Matrix metalloproteinase-9 activates TGF-β and stimulates fibroblast contraction of collagen gels

Kobayashi, Tetsu; Kim, Hui Jung; Liu, Xiangde; Sugiura, Hiroaki; Kohyama, Tadashi; Fang, Qiuhong; Wen, Fu Qiang; Abe, Shinji; Wang, Xingqi; Atkinson, Jeffrey J.; Shipley, J. Michael; Senior, Robert M.; Rennard, Stephen I.

doi:10.1152/ajplung.00015.2014

Cited by 174 publications

(140 citation statements)

References 49 publications

(48 reference statements)

Supporting

Mentioning

133

Contrasting

Unclassified

Order By: Relevance

“…Mechanical stretch after TO Table 4. Literature overview about the consequences of prenatal tracheal occlusion on TGF-␤ signaling, extracellular matrix, and epithelial homeostasis induces TGF-␤ isoform transcription (47,64) and activates matrix metalloproteinases (20) and thrombospondin-1 (52), which favor mature TGF-␤ release (33,47). Besides, ROCKinduced cytoskeleton reorganization is rapidly initiated after TO in the terminal airways (13).…”

Section: Discussionmentioning

confidence: 99%

“…The three TGF-␤ isoforms are secreted as latent complexes bound to the extracellular matrix. Latent complexes release mature TGF-␤ upon proteolytic cleavage by matrix metalloproteinases (33), acidification (34), mechanical stretch (65), or conformational changes induced by thrombospondin-1 (5). Following binding of mature forms to TGF-␤ type I and II receptors, signal transduction is initiated through Smad-dependent or -independent routes that modify transcription of genes controlling extracellular matrix homeostasis and various cell functions (5).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Increased TGF-β: a drawback of tracheal occlusion in human and experimental congenital diaphragmatic hernia?

Vuckovic

Herber-Jonat

Flemmer

et al. 2016

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

Survivors of severe congenital diaphragmatic hernia (CDH) present significant respiratory morbidity despite lung growth induced by fetal tracheal occlusion (TO). We hypothesized that the underlying mechanisms would involve changes in lung extracellular matrix and dysregulated transforming growth factor (TGF)-β pathway, a key player in lung development and repair. Pulmonary expression of TGF-β signaling components, downstream effectors, and extracellular matrix targets were evaluated in CDH neonates who died between birth and the first few weeks of life after prenatal conservative management or TO, and in rabbit pups that were prenatally randomized for surgical CDH and TO vs. sham operation. Before tissue harvesting, lung tissue mechanics in rabbits was measured using the constant-phase model during the first 30 min of life. Human CDH and control fetal lungs were also collected from midterm onwards. Human and experimental CDH did not affect TGF-β/Smad2/3 expression and activity. In human and rabbit CDH lungs, TO upregulated TGF-β transcripts. Analysis of downstream pathways indicated increased Rho-associated kinases to the detriment of Smad2/3 activation. After TO, subtle accumulation of collagen and α-smooth muscle actin within alveolar walls was detected in rabbit pups and human CDH lungs with short-term mechanical ventilation. Despite TO-induced lung growth, mediocre lung tissue mechanics in the rabbit model was associated with increased transcription of extracellular matrix components. These results suggest that prenatal TO increases TGF-β/Rho kinase pathway, myofibroblast differentiation, and matrix deposition in neonatal rabbit and human CDH lungs. Whether this might influence postnatal development of sustainably ventilated lungs remains to be determined.

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Increased TGF-β: a drawback of tracheal occlusion in human and experimental congenital diaphragmatic hernia?

Vuckovic

Herber-Jonat

Flemmer

et al. 2016

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

show abstract

“…For example, as described above, an α3β1-to-MMP-9 signaling axis (Iyer et al, 2005) may contribute to pro-angiogenic communication from the epidermis to the wound vasculature (Mitchell et al, 2009). Similar communication may occur from the epidermis to dermal fibroblasts/myofibroblasts, given the important roles that some MMPs play in myofibroblast differentiation and wound contraction (Hattori et al, 2009; Kobayashi et al, 2014; Mirastschijski et al, 2004). …”

Section: Potential Mechanisms Of Integrin-mediated Long-distance Sigmentioning

confidence: 91%

“…For example, keratinocyte integrins αvβ6 and α3β1 can induce expression and secretion of MMP-9, MMP-3, uPA, and/or other extracellular proteases (Ghosh et al, 2000; Iyer et al, 2005; Ramos et al, 2002; Thomas et al, 2001b) into the wound stroma. Indeed, recruitment of MMP-9 to the fibroblast surface triggers TGFβ activation, which coupled with mechanical tension and other ECM signals can induce myofibroblast differentiation (Dayer and Stamenkovic, 2015; Kobayashi et al, 2014; Van De Water et al, 2013). Other studies support integrin-mediated induction of IL-1α from the epidermis (Hobbs and Watt, 2003).…”

Section: Epidermal Integrins Regulate Crosstalk To Other Cellular Commentioning

confidence: 99%

Integrin-mediated regulation of epidermal wound functions

et al. 2016

View full text Add to dashboard Cite

During cutaneous wound healing, keratinocyte proliferation and migration are critical for re-epithelialization. In addition, the epidermis secretes growth factors, cytokines, proteases, and matricellular proteins into the wound microenvironment that modify the extracellular matrix and stimulate other wound cells that control the inflammatory response, promote angiogenesis, and facilitate tissue contraction and remodeling. Wound keratinocytes express at least seven different integrins - the major cell adhesion receptors for the extracellular matrix - that collectively control essential cell-autonomous functions to ensure proper re-epithelialization, including migration, proliferation, survival, and basement membrane assembly (Fig. 1, arrow 1). Moreover, it has become evident in recent years that some integrins can regulate paracrine signals from wound epidermis that stimulate other wound cells involved in angiogenesis, contraction and inflammation (Fig. 1, arrows 2 and 3). Importantly, it is likely that abnormal integrin expression or function in the epidermis contributes to wound pathologies such as over-exuberant healing (e.g., hypertrophic scar formation) or diminished healing (e.g., chronic wounds). In this review, we discuss current knowledge of integrin function in the epidermis, which implicates them as attractive therapeutic targets to promote wound healing or treat wound pathologies. We also discuss challenges that arise from the complex roles that multiple integrins play in wound epidermis, which may be regulated through extracellular matrix remodeling that determines ligand availability. Indeed, understanding how different integrin functions are temporally coordinated in wound epidermis, and which integrin functions go awry in pathological wounds, will be important to determine how best to target them clinically to achieve maximum therapeutic benefit.

show abstract

“…and other important lung ECM components. Indeed, there is now increasing evidence that mechanical forces per se can, on the one hand, influence ECM composition (200), whereas on the other, the ECM influences the cellular properties in the lung (33,88,134,164,173,195). Mechanical properties and forces can further modulate cell fate, particularly the differentiation of stem cells on the basis of mechanotransduction (48,49,149,161,204).…”

Section: Materials Matrix and Mechanobiologymentioning

confidence: 99%