Role of β-catenin-regulated CCN matricellular proteins in epithelial repair after inflammatory lung injury

Zemans, Rachel L.; McClendon, Jazalle; Aschner, Yael; Briones, Natalie; Young, Shamar; Lau, Lester F.; Kahn, Michaël; Downey, Gregory P.

doi:10.1152/ajplung.00180.2012

Cited by 57 publications

(46 citation statements)

References 76 publications

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“…Alveolar epithelial cell injury was shown to be dependent on the activation of neutrophils and the release of proteinases and elastase, although independent of ROS generation or direct cytolysis (7, 156). Zemans et al (191) demonstrated that neutrophil migration across human epithelial type II cells causes disruption of the monolayer, quickly followed by reepithelialization, a process that was dependent on ␤-catenin signaling (193). Therefore, this would suggest that excessive neutrophil migration across the alveolar epithelium, and the associated release of degrading enzymes, overwhelms normal physiological migration pathways and directly contributes to epithelial damage and permeability within the inflamed lung.…”

Section: Mechanisms Of Neutrophil Recruitment Into the Lungmentioning

confidence: 99%

The mercurial nature of neutrophils: still an enigma in ARDS?

Williams

Chambers

2014

American Journal of Physiology-Lung Cellular and Molecular Phys

364

304

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Section: Mechanisms Of Neutrophil Recruitment Into the Lungmentioning

confidence: 99%

The mercurial nature of neutrophils: still an enigma in ARDS?

Williams

Chambers

2014

American Journal of Physiology-Lung Cellular and Molecular Phys

364

304

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“…Experimental research on the multifunctional CCN1 protein have revealed that it is a potential key player in tissue injury repair [6,7]. It has diverse roles in regulating fibroblast behavior [7][8][9], promoting angiogenesis [10,11], and regulating vascular injury repair [12,13], and it displays organ-protective and regenerative capabilities in some contexts [14,15], while in others, it has been associated with detrimental effects to organ functioning [16].…”

Section: Introductionmentioning

confidence: 99%

Postoperative Accumulation of Cyr61/CCN1 in Surgical Wound Fluid Precedes Cytokine Activation and is Disparate from Systemic Alterations

Hviid¹,

Pripp²,

Aasen³

et al. 2014

J Infect Dis Ther

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Background: Cysteine-rich protein 61 (Cyr61/CCN1) is a multifunctional matricellular protein that has recently emerged as a potential player in injury-repair mechanisms involving the regulation of inflammatory responses. Experimental research has revealed the pro-inflammatory effects and chemotactic capacities of this protein, and clinical investigations have found it to be elevated in patients with chronic inflammatory conditions. However, its regulation at sites of acute tissue injury and inflammation in humans has not been investigated.

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“…Notably, overexpression of CYR61 in breast, prostate or ovarian cancer cells enhances tumour growth 21,22,40 , whereas CYR61 silencing in pancreatic and prostate cancer cells decreases tumour growth 22,23 . Finally, recombinant CYR61 treatment accelerates repair of epithelium in vitro in a model of inflammatory lung epithelium injury 41 . As thymocytes and TEC ARTICLE undergo intense proliferation and apoptosis, we investigated whether matricellular CYR61 could improve TEC status and thymocyte development.…”

Section: Discussionmentioning

confidence: 99%

Thymic epithelial cell expansion through matricellular protein CYR61 boosts progenitor homing and T-cell output

et al. 2013

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Thymic epithelial cells (TEC) are heterogeneous stromal cells that generate microenvironments required for the formation of T cells within the thymus. Defects in TEC lead to immunodeficiency or autoimmunity. Here we identify TEC as the major source of cysteinerich protein 61 (CYR61), a matricellular protein implicated in cell proliferation and migration. Binding of CYR61 to LFA-1, ICAM-1 and integrin a6 supports the adhesion of TEC and thymocytes as well as their interaction. Treatment of thymic lobes with recombinant CYR61 expands the stromal compartment by inducing the proliferation of TEC and activates Akt signalling. Engraftment of CYR61-overexpressing thymic lobes into athymic nude mice drastically boosts the yield of thymic output via expansion of TEC. This increases the space for the recruitment of circulating hematopoietic progenitors and the development of T cells. Our discovery paves the way for therapeutic interventions designed to restore thymus stroma and T-cell generation.

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Role of β-catenin-regulated CCN matricellular proteins in epithelial repair after inflammatory lung injury

Cited by 57 publications

References 76 publications

The mercurial nature of neutrophils: still an enigma in ARDS?

The mercurial nature of neutrophils: still an enigma in ARDS?

Postoperative Accumulation of Cyr61/CCN1 in Surgical Wound Fluid Precedes Cytokine Activation and is Disparate from Systemic Alterations

Thymic epithelial cell expansion through matricellular protein CYR61 boosts progenitor homing and T-cell output

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