammatory Cytokines

Cytokine and Chemokine Retention Profile in COVID-19 Patients with Chronic Kidney Disease

Administration of SB239063 Ameliorates Ovariectomy-Induced Bone Loss via Suppressing Osteoclastogenesis in Mice

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