Expression of Wnt and Notch signaling pathways in inflammatory bowel disease treated with mesenchymal stem cell transplantation: evaluation in a rat model

Xing, Yanfen; Chen, Xiaojie; Cao, Yanwen; Huang, Jian; Xie, Xuhong; Wei, Yaming

doi:10.1186/s13287-015-0092-3

Cited by 31 publications

(29 citation statements)

References 32 publications

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“…Studies in a rat IBD model, in which the activation of Wnt/β-catenin signaling was observed, suggested that this activation may lead to the suppression of transplanted mesenchymal stem cells to differentiate into intestinal epithelium [47]. Wnt signaling components have been tested as potential markers for the diagnosis and treatment of IBD [48].…”

Section: Wnt/β-catenin Signaling In Spamentioning

confidence: 99%

Wnt/β-catenin Signaling in Osteoarthritis and in Other Forms of Arthritis

et al. 2017

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Purpose of Review Arthritis defines a large group of diseases primarily affecting the joint. It is the leading cause of pain and disability in adults. Osteoarthritis (OA) affecting the knee or hip is the most common form among over 100 types of arthritis. Other types of arthritis include erosive hand OA, tempo-romandibular joint (TMJ) OA, facet joint OA, diffuse idiopathic skeletal hyperostosis (DISH), and spondyloarthritis (SpA). However, the specific molecular signals involved in the development and progression of OA and related forms of arthritis remain largely unknown. The canonical wingless/integrated (Wnt)/β-catenin signaling pathway could play a unique role in the pathogenesis of arthritis. In this review article, we will focus on the molecular mechanisms of Wnt/β-catenin signaling in the pathogenesis of OA and other types of arthritis. Recent Findings Emerging evidence demonstrates that Wnts and Wnt-related molecules are involved in arthritis development and progression in human genetic studies and in vitro studies. Also, mouse models have been generated to determine the role of Wnt/β-catenin signaling in the pathogenesis of arthritis. Summary Wnt/β-catenin signaling represents a unique signaling pathway regulating arthritis development and progression, and the molecules in this particular pathway may serve as targets for the therapeutic intervention of arthritis. Mediators and downstream effectors of Wnt/β-catenin signaling are increased in OA as well other forms of arthritis, including DISH and SpA. Through extensive investigations, including pre-clinical studies in transgenic mice and translational and human studies, the Wnt/β-catenin signaling pathway has been proven to play roles in bone and joint pathology by directly affecting bone, cartilage, and synovial tissue; further, these pathologies can be reduced through targeting this pathway. Continued investigation into the distinct molecular signaling of the Wnt/β-catenin pathway will provide additional insights toward the therapeutic intervention in arthritis.

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Section: Wnt/β-catenin Signaling In Spamentioning

confidence: 99%

Wnt/β-catenin Signaling in Osteoarthritis and in Other Forms of Arthritis

et al. 2017

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“…Mesenchymal stem cell transplantation (MSCT) has been reported effective in the treatment of IBD as it can restore epithelial barrier integrity, induce immune suppression, and stimulate regeneration of endogenous host progenitor cells[ 74 - 78 ]. Mesenchymal stem cells can be engrafted into the damaged mucosa and even differentiated into colonic interstitial cells[ 79 ].…”

Section: Anti-inflammatory Therapeutic Aspects Of C-myc In the Colonmentioning

confidence: 99%

Therapeutic aspects of c-MYC signaling in inflammatory and cancerous colonic diseases

Sípos¹,

Firneisz²,

Műzes³

2016

WJG

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Colonic inflammation is required to heal infections, wounds, and maintain tissue homeostasis. As the seventh hallmark of cancer, however, it may affect all phases of tumor development, including tumor initiation, promotion, invasion and metastatic dissemination, and also evasion immune surveillance. Inflammation acts as a cellular stressor and may trigger DNA damage or genetic instability, and, further, chronic inflammation can provoke genetic mutations and epigenetic mechanisms that promote malignant cell transformation. Both sporadical and colitis-associated colorectal carcinogenesis are multi-step, complex processes arising from the uncontrolled proliferation and spreading of malignantly transformed cell clones with the obvious ability to evade the host’s protective immunity. In cells upon DNA damage several proto-oncogenes, including c-MYC are activated in parelell with the inactivation of tumor suppressor genes. The target genes of the c-MYC protein participate in different cellular functions, including cell cycle, survival, protein synthesis, cell adhesion, and micro-RNA expression. The transcriptional program regulated by c-MYC is context dependent, therefore the final cellular response to elevated c-MYC levels may range from increased proliferation to augmented apoptosis. Considering physiological intestinal homeostasis, c-MYC displays a fundamental role in the regulation of cell proliferation and crypt cell number. However, c-MYC gene is frequently deregulated in inflammation, and overexpressed in both sporadic and colitis-associated colon adenocarcinomas. Recent results demonstrated that endogenous c-MYC is essential for efficient induction of p53-dependent apoptosis following DNA damage, but c-MYC function is also involved in and regulated by autophagy-related mechanisms, while its expression is affected by DNA-methylation, or histone acetylation. Molecules directly targeting c-MYC, or agents acting on other genes involved in the c-MYC pathway could be selected for combined regiments. However, due to its context-dependent cellular function, it is clinically essential to consider which cytotoxic drugs are used in combination with c-MYC targeted agents in various tissues. Increasing our knowledge about MYC-dependent pathways might provide direction to novel anti-inflammatory and colorectal cancer therapies.

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“…Some studies examined the role of Wnt/␤-catenin pathway in AS related to IBD. [61][62][63] Xing et al 61 recently created a rat IBD model and found that canonical Wnt signaling was activated in rats with IBD, possibly leading to the suppression of mesenchymal stem cell transplants differentiating into intestinal epithelium. This research suggests that the canonical Wnt signaling pathway is activated to promote proliferation of intestinal stem cells in IBD.…”

Section: Wnt Signaling In Spa Associated With Ibdmentioning

confidence: 99%

Wnt/β‐catenin signaling plays a key role in the development of spondyloarthritis

Xie

Zhou

et al. 2015

Annals of the New York Academy of Sciences

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Spondyloarthritis (SpA) is a group of diseases consisting of psoriatic arthritis (PsA), reactive arthritis, arthritis related to inflammatory bowel disease (a subgroup of juvenile idiopathic arthritis), and ankylosing spondylitis (the prototype of SpA). Axial bone formation and the combination of concurrent erosion and new bone formation are specific characteristics of SpA disease. The use of anti-proinflammatory cytokines, such as inhibitors of tumor necrosis factor α (TNF-α), appears to be the greatest advance in the treatment of SpA over the past 20 years. However, TNF-α blockers do not halt new bone formation. Recent clinical observations and animal studies demonstrate that Wnt signaling proteins and natural Wnt inhibitors, such as DKK1 and sclerostin, are likely to play important roles in the process of ankylosis in SpA, and could potentially serve as therapeutic targets for the treatment of SpA.

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Expression of Wnt and Notch signaling pathways in inflammatory bowel disease treated with mesenchymal stem cell transplantation: evaluation in a rat model

Cited by 31 publications

References 32 publications

Wnt/β-catenin Signaling in Osteoarthritis and in Other Forms of Arthritis

Wnt/β-catenin Signaling in Osteoarthritis and in Other Forms of Arthritis

Therapeutic aspects of c-MYC signaling in inflammatory and cancerous colonic diseases

Wnt/β‐catenin signaling plays a key role in the development of spondyloarthritis

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