Regulation of collagenase gene expression by IL–1β requires transcriptional and post-transcriptional mechanisms

Vincenti, Matthew P.; Coon, Charles I.; Lee, Oneil; Brinckerhoff, Constance E.

doi:10.1093/nar/22.22.4818

Cited by 74 publications

(62 citation statements)

References 52 publications

(72 reference statements)

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“…In most tumor cells, proMMP-1 mRNA levels are very low but can be induced by a wide variety of stimuli (7,8,(26)(27)(28). For instance, interleukin-1β, UV radiations or phorbol esters, increase proMMP-1 gene expression through histone posttranslational modifications (22,29).…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, MMP-1 overexpression is associated with several pathological conditions such as irreversible degradation of cartilage, tendon and bone in arthritis, and tumor invasion and metastasis (5-7). Transcriptional activation of proMMP-1 has been extensively studied, whereas the mechanisms involved in its expression remain largely unclear (7,8).…”

Section: Introductionmentioning

confidence: 99%

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Epigenetic regulation of proMMP-1 expression in the HT1080 human fibrosarcoma cell line

Poplineau

Dufer²,

Antonicelli³

et al. 2011

Int J Oncol

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Abstract. The matrix metalloproteinase (MMP) family members play an important role in various physiological and pathological processes. Although MMP-1 (collagenase-1) has been shown to be involved in tumor invasiveness, the regulation of its expression is still not fully elucidated and could implicate epigenetic mechanisms. The aim of this study was to analyze the effects of the Histone Deacetylase Inhibitor (HDI) trichostatin A (TSA) and the inhibitor of DNA methylation 5-aza-2'-deoxycytidine (5-azadC) on the proMMP-1 expression in the human HT1080 fibrosarcoma cell line. Real-time RT-PCR revealed that 5-azadC or 5-azadC + TSA but not TSA alone, despite global histone H4 hyperacetylation, increased proMMP-1 mRNA levels. This transcription activation was correlated with chromatin decondensation determined by nuclear texture image analysis technique. Western blot analysis of cell culture conditioned media revealed a significant increase in proMMP-1 secretion after 5-azadC or 5-azadC + TSA treatment compared to untreated cells. These results suggested that epigenetic mechanisms could be involved in proMMP-1 gene expression including chromatin supra-organization changes. Indeed, although the proMMP-1 gene promoter does not appear to contain CpG islands, its expression can be induced by the demethylating agent 5-azadC. Further experiments revealed that inhibition of protein neosynthesis by cycloheximide decreased 5-azadC-induced proMMP-1 mRNA, suggesting that epigenetically regulated intermediate molecules could be involved in proMMP-1 expression regulation in these cells.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Epigenetic regulation of proMMP-1 expression in the HT1080 human fibrosarcoma cell line

Poplineau

Dufer²,

Antonicelli³

et al. 2011

Int J Oncol

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“…Furthermore, an earlier report demonstrated ERK1/2 activation alone potently up-regulates MMP-1 mRNA levels whereas p38 activation has no effect on the MMP-1 promoter (68). IL-1 itself has been shown to stabilize human collagenase mRNA (69). It is likely that IL-1 modulates MMP-13 production in an autocrine manner that augments the effects of serotonin and thus, amplifies the signaling cascade in myometrial SMCs.…”

Section: Discussionmentioning

confidence: 99%

Serotonin-induced MMP-13 Production Is Mediated via Phospholipase C, Protein Kinase C, and ERK1/2 in Rat Uterine Smooth Muscle Cells

