Interleukin-1β and tumor necrosis factor-α have opposite effects on fibroblasts and epithelial cells during basement membrane formation

Furuyama, Akiko; Hosokawa, Toshiyuki; Mochitate, Katsumi

doi:10.1016/j.matbio.2008.02.005

Cited by 20 publications

(12 citation statements)

References 27 publications

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“…Interestingly, the negative immunostaining for laminin-1 was observed in three RCs (23.1%) that showed severe inflammatory reaction in the connective tissue wall of the cysts. This result is in accordance to that reported by Furuyama et al, [15] who stated that the ability of epithelial cells to form continuous basement membrane was lost in the presence of inflammatory cytokines which enhances the secretion of matrix metalloproteinase (MMP-9) and (MMP-2).…”

Section: Discussionsupporting

confidence: 93%

Immunohistochemical detection of laminin-1 and Ki-67 in radicular cysts and keratocystic odontogenic tumors

2011

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BackgroundOdontogenic cysts are those which arise from the epithelium associated with the development of teeth. Some odontogenic cysts were found to have special biological features that make them distinct from other lesions. This study was conducted to detect the immunoepxression of laminin-1 and Ki-67 in both radicular cysts (RCs) and keratocystic odontogenic tumors (KCOTs) and to examine the possible predictive value of these markers.MethodsThirteen cases of RCs and twelve cases of KCOTs were included in this study. Antibodies against laminin-1 and Ki-67 were used as primary antibodies.Resultsten cases out of thirteen cases of RCs were immunopositive to laminin-1. The immunonegative cases of RCs showed high degree of inflammation inside the connective tissue wall. One case out of twelve cases of KCOTs was immunopositive to laminin-1 and the rest were immunonegative. Seven cases out of thirteen cases of RCs showed immunopositivity for Ki-67 with increased numbers of immunopositive cells when the inflammation was severe in the connective tissue wall. All KCOTS were immunopositive to Ki-67.ConclusionsThe benign nature of radicular cysts and the aggressive behavior of keratocystic odontogenic tumors could be explained by the expression of laminin and Ki-67. Laminin-1 and Ki-67 could be valuable markers for the prediction of the biologic behavior of cystic lesions.

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Section: Discussionsupporting

confidence: 93%

Immunohistochemical detection of laminin-1 and Ki-67 in radicular cysts and keratocystic odontogenic tumors

2011

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“…TNF-a, a proinflammatory cytokine (Furuyama et al, 2008), is known to stimulate tenocytes in vitro to produce both pro and anti-inflammatory cytokines (e.g., IL-1 b, IL-6, and IL-10) and collagen, degrading enzymes such as metalloproteinases (MMPs) (Riley, 2008;Tsai et al, 2014). Tendon breakdown was demonstrated to be caused by an increase of MMPs activity and reduction of their inhibitors (i.e., TIMP) (Vieira et al, 2012;De Oliveira et al, 2013;Del Buono et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Glycine improves the remodeling process of tenocytes in vitro

Vieira

Viola

Carneiro

et al. 2018

Cell Biology International

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Tendinitis changes the biochemical and morphological properties of the tendon, promoting an increase of activity of metalloproteinases and disorganization of collagen bundles. Tenocytes, the primary cells in tendon, are scattered throughout the collagenic fibers, and are responsible of tendon remodeling and tissue repair in pathological condition. In vivo, glycine, component of the typical Gly-X-Y collagen tripeptide, showed beneficial effects in biochemical and biomechanical properties of Achilles tendon with tendinitis. In this study, we analyzed the effect of glycine in tenocytes subjected to inflammation. Tenocytes from Achilles tendon of rats were treated with TNF-α (10 ng/mL) with and without previous treatment with glycine (20 mM). Cell proliferation and migration were evaluated, as well as the expression of matrix molecules such as glycosaminoglycans, metalloproteinases (MMPs), TIMPs, and collagen I. Glycine can revert the inflammation due to the action of TNF-α by controlling the MMPs quantity and activity. These data indicated that the molecules involved to remodeling process of extracellular matrix are modulated both by TNF-α and the availability of collagen precursors; in fact, this study indicates the glycine can be useful for treatment of inflammation and for modulating tenocytes metabolism in tendons.

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“…However, the direct effect of IL1β on fibroblasts is unclear. It has been known for a long time that fibroblasts exposed to IL1β invariably increase the expression of a variety of MMPs, and subsequently the breakdown of collagen [22], [23], [24], [25], [26], [27], [28]. This anti-fibrotic phenomenon shows a dual role for IL1β in fibrosis, as this should diminish the excessive accumulation of ECM.…”

Section: Introductionmentioning

confidence: 99%

Interleukin-1β Attenuates Myofibroblast Formation and Extracellular Matrix Production in Dermal and Lung Fibroblasts Exposed to Transforming Growth Factor-β1

2014

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One of the most potent pro-fibrotic cytokines is transforming growth factor (TGFβ). TGFβ is involved in the activation of fibroblasts into myofibroblasts, resulting in the hallmark of fibrosis: the pathological accumulation of collagen. Interleukin-1β (IL1β) can influence the severity of fibrosis, however much less is known about the direct effects on fibroblasts. Using lung and dermal fibroblasts, we have investigated the effects of IL1β, TGFβ1, and IL1β in combination with TGFβ1 on myofibroblast formation, collagen synthesis and collagen modification (including prolyl hydroxylase, lysyl hydroxylase and lysyl oxidase), and matrix metalloproteinases (MMPs). We found that IL1β alone has no obvious pro-fibrotic effect on fibroblasts. However, IL1β is able to inhibit the TGFβ1-induced myofibroblast formation as well as collagen synthesis. Glioma-associated oncogene homolog 1 (GLI1), the Hedgehog transcription factor that is involved in the transformation of fibroblasts into myofibroblasts is upregulated by TGFβ1. The addition of IL1β reduced the expression of GLI1 and thereby also indirectly inhibits myofibroblast formation. Other potentially anti-fibrotic effects of IL1β that were observed are the increased levels of MMP1, −2, −9 and −14 produced by fibroblasts exposed to TGFβ1/IL1β in comparison with fibroblasts exposed to TGFβ1 alone. In addition, IL1β decreased the TGFβ1-induced upregulation of lysyl oxidase, an enzyme involved in collagen cross-linking. Furthermore, we found that lung and dermal fibroblasts do not always behave identically towards IL1β. Suppression of COL1A1 by IL1β in the presence of TGFβ1 is more pronounced in lung fibroblasts compared to dermal fibroblasts, whereas a higher upregulation of MMP1 is seen in dermal fibroblasts. The role of IL1β in fibrosis should be reconsidered, and the differences in phenotypical properties of fibroblasts derived from different organs should be taken into account in future anti-fibrotic treatment regimes.

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Interleukin-1β and tumor necrosis factor-α have opposite effects on fibroblasts and epithelial cells during basement membrane formation

Cited by 20 publications

References 27 publications

Immunohistochemical detection of laminin-1 and Ki-67 in radicular cysts and keratocystic odontogenic tumors

Immunohistochemical detection of laminin-1 and Ki-67 in radicular cysts and keratocystic odontogenic tumors

Glycine improves the remodeling process of tenocytes in vitro

Interleukin-1β Attenuates Myofibroblast Formation and Extracellular Matrix Production in Dermal and Lung Fibroblasts Exposed to Transforming Growth Factor-β1

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