[citation report] The CCN family: A new class of inflammation modulators? (2024)

“…Matricellular proteins are emerging as essential regulators of inflammation and repair (4,6). CCN1, a matricellular protein, is highly expressed in injury repair and mediates varied and divergent cellular responses in cell-type and context-dependent manner (40).…”

Section: Discussionmentioning

confidence: 99%

“…Matricellular proteins play major roles in development and tissue injury repair responses (3,4). CCN1 (or cysteine-rich protein 61) belongs to the CCN family of matricellular proteins that regulate a number of biologic processes such as inflammation, angiogenesis, wound healing, and fibrosis (5,6). The CCN acronym derives from the first 3 members of the 6-member family, namely cysteine-rich protein 61, connective tissue growth factor, and nephroblastoma overexpressed gene.…”

mentioning

confidence: 99%

See 1 more Smart Citation

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 of human subjects with rapidly progressive idiopathic pulmonary fibrosis (IPF). Elevated levels of CCN1 mRNA were confirmed in lung tissues of IPF subjects undergoing lung transplantation, and CCN1 protein was predominantly localized to fibroblastic foci. CCN1 expression in ex vivo IPF lung fibroblasts correlated with gene expression of the extracellular matrix proteins, collagen (Col)1a1, Col1a2, and fibronectin as well as the myofibroblast marker, a-smooth muscle actin. RNA interference (RNAi)-mediated knockdown of CCN1 down-regulated the constitutive expression of these profibrotic genes in IPF fibroblasts. TGF-b1, a known mediator of tissue fibrogenesis, induces gene and protein expression of CCN1 via a mothers against decapentaplegic hom*olog 3 (SMAD3)-dependent mechanism. Importantly, endogenous CCN1 potentiates TGF-b1-induced SMAD3 activation and induction of profibrotic genes, supporting a positive feedback loop leading to myofibroblast activation. In vivo RNAi-mediated silencing of CCN1 attenuates fibrogenic responses to bleomycin-induced lung injury. These studies support previously unrecognized, cooperative interaction between the CCN1 matricellular protein and canonical TGF-b1/SMAD3 signaling that promotes lung

“…Matricellular proteins are emerging as essential regulators of inflammation and repair (4,6). CCN1, a matricellular protein, is highly expressed in injury repair and mediates varied and divergent cellular responses in cell-type and context-dependent manner (40).…”

Section: Discussionmentioning

confidence: 99%

“…Matricellular proteins play major roles in development and tissue injury repair responses (3,4). CCN1 (or cysteine-rich protein 61) belongs to the CCN family of matricellular proteins that regulate a number of biologic processes such as inflammation, angiogenesis, wound healing, and fibrosis (5,6). The CCN acronym derives from the first 3 members of the 6-member family, namely cysteine-rich protein 61, connective tissue growth factor, and nephroblastoma overexpressed gene.…”

mentioning

confidence: 99%

The matricellular protein CCN1 enhances TGF‐β1/SMAD3‐dependent profibrotic signaling in fibroblasts and contributes to fibrogenic responses to lung injury
62239

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 of human subjects with rapidly progressive idiopathic pulmonary fibrosis (IPF). Elevated levels of CCN1 mRNA were confirmed in lung tissues of IPF subjects undergoing lung transplantation, and CCN1 protein was predominantly localized to fibroblastic foci. CCN1 expression in ex vivo IPF lung fibroblasts correlated with gene expression of the extracellular matrix proteins, collagen (Col)1a1, Col1a2, and fibronectin as well as the myofibroblast marker, a-smooth muscle actin. RNA interference (RNAi)-mediated knockdown of CCN1 down-regulated the constitutive expression of these profibrotic genes in IPF fibroblasts. TGF-b1, a known mediator of tissue fibrogenesis, induces gene and protein expression of CCN1 via a mothers against decapentaplegic hom*olog 3 (SMAD3)-dependent mechanism. Importantly, endogenous CCN1 potentiates TGF-b1-induced SMAD3 activation and induction of profibrotic genes, supporting a positive feedback loop leading to myofibroblast activation. In vivo RNAi-mediated silencing of CCN1 attenuates fibrogenic responses to bleomycin-induced lung injury. These studies support previously unrecognized, cooperative interaction between the CCN1 matricellular protein and canonical TGF-b1/SMAD3 signaling that promotes lung

“…These time-dependent regulations, in combination with the known inflammatory roles of CCN1, support its function as an early mediator of inflammatory activation. However, a large body of evidence has demonstrated that CCN1 is activated by cytokine exposure [39], and NF-B binding-sites have been reported in its promoter region [40]. While this would indicate the reverse to be true, i.e., that CCN1 is regulated by proinflammatory stimulation, it is crucial to emphasize that cytokines, in general, work in an interacting network of mutual promotion and inhibition to fine-tune the inflammatory response [1].…”

Section: Discussionmentioning

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

11

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.

“…In contrast, in vitro studies support the novel concept of CCN2 as a proinflammatory cytokine. 19 CCN2 is a chemotactic factor for immune cells, 20 has promoted cell adhesion and migration, and has upregulated proinflammatory factor production, including cytokines, chemokines, and adhesion molecules. 19 We have previously demonstrated that systemic administration of CCN2(IV) elicited the recruitment of inflammatory cells in the murine kidney after 24 h, suggesting that CCN2(IV) could induce acute inflammation in vivo, 21 but there are no data on sustained inflammation.…”

mentioning

confidence: 99%

The C-terminal module IV of connective tissue growth factor is a novel immune modulator of the Th17 response

Rodrigues‐Díez

1

,

Rodrigues-Díez

2

,

Rayego‐Mateos

3

et al. 2013

Laboratory Investigation

43357

No abstract

[citation report] The CCN family: A new class of inflammation modulators? (2024)

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