Idiopathic Pulmonary Fibrosis: Cellular and Molecular Pathogenesis

Weissler, Jonathan C.

doi:10.1097/00000441-198902000-00005

Cited by 58 publications

(28 citation statements)

References 84 publications

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“…IL13-PE also effectively inhibited the gene expression of procollagen III, a major procollagen produced by pulmonary fibroblasts during clinical pulmonary fibrosis. 72 Of particular interest was the observation that IL13-PE induced the expression of IL-13R␣2 in the surviving cells.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-13 Fusion Cytotoxin Arrests Schistosoma mansoni Egg-Induced Pulmonary Granuloma Formation in Mice

Jakubzick

Kunkel

Joshi

et al. 2002

The American Journal of Pathology

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Section: Discussionmentioning

confidence: 99%

Interleukin-13 Fusion Cytotoxin Arrests Schistosoma mansoni Egg-Induced Pulmonary Granuloma Formation in Mice

Jakubzick

Kunkel

Joshi

et al. 2002

The American Journal of Pathology

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“…This is achieved by a complex series of events that is spatio-temporally coordinated and leads to release of chemokines, pro-and anti-inflammatory mediators including cytokines, migration and activation of inflammatory and mesenchymal cells, and a return to homeostatic tissue function (Clark, 1996;Davidson, 1992). An imbalance in the pro-and anti-inflammatory mediators produced can lead to the development of chronic inflammatory diseases (Weissler, 1989;Selman et al, 2001). In addition to the regulation of the inflammatory response, a transition from an early stage of inflammation to a later stage of repair is required to re-establish normal tissue function following injury.…”

Section: Introductionmentioning

confidence: 99%

Fibroblast migration is mediated by CD44-dependent TGFβ activation

Acharya

Majumdar

Jacob

et al. 2008

Journal of Cell Science

139

105

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CD44 contributes to inflammation and fibrosis in response to injury. As fibroblast recruitment is critical to wound healing, we compared cytoskeletal architecture and migration of wild-type (CD44WT) and CD44-deficient (CD44KO) fibroblasts. CD44KO fibroblasts exhibited fewer stress fibers and focal adhesion complexes, and their migration was characterized by increased velocity but loss of directionality, compared with CD44WT fibroblasts. Mechanistically, we demonstrate that CD44WT cells generated more active TGFβ than CD44KO cells and that CD44 promotes the activation of TGFβ via an MMP-dependent mechanism. Reconstitution of CD44 expression completely rescued the phenotype of CD44KO cells whereas exposure of CD44KO cells to exogenous active TGFβ rescued the defect in stress fibers and migrational velocity, but was not sufficient to restore directionality of migration. These results resolve the TGFβ-mediated and TGFβ-independent effects of CD44 on fibroblast migration and suggest that CD44 may be critical for the recruitment of fibroblasts to sites of injury and the function of fibroblasts in tissue remodeling and fibrosis.

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“…PULMONARY FIBROSIS IS A DISEASE characterized by excessive mesenchymal cell proliferation and concomitant collagen accumulation within the alveolar and interstitial compartments of the lung (36). This inflammatory and fibroproliferative response to lung injury occurs via concerted interaction of various cytokines and growth factors within the tissue microenvironment (7).…”

mentioning

confidence: 99%