A cytokine axis regulates elastin formation and degradation

Sproul, Erin P.; Argraves, W. Scott

doi:10.1016/j.matbio.2012.11.004

Cited by 63 publications

(48 citation statements)

References 128 publications

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“…The proliferative effect on tenocytes and tenoblasts supports the intrinsic healing mechanism, by attracting these cell populations from the endotenon, which in turn can synthesise and remodel the ECM. On the other hand, there is an evidence that the effect of PDGF-BB on elastin synthesis is inhibitory, where the MAPK/ERK signalling pathway acts in opposition to canonical TGFβ1 signalling (Sproul and Argraves, 2013). However, its mechanism and role in tendon healing are yet unknown.…”

Section: Pdgf-bb Is Predominantly Expressed During Tendon Healingmentioning

confidence: 99%

In vitro and in vivo effects of PDGF-BB delivery strategies on tendon healing: a review

Evrova

Buschmann

2017

eCM

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To promote and support tendon healing, one viable strategy is the use or administration of growth factors at the wound/rupture site. Platelet derived growth factor-BB (PDGF-BB), together with other growth factors, is secreted by platelets after injury. PDGF-BB promotes mitogenesis and angiogenesis, which could accelerate tendon healing. Therefore, in vitro studies with PDGF-BB have been performed to determine its effect on tenocytes and tenoblasts. Moreover, accurate and sophisticated drug delivery devices, aiming for a sustained release of PDGF-BB, have been developed, either by using heparin-binding and fibrin-based matrices or different electrospinning techniques.In this review, the structure and composition, as well as the healing process of tendons, are described. Part A deals with in vitro studies. They focus on the multiple effects evoked by PDGF-BB on the cellular level. Moreover, they address strategies for the sustained delivery of PDGF-BB. Part B focuses on animal models used to test different delivery strategies for PDGF-BB, in the context of tendon reconstruction. These studies showed that dosage and timing of PDGF-BB application are the most important factors for deciding which delivery device should be applied for a specific tendon laceration.

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Section: Pdgf-bb Is Predominantly Expressed During Tendon Healingmentioning

confidence: 99%

In vitro and in vivo effects of PDGF-BB delivery strategies on tendon healing: a review

Evrova

Buschmann

2017

eCM

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“…Because the GLP-1R could not be detected in cardiac fibroblasts, we explored the possibility that the elastogenic effect of GLP-1 might be induced through other receptor(s) previously identified to be involved in elastinproducing signaling pathways (22,23,29,30). Results of a series of experiments indicated that treatments with selected inhibitors of the well-established elastogenic pathways, triggered either by TGF␤-1 (SB431542) or insulin (AG1024), as well as treatment with dimethyloxaloylglycine, an inhibitor of proline hydroxylase that blocks collagen fibrogenesis, did not interfere with the elastogenic effect of GLP-1 peptides (data not shown).…”

Section: Glp-1 (7-36) and Glp-1 (9-36) Stimulate Elastinencoding Mrnamentioning

confidence: 99%

“…After confirming that the known GLP-1R is not expressed in cardiac fibroblasts (Figure 2), we considered the involvement of alternate pathways involved in elastic fibers deposition (30). Although GLP-1 had been previously documented to engage its own receptor to trigger either the IGF-IR-dependent protection against apoptosis (51), or the EGF-1-dependent proliferative signals in pancreatic ␤-cells (52), here, we provide the first experimental evidence that GLP-1 can also cross-activate the IGF-IR in cardiac fibroblasts lacking the known GLP-1R.…”

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confidence: 92%

The Antidiabetic Hormone Glucagon-Like Peptide-1 Induces Formation of New Elastic Fibers in Human Cardiac Fibroblasts After Cross-Activation of IGF-IR

