Signal pathways involved in the production of MMP‐1 and MMP‐3 in human gingival fibroblasts

Domeij, Helena; Yucel‐Lindberg, Tülay; Modéer, Thomas

doi:10.1034/j.1600-0722.2002.21247.x

Cited by 90 publications

(111 citation statements)

References 35 publications

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“…Our results are consistent with the previous observation that exogenous PGE 2 up-regulates MMPs in gingival fibroblasts (Sakaki et al, 2004). Other studies have reported that PGE 2 mediates IL-1β-induced MMP-1 up-regulation in tendon and gingival fibroblasts (Domeij et al, 2002;Tsuzaki et al, 2003). It is noted that tendon consists predominantly of collagen type I with a triple helical structure that resists general proteolytic degradation but is susceptible to MMPs.…”

Section: Discussionsupporting

confidence: 93%

Leukotriene B4 at low dosage negates the catabolic effect of prostaglandin E2 in human patellar tendon fibroblasts

Thampatty¹,

Im²,

Wang³

2006

Gene

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Tendinopathy often involves inflammation and matrix degeneration. The inflammatory mediators such as prostaglandin E 2 (PGE 2 ) and leukotriene B 4 (LTB 4 ) are implicated in the development of tendinopathy. Therefore, the purpose of this study was to determine the effect of PGE 2 and LTB 4 on the proliferation of human patellar tendon fibroblasts (HPTFs), the gene expression of collagen type I, MMP-1 and MMP-3, as well as the protein secretion of these gene products by the cells. The results showed that LTB 4 at low doses (0.1 and 1 nM) significantly increased cell proliferation compared to controls and LTB 4 at 0.1 nM negated the PGE 2 -induced decrease in cell proliferation. In addition, PGE 2 at 100 ng/ml significantly increased the expression of MMP-1 and MMP-3 at both mRNA and protein levels. These stimulatory effects were significantly diminished by co-treatment with LTB 4 at 0.1 nM. Finally, neither PGE 2 nor LTB 4 treatment affected collagen type I gene expression. These results suggest that low levels of LTB 4 counterbalance the negative effects mediated by PGE 2 on tendon fibroblast proliferation and MMP production, which may lead to matrix degradation. Thus, our findings suggest that although LTB 4 is generally thought to be pathogenic, low levels of LTB 4 are actually beneficial in maintaining tendon tissue homeostasis.

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Section: Discussionsupporting

confidence: 93%

Leukotriene B4 at low dosage negates the catabolic effect of prostaglandin E2 in human patellar tendon fibroblasts

Thampatty¹,

Im²,

Wang³

2006

Gene

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“…However, the induction of MMP1 by IL-1b was less powerful in comparison with the MC medium, suggesting the involvement of other factors derived from macrophages. The stimulatory effects of IL-1b on MMP1 and MMP3 release have been described in other cell types such as chondrocytes (Liacini et al, 2005) and gingival fibroblasts (Domeij et al, 2002). In the present study, TNFa alone also induced a small increase in protein release of both MMPs but the induction was much less potent than the MC medium, and this observation suggests that other macrophagederived factors, such as IL-1b, could be the key mediators.…”

Section: Discussionmentioning

confidence: 64%

Macrophage‐induced expression and release of matrix metalloproteinase 1 and 3 by human preadipocytes is mediated by IL‐1β via activation of MAPK signaling

