Spatio-temporal expression of MMP-2, MMP-9 and tissue kallikrein in uteroplacental units of the pregnant guinea-pig (Cavia porcellus)

Corthorn, Jenny; Rey, Sergio; Chacón, Cecília; Valdés, Gloría

doi:10.1186/1477-7827-5-27

Cited by 21 publications

(23 citation statements)

References 40 publications

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“…Stimulation of the B2R induces MMP overexpression and cell migration in a rat astroglial cell line [39], while the B1R induces release of MMP-2 and MMP-9 in breast cancer cells [37]. Co-localization of MMP-9 and the B2R was observed in our previous studies in guinea-pig extravillous trophoblast [46]. The co-localization of MMP-9 and MMP-2 with the B2R was confirmed in HTR-8/SVneo cells by immunohistochemistry and enzymatic activity in this study.…”

Section: Discussionmentioning

confidence: 96%

Bradykinin promotes migration and invasion of human immortalized trophoblasts

Erices

Corthorn

Lisboa

et al. 2011

Reprod Biol Endocrinol

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Having demonstrated that the bradykinin B2 receptor (B2R) is expressed in cells that participate in trophoblast invasion in humans and guinea-pigs, we investigated the role of bradykinin (BK) on cell migration and invasion in the HTR-8/SVneo trophoblast cell line using wound healing and invasion assays. First, we documented that HTR-8/SVneo cells expressed kallikrein, B2R, B1R, MMP-2 and MMP-9 using immunocytochemistry. Incubation with BK (10.0 microMol/L) for 18 hours increased the migration index 3-fold in comparison to controls or to cells preincubated with the B2R antagonist HOE-140. BK (10.0 microMol/L) incubation yielded a similar number of proliferating and viable cells as controls, therefore the enhanced closure of the wound cannot be attributed to proliferating cells. Incubation with BK (10.0 microMol/L) for 18 hours increased the invasion index 2-fold in comparison to controls or to cells preincubated with the antagonist of the B2R. Neither the B1R ligand Lys-des-Arg9 BK, nor its antagonist Lys-(des-Arg9-Leu8), modified migration and invasion. Further support for the stimulatory effect of B2R activation on migration and invasion is provided by the 3-fold increase in the number of filopodia per cell versus controls or cells preincubated with the B2R antagonist. Bradykinin had no effect on the cellular protein content of the B2R, nor the MMP-9 and MMP-2 gelatinase activity in the culture media varied after incubation with BK. This study adds bradykinin-acting on the B2R-to the stimuli of trophoblast migration and invasion, an effect that should be integrated to other modifications of the kallikrein-kinin system in normal and pathological pregnancies.

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Section: Discussionmentioning

confidence: 96%

Bradykinin promotes migration and invasion of human immortalized trophoblasts

Erices

Corthorn

Lisboa

et al. 2011

Reprod Biol Endocrinol

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“…Gelatinase activity was detected by zymography using methods described previously with some modifications [16]. PVAT homogenates (50 μg/lane) were resolved under non-reducing conditions in an 8% polyacrylamide gel containing 0.5 mg/ml gelatin (Merck, Darmstadt, Germany).…”

Section: Methodsmentioning

confidence: 99%

Tumor Necrosis Factor-α Induces Aortic Intima-Media Thickening via Perivascular Adipose Tissue Inflammation

