Elevated protease activities in human amnion and chorion correlate with preterm premature rupture of membranes

Draper, Deborah; McGregor, James A.; Hall, Jenny; Jones, Ward; Beutz, Michelle; Heine, R. Phillips; Porreco, Richard P.

doi:10.1016/0002-9378(95)90640-1

Cited by 92 publications

(46 citation statements)

References 16 publications

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“…Candida albicans, an opportunistic yeast, attaches to ECM and BM molecules, and it is presumed that the interaction with immobilized FN and other ECM molecules enhances the establishment and maintenance of infection at sites outside its normal niche (Calderone & Scheld, 1987 ;Klotz, 1994). Other mucosal pathogens, such as the streptococci, adhere to immobilized FN in a time-and dose-dependent manner (Kuusela et al, 1985 ;van der Flier et al, 1995 such as FN and LM, to establish colonization and cause persistent infection.…”

Section: Discussionmentioning

confidence: 99%

Trichomonas vaginalis interactions with fibronectin and laminin

Crouch

Alderete

1999

Microbiology

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The sexually transmitted protozoan Trichomonas vaginalis cytoadheres to vaginal epithelial cells and causes contact-dependent cytotoxicity which, when combined with the normal exfoliation process, leads to erosion of the epithelium, which may allow trichomonads into extracellular matrix and basement membrane sites. Therefore, the association of T. vaginalis with immobilized fibronectin (FN) and laminin (LM) on cover-slips was examined. Binding of live parasites to coated cover-slips was time-and parasite-densitydependent. Coincubation with an inhibitor of trichomonad cysteine proteinases resulted in an increased attachment of parasites to FN but had no effect on binding to LM, denoting that protease activity influenced optimal FN associations. Further, 20 h mid-exponential phase trichomonads placed in fresh culture medium for 3 h gave higher levels of binding to FN, suggesting that changes during growth in vitro to T. vaginalis organisms affect maximal levels of binding to FN. Extended incubation with substrates diminished the capacity of parasites to bind FN and LM. Treatment of live organisms with periodate reduced binding to LM but not FN, suggesting a role for carbohydrates. In addition, trypsinization of live parasites decreased numbers bound to both substrates. Placement of trypsinized parasites in medium for 2 h fully regenerated binding to FN but not LM. Incubation of trypsinized parasites with cycloheximide abrogated regeneration of attachment to FN, affirming a role for synthesized surface proteins in FN binding. Importantly, the T. vaginalis adhesin proteins that mediate cytoadherence, and iron, a factor that regulates adhesin synthesis, were not involved in FN and LM recognition. These results suggest a role for surface proteins and carbohydrates in trichomonal associations with FN and LM, respectively.

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Section: Discussionmentioning

confidence: 99%

Trichomonas vaginalis interactions with fibronectin and laminin

Crouch

Alderete

1999

Microbiology

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“…The presence of intrauterine infection has been shown to result in the local expression and secretion of proinflammatory cytokines such as interleukin (IL)-1␤, tumor necrosis factor-␣, IL-6, and IL-8 (Romero et al, 1993;Dudley et al, 1996;Keelan et al, 1999a), which act locally on intrauterine cells to induce the release of inflammatory mediators, extracellular matrix-remodeling enzymes (So et al, 1992;Draper et al, 1995), and prostaglandins (PGs) through altered expression of prostanoid biosynthetic enzymes including fatty acid cyclooxygenase-2 (COX-2) Hansen et al, 1999;Kniss, 1999;Rauk and Chiao, 2000).…”

mentioning

confidence: 99%

Nanomolar and Micromolar Effects of 15-Deoxy-Δ^12,14-prostaglandin J₂on Amnion-Derived WISH Epithelial Cells: Differential Roles of Peroxisome Proliferator-Activated Receptors γ and δ and Nuclear Factor κB