Shum

Melendez

Jeffrey

2002

Journal of Biological Chemistry

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Serotonin (5-hydroxytryptamine; 5-HT), acting via the 5-HT 2A receptor, up-regulates the transcription and production of interstitial collagenase (matrix metalloproteinase-13; MMP-13), a critical enzyme responsible for maintaining the integrity of the uterus, after parturition. Serotonin treatment of rat uterine myometrial smooth muscle cells induced inositol phosphate (IP) turnover, which was abolished by the 5-HT 2A receptorspecific antagonists ketanserin and spiperone. The phospholipase C (PLC) inhibitors U73122 and D609 attenuated serotonin-mediated-IP turnover with a corresponding inhibition of MMP-13 protein production. Subsequent recovery of both MMP-13 protein expression and IP generation was seen following the removal of D609. Protein kinase C (PKC) activators, the diacylglycerol analogue 1,2-dioctanoyl-sn-glycerol and phorbol myristate acetate (PMA), mimicked the effect of serotonin on MMP-13 protein expression; prolonged PMA treatment (which down-regulates PKC) lowered MMP-13 protein levels. The PKC-specific inhibitors bisindolylmaleimide I, calphostin C, CGP 41251, and the PKC␦-selective inhibitor rottlerin were able to suppress serotonin up-regulation of MMP-13. Furthermore, the mitogen-activated protein kinase kinase (MEK) inhibitor PD98059 blocked serotonin-dependent activation of p44/42 MAPK (pERK1/2), a downstream effector of PKC and also down-regulated MMP-13 protein expression. Similarly, calphostin C and rottlerin depressed activation of p44/42 MAPK. From these studies, serotonin, binding through the 5-HT 2A receptor, initiates a signaling cascade whereby stimulation of PLC leads to the activation of PKC and subsequently the ERK1/2 pathway, which ultimately results in MMP-13 production.The maintenance of the three-dimensional architecture of the mammalian uterus is carefully regulated during pregnancy and after parturition. Production of fibrillar collagens (Types I and III) is up-regulated 10-fold in the uterus during pregnancy (1, 2). These collagens possess a rigid superhelical structure, which is responsible for providing the tensile strength necessary to accommodate the force exerted by the growing fetus. After parturition, a precisely programmed non-necrotic and non-inflammatory process of connective tissue remodeling occurs, which results in the rapid and dramatic degradation of the collagen amassed and returns the uterus to reproductive competence (3). This transition is initiated by the enzyme interstitial collagenase (matrix metalloproteinase-13; MMP-13), 1 a member of the matrix metalloproteinase family. It acts as not only the rate-limiting step but also the committed step in the catalysis of the degradation of extracellular collagen (4, 5). The expression of MMP-13 occurs during postpartum involution and is not present either during the pregnancy or even within hours prior to parturition. The myometrial smooth muscle cell of the uterus has been identified not only as the source for MMP-13 (6) but also that of its natural substrate, collagen (7). Thus, the myometrial smooth muscle...

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“…GST subunits from untreated (C) or IL-1-treated (IL-1) (100 units/ml) hepatocytes were purified by glutathione-affinity column and separated by HPLC as described under "Experimental Procedures." the regulation of collagenase mRNA by IL-1 (35). However, in this case, this cytokine increased the stability of this transcript by reversing the destabilizing effects of sequences located in the 3Ј-untranslated regions.…”

Section: Figmentioning

confidence: 92%

Modulation of Glutathione S-Transferase Subunits A2, M1, and P1 Expression by Interleukin-1β in Rat Hepatocytes in Primary Culture

Mahéo¹,

Antras-Ferry

Morel

et al. 1997

Journal of Biological Chemistry

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The influence of various cytokines on the expression of glutathione S-transferases (GSTs) was investigated in rat hepatocytes in primary culture. Only treatment of hepatocytes with interleukin-1␤ (IL-1) was effective, resulting in a marked decrease in GSTs. Steady-state mRNA levels of rGSTA2 and M1 were strongly downregulated by IL-1 in a dose-dependent manner after a 24-h exposure while rGSTP1 mRNA level was increased by a 48-h treatment. Similar effects of IL-1 were observed at the protein level. The response to IL-1 appeared to be specific for each subunit within GST gene families. In addition, IL-1 strongly suppressed the induction of rGSTA2 by 3-methylcholanthrene, oltipraz (a synthetic derivative of 1,2-dithiole-3-thione), and phenobarbital and that of rGSTM1 by oltipraz and phenobarbital, whereas it was ineffective on rGSTP1 induction by these compounds. Using in vitro nuclear run-on transcription assay and Northern blot analysis of ␣-amanitin-treated cells, IL-1-mediated rGSTM1 mRNA decrease was found to result from mRNA destabilization. These results provide the first demonstration that IL-1 regulates some major GST subunits in hepatocytes by a post-transcriptional mechanism.

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Regulation of collagenase gene expression by IL–1β requires transcriptional and post-transcriptional mechanisms

Cited by 74 publications

References 52 publications

Epigenetic regulation of proMMP-1 expression in the HT1080 human fibrosarcoma cell line

Epigenetic regulation of proMMP-1 expression in the HT1080 human fibrosarcoma cell line

Serotonin-induced MMP-13 Production Is Mediated via Phospholipase C, Protein Kinase C, and ERK1/2 in Rat Uterine Smooth Muscle Cells

Modulation of Glutathione S-Transferase Subunits A2, M1, and P1 Expression by Interleukin-1β in Rat Hepatocytes in Primary Culture

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