et al. 2013

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Background/Aims: Neointimal thickening results from inflammation in association with vascular smooth muscle cell (VSMC) proliferation. We studied the role of perivascular adipose tissue (PVAT) on VSMC proliferation and intima-media thickening (IMT) in a rodent model of chronic inflammation. Methods: The abdominal aorta and surrounding PVAT of tumour necrosis factor (TNF)-α-injected mice were examined 28 days after administration. Plasma and PVAT cytokines were measured with Milliplex™ assays. Inflammatory cells were examined with immunofluorescence. Expression of transforming growth factor (TGF)-β1, matrix metalloproteinase (MMP)-2, MMP-9 and MMP-12 was examined with immunohistochemistry, immunoblotting and zymography. IMT was determined. Cell proliferation and TGF-β1 mRNA levels were examined after treating VSMC with PVAT homogenates ± MMP-2 inhibitors (batimastat, ARP 100 or TIMP-2) and SB-431542, a selective inhibitor of the TGF-β-type 1 receptor. Results: Significant increases in CD3, CD68, neutrophils, vascular cell adhesion molecule-1 and MMP-2 in PVAT, and TGF-β1 and IMT of the aorta of TNF-α-injected mice were observed. PVAT of TNF-α-injected mice significantly up-regulated TGF-β1 and increased cell proliferation in a dose-dependent manner and was attenuated by SB-431542, batimastat, ARP 100 and TIMP-2. Conclusions: Our study shows that chronic PVAT inflammation leads to MMP-mediated increase in TGF-β1 and hence VSMC proliferation.

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“…Under normal physiological conditions, MMPs are known to regulate cellular migration, invasion, and angiogenesis during embryonic implantation, whereas under pathological conditions, increased expression and activity of MMPs result in tumor growth, migration, and metastasis, leading to the development of cancer (Corthorn et al 2007). The controlled expression and a proper balance between MMPs and their inhibitors (TIMPs), which determine the net MMP activity (Seval et al 2004) and hence regulate the invasive potential of placental trophoblasts, are pivotal for maintaining normal placentation (Staun-Ram & Shalev 2005).…”

Section: Introductionmentioning

confidence: 99%

Imbalance between matrix metalloproteinases and their tissue inhibitors in preeclampsia and gestational trophoblastic diseases

Rahat¹,

Sharma²,

Bagga³

et al. 2016

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The invasion cascade exhibited by placental trophoblasts and cancerous cells bears many similarities, and it is attributed to extracellular matrix degradation mediated by matrix metalloproteinases (MMPs). Although proper and controlled invasion by trophoblasts into the maternal uterus is an essential requirement for maintenance of normal pregnancy, any abnormality in this phenomenon results in the development of invasion-related disorders such as gestational trophoblastic diseases (GTDs) and preeclampsia. We studied the epigenetic basis of differential expression of two placental MMPs (MMP2 and MMP9) and tissue inhibitors of metalloproteinases (TIMP2 and TIMP1) during normal gestation and invasion-related disorders, i.e., preeclampsia and GTDs. Our study suggests the association of H3K9/27me3 with differential expression of these MMPs and their inhibitors, which regulate the placental invasion during normal pregnancy, whereas no role of CpG methylation was observed in the differential expression of MMPs/TIMPs. Further, development of GTDs was associated with abnormally higher expression of these MMPs and lower levels of their inhibitors, whereas the reverse trends were observed for MMPs and their TIMPs in case of preeclampsia, in association with abnormal changes in H3K9/27me3. These results suggest the involvement of higher levels of MMPs in an aggressive invasive behavior depicted by GTDs, whereas lower levels of these MMPs in shallow and poor invasive phenotype associated with preeclampsia. Thus, our study shows the significance of a proper balance regulated by histone trimethylation between differential expression of MMPs and their TIMPs for maintaining normal pregnancy and its deregulation as a contributing factor for pathogenesis of invasive disorders during pregnancy.

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Spatio-temporal expression of MMP-2, MMP-9 and tissue kallikrein in uteroplacental units of the pregnant guinea-pig (Cavia porcellus)

Cited by 21 publications

References 40 publications

Bradykinin promotes migration and invasion of human immortalized trophoblasts

Bradykinin promotes migration and invasion of human immortalized trophoblasts

Tumor Necrosis Factor-α Induces Aortic Intima-Media Thickening via Perivascular Adipose Tissue Inflammation

Imbalance between matrix metalloproteinases and their tissue inhibitors in preeclampsia and gestational trophoblastic diseases

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