Leptin‐induced migration and angiogenesis in rheumatoid arthritis is mediated by reactive oxygen species

Sun, Xiaotong; Wei, Jing; Tang, Yawei; Wang, Bing; Zhang, Yan; Shi, Lei; Guo, Jianping; Hu, Fanlei; Li, Xia

doi:10.1002/2211-5463.12326

Cited by 29 publications

(18 citation statements)

References 37 publications

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“…Leptin, a hormone secreted by adipose tissue, has been observed to play an important role in both autoimmune and inflammatory rheumatic diseases. Leptin can induce ROS formation and aid in inflammation by causing angiogenesis, while inhibition of this hormone could be a therapeutic treatment in RA to decrease angiogenesis and thereby infiltration as well (Table 1) [97].…”

Section: Inflammaging In Rheumatoid Arthritis (Ra)mentioning

confidence: 99%

Inflammaging and Oxidative Stress in Human Diseases: From Molecular Mechanisms to Novel Treatments

Zuo

Stetskiv

et al. 2019

IJMS

360

201

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It has been proposed that a chronic state of inflammation correlated with aging known as inflammaging, is implicated in multiple disease states commonly observed in the elderly population. Inflammaging is associated with over-abundance of reactive oxygen species in the cell, which can lead to oxidation and damage of cellular components, increased inflammation, and activation of cell death pathways. This review focuses on inflammaging and its contribution to various age-related diseases such as cardiovascular disease, cancer, neurodegenerative diseases, chronic obstructive pulmonary disease, diabetes, and rheumatoid arthritis. Recently published mechanistic details of the roles of reactive oxygen species in inflammaging and various diseases will also be discussed. Advancements in potential treatments to ameliorate inflammaging, oxidative stress, and consequently, reduce the morbidity of multiple disease states will be explored.

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Section: Inflammaging In Rheumatoid Arthritis (Ra)mentioning

confidence: 99%

Inflammaging and Oxidative Stress in Human Diseases: From Molecular Mechanisms to Novel Treatments

Zuo

Stetskiv

et al. 2019

IJMS

360

201

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“…Resistin promotes endothelial progenitor cell (EPC) homing into the synovium during RA angiogenesis via a signal transduction pathway involving VEGF expression in primary EPCs [ 22 ]. Others suggest that it may be useful to inhibit leptin in RA disease, as leptin promotes RA FLS migration by increasing reactive oxygen species (ROS) expression [ 23 ]. Leptin is also capable of enhancing HUVEC tube formation in a ROS/HIF-1α-dependent manner, and promoting production of VEGF and IL-6 in RA FLS.…”

Section: Cytokines Show Angiogenic Activitymentioning

confidence: 99%

Implications of Angiogenesis Involvement in Arthritis

MacDonald

Liu

et al. 2018

IJMS

160

117

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Angiogenesis, the growth of new blood vessels, is essential in the pathogenesis of joint inflammatory disorders such as rheumatoid arthritis (RA) and osteoarthritis (OA), facilitating the invasion of inflammatory cells and increase in local pain receptors that contribute to structural damage and pain. The angiogenic process is perpetuated by various mediators such as growth factors, primarily vascular endothelial growth factor (VEGF) and hypoxia-inducible factors (HIFs), as well as proinflammatory cytokines, various chemokines, matrix components, cell adhesion molecules, proteases, and others. Despite the development of potent, well-tolerated nonbiologic (conventional) and biologic disease-modifying agents that have greatly improved outcomes for patients with RA, many remain resistant to these therapies, are only partial responders, or cannot tolerate biologics. The only approved therapies for OA include symptom-modifying agents, such as analgesics, non-steroidal anti-inflammatory drugs (NSAIDs), steroids, and hyaluronic acid. None of the available treatments slow the disease progression, restore the original structure or enable a return to function of the damaged joint. Moreover, a number of safety concerns surround current therapies for RA and OA. New treatments are needed that not only target inflamed joints and control articular inflammation in RA and OA, but also selectively inhibit synovial angiogenesis, while preventing healthy tissue damage. This narrative review of the literature in PubMed focuses on the evidence illustrating the therapeutic benefits of modulating angiogenic activity in experimental RA and OA. This evidence points to new treatment targets in these diseases.

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“…Therefore, the role of AQP5 in tumor vascularisation was investigated using HUVECs. These cells exhibit the ability to grow and form tube-like structures, depending on the growth factors contained in the supernatant (22). HUVECs were treated with the supernatant of NC cultures as control medium (Fig.…”

Section: Downregulation Of Aqp5 Inhibits Angiogenesis and Decreases Amentioning

confidence: 99%

Aquaporin 5 promotes tumor migration and angiogenesis in non‑small cell lung cancer cell line H1299

et al. 2020

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Non-small cell lung cancer (NSCLC) constitutes the majority of all lung-cancer cases. Aquaporin 5 (AQP5) may be involved in NSCLC by promoting lung-cancer initiation and progression. The present study aimed to determine the role of AQP5 in migration and angiogenesis using NSCLC cells and HUVECs. AQPs 1, 3, 4, 5, 8 and 9 were screened in the NSCLC cell line H1299, and the present results showed that AQP5 mRNA was upregulated compared with the other AQP genes. At the protein level, AQP5 was significantly increased in H1299 cells compared with 16HBE cells. AQP5 knockdown in H1299 cells significantly decreased cell migration compared with untransfected cells, as demonstrated by both Transwell and wound closure assays. The present study further investigated H1299 ability to promote HUVEC vascularisation. The supernatants of both transfected and untransfected H1299 cells were used as conditioned medium for HUVECs, and tube formation was measured. The supernatant of AQP5-downregulated cells exhibited significantly low tube formation potential compared with untransfected cells. Similarly, vascular endothelial growth factor was significantly increased in control cells (si-NC) compared with cells transfected with small interfering RNA targeting AQP5. The present study found that AQP5 downregulation significantly decreased the phosphorylation level of epidermal growth factor receptor and the activity of the ERK1/2 pathway. In summary, the present study suggested that AQP5 influenced migration and angiogenesis in NSCLCs in vitro and may potentially exhibit similar in vivo effects.

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Leptin‐induced migration and angiogenesis in rheumatoid arthritis is mediated by reactive oxygen species

Cited by 29 publications

References 37 publications

Inflammaging and Oxidative Stress in Human Diseases: From Molecular Mechanisms to Novel Treatments

Inflammaging and Oxidative Stress in Human Diseases: From Molecular Mechanisms to Novel Treatments

Implications of Angiogenesis Involvement in Arthritis

Aquaporin 5 promotes tumor migration and angiogenesis in non‑small cell lung cancer cell line H1299

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