Berry¹,

Keelan²,

Helliwell³

et al. 2005

Mol Pharmacol

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15-Deoxy ⌬12,14 -prostaglandin J 2 (15d-PGJ 2 ), an activator of peroxisome proliferator-activated receptor (PPAR)-␥ and -␦, is a prostanoid metabolite with anti-inflammatory actions. In intrauterine tissues, proinflammatory cytokines and prostaglandins have been identified as playing key roles in the maintenance of pregnancy and the onset of labor. We investigated and compared the early (Ͻ3 h) effects of 15d-PGJ 2 with rosiglitazone (PPAR-␥ ligand) and 2-methyl-4-((4-methyl-2-(4-trifluoromethylphenyl)-1,3-thiazol-5-yl)-methylsulfanyl)phenoxy-acetic acid (GW501516) (PPAR-␦ ligand) on interleukin (IL)-1␤-induced prostaglandin and cytokine production by amnion-derived WISH cells. We show that 15d-PGJ 2 exerts differential effects depending on concentration. At low concentrations (Ͻ0.1 M), 15d-PGJ 2 inhibited IL-1␤-stimulated prostaglandin E 2 (PGE 2 ) but not cytokine (IL-6/IL-8) production or cyclooxygenase-2 (COX-2) expression. This effect was attenuated by a PPAR-␥ inhibitor [2-chloro-5-nitro-N-phenylbenzamide (GW9662)], by transfection with a dominant-negative PPAR construct, and was reproduced by the PPAR-␥ ligand rosiglitazone. At higher concentrations (1-10 M), 15d-PGJ 2 inhibited IL-1␤-stimulated PGE 2 and cytokine production and COX-2 expression, and this effect was not blocked by GW9662. Rosiglitazone at high concentrations (1-10 M) stimulated PGE 2 production in the absence or presence of the dominant-negative PPAR. The PPAR-␦ ligand GW501516 also inhibited IL-1␤-stimulated PGE 2 production but only at high concentrations (1 M). IL-1␤-induced nuclear factor-B (NF-B) DNA binding activity was significantly inhibited by 15d-PGJ 2 (10 M) and GW501516 (1 M) but increased with 10 M rosiglitazone. We conclude that 1) at low concentrations, 15d-PGJ 2 acts through a PPAR-␥ signaling pathway; b) at higher concentrations, its actions are mediated most likely through other pathways such as activation of PPAR-␦ and/or inhibition of NF-B; and 3) rosiglitazone exerts PPAR-independent effects at high concentrations (Ͼ1 M).Proinflammatory cytokines have been shown to play crucial roles in the maintenance of human pregnancy and the initiation of parturition (Romero et al., 1993;Mitchell et al., 1995). The presence of intrauterine infection has been shown to result in the local expression and secretion of proinflammatory cytokines such as interleukin (IL)-1␤, tumor necrosis factor-␣, IL-6, and IL-8 (Romero et al., 1993;Dudley et al., 1996;Keelan et al., 1999a), which act locally on intrauterine cells to induce the release of inflammatory mediators, extracellular matrix-remodeling enzymes (So et al., 1992;Draper et al., 1995), and prostaglandins (PGs) through altered expression of prostanoid biosynthetic enzymes including fatty acid cyclooxygenase-2 (COX-2) Hansen et al., 1999;Kniss, 1999;Rauk and Chiao, 2000).Although most studies to date have focused on the produc- Article, publication date, and citation information can be found at http://molpharm.aspetjournals.org. doi:10.1124/mol.104.009449.ABBREVIATIONS: IL, ...

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“…We have demonstrated a decline in amniotic fluid TIMP activity in association with labour. At the same time the activity of MMP-9 increases in amniotic fluid and in tissues at term and preterm (Draper et al 1995, Athayde et al 1998. The net effect is likely to be breakdown of connective tissue in the fetal membranes (Bryant-Greenwood & Yamamoto 1995).…”

Section: Discussionmentioning

confidence: 98%

Secretion of tissue inhibitors of matrix metalloproteinases by human fetal membranes, decidua and placenta at parturition

Riley

Leask²,

Denison³

et al. 1999

Journal of Endocrinology

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At parturition, breakdown of extracellular matrix in the fetal membranes may play a part in the rupture of the membranes and in the aetiology of premature rupture, in addition to having a regulatory role in the cell-cell interactions and signalling at the feto-maternal interface to stimulate myometrial contractility. The matrix metalloproteinases (MMPs) are important enzymes for the breakdown of extracellular matrix and their activity is regulated by a family of endogenous inhibitors, the tissue inhibitors of matrix metalloproteinases (TIMPs). At parturition, alteration in the balance between MMPs and TIMPs may mediate this extracellular matrix breakdown during rupture of fetal membranes. The aims of this study were to determine if the intrauterine secretion of TIMPs changes at labour, and to characterise their cellular sources. A broad range of TIMP activities (27-30 kDa, 24 kDa and 21 kDa) were detected by reverse zymography in term amniotic fluid. There was a significant (P<0·05) decrease in the amount of TIMPs in amniotic fluid and their release with the onset of labour. The TIMPs were characterised by immunoblot as TIMPs-1, -2, -3 and -4. High levels of TIMPs were secreted by explants of chorio-decidua, decidua parietalis and placenta, with less being released by amnion. Immunolocalisation studies revealed a specific distribution pattern for each of the TIMP isoforms. Trophoblast cells of chorion laeve, decidua parietalis and placental syncytiotrophoblast demonstrated specific immunoreactivity for all four isoforms. TIMPs were also found bound to selective regions of extracellular matrix. The decrease in TIMPs during labour may permit increased breakdown of extracellular matrix in the fetal membranes and decidua at parturition, thus altering cell signalling at the feto-maternal interface and facilitating membrane rupture.

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Elevated protease activities in human amnion and chorion correlate with preterm premature rupture of membranes

Cited by 92 publications

References 16 publications

Trichomonas vaginalis interactions with fibronectin and laminin

Trichomonas vaginalis interactions with fibronectin and laminin

Nanomolar and Micromolar Effects of 15-Deoxy-Δ^12,14-prostaglandin J₂on Amnion-Derived WISH Epithelial Cells: Differential Roles of Peroxisome Proliferator-Activated Receptors γ and δ and Nuclear Factor κB

Secretion of tissue inhibitors of matrix metalloproteinases by human fetal membranes, decidua and placenta at parturition

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Elevated protease activities in human amnion and chorion correlate with preterm premature rupture of membranes

Cited by 92 publications

References 16 publications

Trichomonas vaginalis interactions with fibronectin and laminin

Trichomonas vaginalis interactions with fibronectin and laminin

Nanomolar and Micromolar Effects of 15-Deoxy-Δ12,14-prostaglandin J2on Amnion-Derived WISH Epithelial Cells: Differential Roles of Peroxisome Proliferator-Activated Receptors γ and δ and Nuclear Factor κB

Secretion of tissue inhibitors of matrix metalloproteinases by human fetal membranes, decidua and placenta at parturition

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Product

Resources

About

Nanomolar and Micromolar Effects of 15-Deoxy-Δ^12,14-prostaglandin J₂on Amnion-Derived WISH Epithelial Cells: Differential Roles of Peroxisome Proliferator-Activated Receptors γ and δ and Nuclear Factor κB