Gao

Chen

2011

Journal Cellular Physiology

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Obesity is associated with a chronic low-grade inflammation and increased macrophage infiltration in adipose tissue. Matrix metalloproteinases (MMPs) are involved in adipose tissue remodeling and inflammatory responses in obesity. This study investigated whether macrophage-derived factors modulate expression and secretion of MMP1 and MMP3 in human preadipocytes. The potential mediators and signaling pathways were also explored. MMP1 and MMP3 were primarily expressed and secreted by preadipocytes and dramatically reduced post-differentiation. Preadipocytes were incubated with RPMI 1640 medium (control) or THP-1 macrophage-conditioned (MC) medium (25% and 100%) for 24 h. MC medium markedly increased mRNA levels of MMP1 (up to 122-fold) and MMP3 (up to 59-fold), as well as protein release of MMP1 (up to 378-fold) and MMP3 (up to 10-fold) in a dose-dependent manner. Treatment with IL-1β or TNFα, the major products of macrophages, also induced MMP1 and MMP3 secretion by preadipocytes. Neutralizing IL-1β abolished the induction of MMP1 and MMP3 in preadipocytes by MC medium while the effects of TNFα neutralization were modest. Furthermore, MC medium or IL-1β led to the phosphorylation of p38, ERK and JNK MAPKs. Inhibition of p38, ERK and JNK reversed the stimulatory effects of MC or IL-1β on MMP1 and MMP3 production. MC medium and IL-1β also activated NF-κB p65 whereas reduced IκBα protein expression in preadipocytes. These results suggest that macrophage accumulation in adipose tissue has a central role in stimulating MMP1 and MMP3 production by preadipocytes, and this is partially mediated by IL-1β via activation of the MAPK and NF-κB signaling pathways.

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“…MMP-1 is an inducible enzyme, and its gene transcription is modulated by several cytokines that play a central role in inflammation (Domeij et al 2002). MMP-1 mRNA levels have been shown to be significantly increased during the course of gingivitis or periodontitis in human gingival tissue (Aiba et al 1996;Ejeil et al 2003).…”

Section: Effects Of Go On Mmp-1mentioning

confidence: 99%

Elevated gene expression of MMP-1, MMP-10, and TIMP-1 reveal changes of molecules involved in turn-over of extracellular matrix in cyclosporine-induced gingival overgrowth

et al. 2006

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In humans, pathogenesis in cyclosporine A (CsA)-induced gingival overgrowth (GO) includes the accumulation of extracellular matrix (ECM) constituents, viz., collagen type-1 and type-3 and proteoglycans, in subgingival connective tissue. However, whether this increase is associated with alterations of molecules pivotal for the turn-over of collagens and proteoglycans remains unclear. The present study explores the status of matrix metalloproteinase MMP-1 and MMP-10, which are important for fibrillar collagen and proteoglycan turn-over, and their tissue inhibitor TIMP-1, on their gene expression and protein levels in frozen sections derived from GO and matched normal tissue. In situ hybridization (ISH) revealed elevated levels of MMP-1 gene expression in the connective tissue of GO compared with normal tissue. This elevation also applied to MMP-10 and TIMP-1, the latter exhibiting the strongest gene transcription in the deep connective tissue. These differences detected by ISH were corroborated by quantitative reverse transcription/polymerase chain reaction; relative gene expression analysis indicated a 1.9-fold increase for MMP-1, a 2.3-fold increase for MMP-10, and a 4.8-fold increase for TIMP-1. Detection of the protein by indirect immunofluorescence showed that normal gingival tissue was devoid of all three proteins, although they were detectable in GO tissue, with emphasis on TIMP-1. Analysis of our data indicates elevated levels of MMP-1 and-10, and particularly TIMP-1. With respect to TIMP-1, this elevation may in turn lead to alterations in ECM turn-over by abrogating MMP-1 and MMP-10, thereby contributing to ECM accumulation associated with GO.

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Signal pathways involved in the production of MMP‐1 and MMP‐3 in human gingival fibroblasts

Cited by 90 publications

References 35 publications

Leukotriene B4 at low dosage negates the catabolic effect of prostaglandin E2 in human patellar tendon fibroblasts

Leukotriene B4 at low dosage negates the catabolic effect of prostaglandin E2 in human patellar tendon fibroblasts

Macrophage‐induced expression and release of matrix metalloproteinase 1 and 3 by human preadipocytes is mediated by IL‐1β via activation of MAPK signaling

Elevated gene expression of MMP-1, MMP-10, and TIMP-1 reveal changes of molecules involved in turn-over of extracellular matrix in cyclosporine-induced gingival overgrowth

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