Matrix protein tenascin-C expands and reversibly blocks maturation of murine eosinophil progenitors

Doan, Ton C.; Jeong, Brian M.; Coden, Mackenzie E.; Loffredo, Lucas F.; Bhattacharyya, Swati; Chiarella, Sergio E.; Varga, John; Abdala‐Valencia, Hiam; Berdnikovs, Sergejs

doi:10.1016/j.jaci.2018.02.054

Cited by 9 publications

(11 citation statements)

References 22 publications

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“…Integrin α9β1 is known to play other potentially important roles in eosinophils. For example, eosinophils use α9β1 to bind to provisional matrix proteins tenascin‐C (TNC) and osteopontin 51–53 . As these matrix proteins play an important role in wound healing at a similar time and context as PAR signaling, it would be interesting and important to investigate whether there is further interaction of α9β1 with PAR1/2 on eosinophils within the context of wound healing and the fibrinolytic system.…”

Section: Eosinophils In Coagulationmentioning

confidence: 99%

Eosinophils in wound healing and epithelial remodeling: Is coagulation a missing link?

Coden

Berdnikovs

2020

Journal of Leukocyte Biology

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Eosinophils are often cited as playing roles in wound healing and epithelial remodeling; however, the exact triggers and mechanisms of such activity remain poorly understood. Eosinophils show the remarkable capacity to partner with coagulation, which is a highly conserved biologic system evolved to protect an organism from injury by promoting hemostasis and tissue repair. Eosinophils contribute directly by producing key factors in coagulation (tissue factor, thrombin) and fibrinolysis (plasminogen). Moreover, they have been shown to interact with other players in these cascades, such as fibrinogen and the urokinase‐type plasminogen activator/urokinase‐type plasminogen activator receptor system, which further promotes coagulation and fibrinolysis. Although primarily thought of in the contexts of blood clotting and vascular repair, coagulation and fibrinolytic systems play key roles within tissue, in particular during epithelial injury and remodeling. Chronic inflammation and remodeling frequently associate with pro‐thrombotic and pro‐coagulation state. There is a striking association between eosinophils and dysregulated coagulation in animal models and human disease. This review will examine the mechanistic links between eosinophils and the coagulation system in the context of epithelial injury and repair, as well as evidence for this interaction in heart disease, type 2 inflammatory diseases, and cancer. Collectively, multiple emerging studies summarized in this review elucidate an overlooked, but potentially fundamental, biologic mechanism to engage eosinophils in processes of epithelial injury and repair.

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Section: Eosinophils In Coagulationmentioning

confidence: 99%

Eosinophils in wound healing and epithelial remodeling: Is coagulation a missing link?

Coden

Berdnikovs

2020

Journal of Leukocyte Biology

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“…In animal experiments, Nakahara et al showed that TNC inactivation was protective against ovalbumin-induced asthma, with less eosinophils in the bronchoalveolar lavage fluid (BALF), decreased lung cell infiltration and reduced Th2 cytokines IL-5 and IL-13 in BALF and plasma 21 . Doan et al further showed that TNC KO lungs exhibited a decreased expansion while accelerated maturation of eosinophil progenitors in the same asthma model 49 . In a model of bleomycin-induced acute lung injury (ALI), Carey et al showed that TNC KO lungs were protected from fibrosis, with less SMA + myofibroblasts in the lung, and TNC inactivation prevented constitutively active TGFβ to induce the differentiation of fibroblasts into myofibroblasts 19 .…”

Section: Discussionmentioning

confidence: 94%

Tenascin-C inactivation impacts lung structure and function beyond lung development

Gremlich

Roth‐Kleiner

Equey

et al. 2020

Sci Rep

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Johannes c. Schittny 4 & tiziana p. cremona 4 tenascin-c (tnc) is an extracellular matrix protein expressed at high levels during lung organogenesis. Later, tnc is only transiently de novo expressed to orchestrate tissue repair in pathological situations. We previously showed that TNC inactivation affects lung development and thus evaluated here the implications on lung function in newborn/adult mice. Respiratory function parameters were measured in anesthetized and mechanically ventilated wild-type (WT) and TNC-deficient mice at 5 (P5) and 90 (P90) days of age under basal conditions, as well as following high tidal volume (HTV) ventilation. At P5, TNC-deficient mice showed an increased static compliance (Cst) and inspiratory capacity (IC) relative to WT at baseline and throughout HTV. At P90, however, Cst and IC were only elevated at baseline. Control non-ventilated newborn and adult TNC-deficient mice showed similar lung morphology, but less alpha smooth muscle actin (α-SMA) around small airways. SMA + cells were decreased by 50% in adult TNCdeficient lungs and collagen layer thickened around small airways. Increased surfactant protein C (SPc) and altered tGfβ and TLR4 signaling pathways were also detected. Thus, TNC inactivation-related defects during organogenesis led to persisting functional impairment in adulthood. this might be of interest in the context of pulmonary diseases with thickened airway smooth muscle layer or ventilation heterogeneity, like asthma and COPD.

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“…Moreover, eosinophils may modulate the polarization and activation of T cells through direct and indirect mechanisms. Tissue remodeling and repair by eosinophils has been shown to be somewhat dependent on the extracellular matrix components that, in turn, may activate or suppress eosinophils [150]. Finally, eosinophils have the capacity to resolve inflammation, whether directly, by the release of resolvins [151], or through activation of phagocytic macrophages [152].…”

Section: Eosinophil Biologymentioning

confidence: 99%

“NETs and EETs, a Whole Web of Mess”

et al. 2020

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Neutrophils and eosinophils are granulocytes that have very distinct functions. Neutrophils are first responders to external threats, and they use different mechanisms to control pathogens. Phagocytosis, reactive oxygen species, and neutrophil extracellular traps (NETs) are some of the mechanisms that neutrophils utilize to fight pathogens. Although there is some controversy as to whether NETs are in fact beneficial or detrimental to the host, it mainly depends on the biological context. NETs can contribute to disease pathogenesis in certain types of diseases, while they are also undeniably critical components of the innate immune response. On the contrary, the role of eosinophils during host immune responses remains to be better elucidated. Eosinophils play an important role during helminthic infections and allergic responses. Eosinophils can function as effector cells in viral respiratory infections, gut bacterial infections, and as modulators of immune responses by driving the balance between Th1 and Th2 responses. In particular, eosinophils have biological activities that appear to be quite similar to those of neutrophils. Both possess bactericidal activity, can activate proinflammatory responses, can modulate adaptive immune responses, can form extracellular traps, and can be beneficial or detrimental to the host according to the underlying pathology. In this review we compare these two cell types with a focus on highlighting their numerous similarities related to extracellular traps.

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Matrix protein tenascin-C expands and reversibly blocks maturation of murine eosinophil progenitors

Cited by 9 publications

References 22 publications

Eosinophils in wound healing and epithelial remodeling: Is coagulation a missing link?

Eosinophils in wound healing and epithelial remodeling: Is coagulation a missing link?

Tenascin-C inactivation impacts lung structure and function beyond lung development

“NETs and EETs, a Whole Web of Mess”

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