The matricellular protein CCN1 enhances TGF-β1/SMAD3-dependent profibrotic signaling in fibroblasts and contributes to fibrogenic responses to lung injury

• Published in: The FASEB journal Vol. 30; no. 6; p. 2135
• Main Authors: Kurundkar, Ashish R, Kurundkar, Deepali, Rangarajan, Sunad, Locy, Morgan L, Zhou, Yong, Liu, Rui-Ming, Zmijewski, Jaroslaw, Thannickal, Victor J
• Format: Journal Article
• Language: English
• Published: United States 01.06.2016
• Subjects: Animals; Cells, Cultured; Cysteine-Rich Protein 61 - genetics; Cysteine-Rich Protein 61 - metabolism; Fibroblasts - metabolism; Gene Expression Regulation - physiology; Gene Knockdown Techniques; Humans; Lung Injury - metabolism; Protein-Serine-Threonine Kinases - genetics; Protein-Serine-Threonine Kinases - metabolism; Pulmonary Fibrosis - metabolism; Receptor, Transforming Growth Factor-beta Type I; Receptors, Transforming Growth Factor beta - genetics; Receptors, Transforming Growth Factor beta - metabolism; RNA Interference; Signal Transduction - physiology; Smad3 Protein - genetics; Smad3 Protein - metabolism; Transforming Growth Factor beta1 - genetics; Transforming Growth Factor beta1 - metabolism; Up-Regulation; idiopathic pulmonary fibrosis; matrix remodeling; wound repair; myofibroblasts

Matricellular proteins mediate pleiotropic effects during tissue injury and repair. CCN1 is a matricellular protein that has been implicated in angiogenesis, inflammation, and wound repair. In this study, we identified CCN1 as a gene that is differentially up-regulated in alveolar mesenchymal cells...