Qa'aty

Wang

et al. 2015

Endocrinology

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Glucagon-like peptide 1 (GLP-1) is a metabolic hormone involved in the stimulation of insulin biosynthesis and secretion. It has been recently reported that GLP-1 also exerts cardioprotective effects and facilitates functional recovery after myocardial infarction through GLP-1 receptor-mediated signaling in cardiomyocytes. GLP-1 treatment has been also demonstrated to produce sustained improvement in cardiac function in long-term studies, suggesting the involvement of mechanisms beyond the acute metabolic and cytoprotective effects. For example, the possible interaction of GLP-1 with the cardiac fibroblasts, which are responsible for the postinfarct remodeling and extracellular matrix production, has not been previously explored. Here, we report that cultures of human cardiac fibroblasts treated with GLP-1 peptides display a selective up-regulation in elastin gene expression and a consequent increase in elastic fibers production, in the absence of the classic GLP-1 receptor. Importantly, we provide experimental evidence that this GLP-1-induced elastogenesis is triggered through the cross-activation of the IGF-I receptor. Because GLP-1 does not stimulate deposition of collagen I, nor promote the proliferation or apoptosis of cultured cardiac fibroblasts, we speculate that its elastogenic effect may also contribute to the beneficial remodeling of the human heart after myocardial infarction.

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“…Furthermore, because MMP2 and MMP9 expression increased after TNF-a stimulation of epithelial cells, and because MMPs were recently associated with the breakdown of elastin in SPC-TNF-a mice and patients with COPD, TNF-a could possibly contribute to the reported degradation of elastin (3,23). This is supported by evidence of research that shows that suppression of tropoelastin in TNF-a stimulated fibroblasts directly, and breakdown of elastin through increased release of elastolytic enzymes (9). In addition, a role for TNF-a in tissue remodeling is evident from a study demonstrating protection of TNF-a receptor knockout mice to cigarette smoke-induced connective tissue breakdown (10).…”

Section: Discussionmentioning

confidence: 90%

“…A role for TNF-a in tissue remodeling is further evident from a study that demonstrated that TNF-a receptor knockout mice were protected from cigarette smoke-induced connective tissue breakdown (9,10). In addition, it was recently shown that, in alveolar epithelial cells, TNF-a can induce JNK signaling (11) and that JNK is involved in TNFa-induced MMP12 expression (12).…”

Section: Clinical Relevancementioning

confidence: 99%

Involvement of c-Jun N-Terminal Kinase in TNF-α–Driven Remodeling

Eurlings

Reynaert

Wetering

et al. 2017

Am J Respir Cell Mol Biol

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Lung tissue remodeling in chronic obstructive pulmonary disease (COPD) is characterized by airway wall thickening and/or emphysema. Although the bronchial and alveolar compartments are functionally independent entities, we recently showed comparable alterations in matrix composition comprised of decreased elastin content and increased collagen and hyaluronan contents of alveolar and small airway walls. Out of several animal models tested, surfactant protein C (SPC)-TNF-a mice showed remodeling in alveolar and airway walls similar to what we observed in patients with COPD. Epithelial cells are able to undergo a phenotypic shift, gaining mesenchymal properties, a process in which c-Jun N-terminal kinase (JNK) signaling is involved. Therefore, we hypothesized that TNF-a induces JNK-dependent epithelial plasticity, which contributes to lung matrix remodeling. To this end, the ability of TNF-a to induce a phenotypic shift was assessed in A549, BEAS2B, and primary bronchial epithelial cells, and phenotypic markers were studied in SPC-TNF-a mice. Phenotypic markers of mesenchymal cells were elevated both in vitro and in vivo, as shown by the expression of vimentin, plasminogen activator inhibitor-1, collagen, and matrix metalloproteinases. Concurrently, the expression of the epithelial markers, E-cadherin and keratin 7 and 18, was attenuated. A pharmacological inhibitor of JNK attenuated this phenotypic shift in vitro, demonstrating involvement of JNK signaling in this process. Interestingly, activation of JNK signaling was also clearly present in lungs of SPC-TNF-a mice and patients with COPD. Together, these data show a role for TNF-a in the induction of a phenotypic shift in vitro, resulting in increased collagen production and the expression of elastin-degrading matrix metalloproteinases, and provide evidence for involvement of the TNF-a-JNK axis in extracellular matrix remodeling.

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A cytokine axis regulates elastin formation and degradation

Cited by 63 publications

References 128 publications

In vitro and in vivo effects of PDGF-BB delivery strategies on tendon healing: a review

In vitro and in vivo effects of PDGF-BB delivery strategies on tendon healing: a review

The Antidiabetic Hormone Glucagon-Like Peptide-1 Induces Formation of New Elastic Fibers in Human Cardiac Fibroblasts After Cross-Activation of IGF-IR

Involvement of c-Jun N-Terminal Kinase in TNF-α–Driven Remodeling

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