Tenascin C upregulates interleukin-6 expression in human cardiac myofibroblasts<i>via</i>toll-like receptor 4

Maqbool, Azhar; Spary, Emma J.; Manfield, Iain W.; Ruhmann, Michaela; Zuliani-Alvarez, Lorena; Gamboa-Esteves, Filomena O; Porter, Karen E.; Drinkhill, Mark J.; Midwood, Kim S.; Turner, Neil A.

doi:10.4330/wjc.v8.i5.340

Cited by 38 publications

(23 citation statements)

References 56 publications

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“…The mechanistic role for TNC in organ transplantation remains to be fully determined; however, a role for TNC as a DAMP in allograft rejection and fibrosis is suggested by studies of cardiac remodeling, wherein TNC-deficient mice are protected against post-myocardial infarction fibrosis (77). Consistent with this observation, TNC augmented expression of proinflammatory cytokines and proteins important to tissue remodeling in cardiac myofibroblasts in a TLR4-dependent manner (78). Still other nontransplant models point to a potential role for TNC in mediating DC maturation and promoting Th17 immunity (79).…”

Section: Evolving Paradigms For Damps In Sotsupporting

confidence: 64%

Danger signals in regulating the immune response to solid organ transplantation

Todd¹,

Palmer²

2017

Journal of Clinical Investigation

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Section: Evolving Paradigms For Damps In Sotsupporting

confidence: 64%

Danger signals in regulating the immune response to solid organ transplantation

Todd¹,

Palmer²

2017

Journal of Clinical Investigation

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“…26 The most widely reported effect of TLR4 activation by tenascin-C is the induction of soluble proinflammatory mediators, such as interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF). This has been observed in a number of cell types, including macrophages, 13,18,21,22 dendritic cells (DCs), 17 fibroblasts, 13,20 and chondrocytes. 14 More recently, tenascin-C signaling through TLR4 has been implicated in inflammasome priming.…”

Section: The Proinflammatory Capabilities Of Tenascin-cmentioning

confidence: 96%

Internal Affairs: Tenascin-C as a Clinically Relevant, Endogenous Driver of Innate Immunity

Marzeda

Midwood

2018

J Histochem Cytochem.

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To protect against danger, the innate immune system must promptly and accurately sense alarm signals, and mount an appropriate response to restore homeostasis. One endogenous trigger of immunity is tenascin-C, a large hexameric protein of the extracellular matrix. Upregulated upon tissue injury and cellular stress, tenascin-C is expressed during inflammation and tissue remodeling, where it influences cellular behavior by interacting with a multitude of molecular targets, including other matrix components, cell surface proteins, and growth factors. Here, we discuss how these interactions confer upon tenascin-C distinct immunomodulatory capabilities that make this matrix molecule necessary for efficient tissue repair. We also highlight in vivo studies that provide insight into the consequences of misregulated tenascin-C expression on inflammation and fibrosis during a wide range of inflammatory diseases. Finally, we examine how its unique expression pattern and inflammatory actions make tenascin-C a viable target for clinical exploitation in both diagnostic and therapeutic arenas.

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“…Serum level of tenascin C (TNC) correlates with the severity of HF [ 67 ]. Maqbool et al [ 68 ] reported that TNC can stimulate TLR4 to upregulate the expression of IL-6, contributing to the worsening and progression of HF.…”

Section: Tlr Signaling and Hfmentioning

confidence: 99%

The Role of Toll-Like Receptor Signaling in the Progression of Heart Failure

Feng

2018

Mediators of Inflammation

112

103

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Medical systems worldwide are being faced with a growing need to understand mechanisms behind the pathogenesis of heart failure (HF) that is considered as a leading cause of morbidity and mortality around the world. Elevated levels of inflammatory mediators have been identified in patients with HF, which are primarily manifestations of innate immune responses mediated by pattern recognition receptors (PRRs). Toll-like receptors (TLRs), which belong to PRRs, are subjected to the release of pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) to generate innate immune responses. More and more emerging data indicate that TLR signaling pathway molecules are involved in the progression of HF. Herein, we present new data with regard to the activation of TLRs in the failing heart, focusing on TLR2, TLR3, TLR4, and TLR9, and suggest the potential use of TLRs in target therapy.

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Tenascin C upregulates interleukin-6 expression in human cardiac myofibroblastsviatoll-like receptor 4

Abstract: TNC up-regulates IL-6 expression in human CMF, an effect mediated through the FBG domain of TNC and via the TLR4 receptor.

Cited by 38 publications

References 56 publications

Danger signals in regulating the immune response to solid organ transplantation

Danger signals in regulating the immune response to solid organ transplantation

Internal Affairs: Tenascin-C as a Clinically Relevant, Endogenous Driver of Innate Immunity

The Role of Toll-Like Receptor Signaling in the Progression of Heart Failure

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