Increased matrix metalloproteinases 2 and 9 in placenta of diabetic rats at midgestation

Pustovrh, María Carolina; Jawerbaum, Alicia; Capobianco, Evangelina; White, Verónica; López‐Costa, Juan José; González, Ezequiel

doi:10.1016/j.placenta.2004.06.011

Cited by 32 publications

(45 citation statements)

References 67 publications

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“…According to the results of other studies, the regulation of CX3CL1 function may be maintained on both protein and gene expression levels. Increased expression of matrix metalloproteinases (MMPs) and disintegrin metalloproteinases (ADAMs, including ADAM17/TACE) or sheddases have been reported in the diabetic placenta [46, 47]. These increases may lead to an increase in the concentration of the soluble form of CX3CL1, which is derived from its membrane form.…”

Section: Discussionmentioning

confidence: 99%

Fractalkine (CX3CL1) and Its Receptor CX3CR1 May Contribute to Increased Angiogenesis in Diabetic Placenta

Szukiewicz

Kochanowski

Pyźlak

et al. 2013

Mediators of Inflammation

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Chemokine CX3CL1 is unique, possessing the ability to act as a dual agent: chemoattractant and adhesive compound. Acting via its sole receptor CX3CR1, CX3CL1 participates in many processes in human placental tissue, including inflammation and angiogenesis. Strongly upregulated by hypoxia and/or inflammation-induced inflammatory cytokines secretion, CX3CL1 may act locally as a key angiogenic factor. Both clinical observations and histopathological studies of the diabetic placenta have confirmed an increased incidence of hypoxia and inflammatory reactions with defective angiogenesis. In this study we examined comparatively (diabetes class C complicated versus normal pregnancy) the correlation between CX3CL1 content in placental tissue, the mean CX3CR1 expression, and density of the network of placental microvessels. A sandwich enzyme immunoassay was applied for CX3CL1 measurement in placental tissue homogenates, whereas quantitative immunohistochemical techniques were used for the assessment of CX3CR1 expression and the microvascular density. Significant differences have been observed for all analyzed parameters between the groups. The mean concentration of CX3CL1 in diabetes was increased and accompanied by augmented placental microvessel density as well as a higher expression of CX3CR1. In conclusion, we suggest involvement of CX3CL1/CX3CR1 signaling pathway in the pathomechanism of placental microvasculature remodeling in diabetes class C.

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Section: Discussionmentioning

confidence: 99%

Fractalkine (CX3CL1) and Its Receptor CX3CR1 May Contribute to Increased Angiogenesis in Diabetic Placenta

Szukiewicz

Kochanowski

Pyźlak

et al. 2013

Mediators of Inflammation

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“…In effect, a decrease in the expression/activity of placental MMP-2 and MMP-9 was observed in late compared with mid-pregnancy in rats. 37 Some studies have shown an increase in MMP-2 and MMP-9 in the placenta of diabetic rats at mid-gestation, 50 but did not follow the changes in MMPs during late-gestation. Other studies have suggested that MMPs are involved in placental remodeling during pregnancy.…”

Section: Vascular and Placental Mmps During Pregnancymentioning

confidence: 97%

“…Other studies have suggested that MMPs are involved in placental remodeling during pregnancy. 50 Serum MMP-2 and MMP-9 activity are increased in pregnant bitches. 51 Also, the expression of MMP-2, MMP-14 and EMMPRIN is increased in the bovine placenta during late gestation.…”

Section: Vascular and Placental Mmps During Pregnancymentioning

confidence: 99%

Matrix Metalloproteinases in Normal Pregnancy and Preeclampsia

Chen

Khalil

2017

Progress in Molecular Biology and Translational Science

229

168

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Normal pregnancy is associated with marked hemodynamic and uterine changes that allow adequate uteroplacental blood flow and uterine expansion for the growing fetus. These pregnancy-associated changes involve significant uteroplacental and vascular remodeling. Matrix metalloproteinases (MMPs) are important regulators of vascular and uterine remodeling. Increases in MMP-2 and MMP-9 have been implicated in vasodilation, placentation and uterine expansion during normal pregnancy. The increases in MMPs could be induced by the increased production of estrogen and progesterone during pregnancy. MMP expression/activity may be altered during complications of pregnancy. Decreased vascular MMP-2 and MMP-9 may lead to decreased vasodilation, increased vasoconstriction, hypertensive pregnancy and preeclampsia. Abnormal expression of uteroplacental integrins, cytokines and MMPs may lead to decreased maternal tolerance, apoptosis of invasive trophoblast cells, inadequate remodeling of spiral arteries, and reduced uterine perfusion pressure (RUPP). RUPP may cause imbalance between the anti-angiogenic factors soluble fms-like tyrosine kinase-1 and soluble endoglin and the pro-angiogenic vascular endothelial growth factor and placental growth factor, or stimulate the release of inflammatory cytokines, hypoxia-inducible factor, reactive oxygen species, and angiotensin AT1 receptor agonistic autoantibodies. These circulating factors could target MMPs in the extracellular matrix as well as endothelial and vascular smooth muscle cells, causing generalized vascular dysfunction, increased vasoconstriction and hypertension in pregnancy. MMP activity can also be altered by endogenous tissue inhibitors of metalloproteinases (TIMPs) and changes in the MMP/TIMP ratio. In addition to their vascular effects, decreases in expression/activity of MMP-2 and MMP-9 in the uterus could impede uterine growth and expansion and lead to premature labor. Understanding the role of MMPs in uteroplacental and vascular remodeling and function could help design new approaches for prediction and management of preeclampsia and premature labor.

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“…However, hyperglycaemia in pregnancy induces placental genes for chronic stress and inflammatory pathways. In contrast to upregulation of MMP-2 and MMP-9 in placentas of rats with streptozocin-induced, MMP-9 activity is lower in the placentas of women with GDM [28,29]. Furthermore, MMP-9 is released in tissue cultures by syncytiotrophoblastic cells and is presumably secreted into the woman's bloodstream both by the placenta and by vascular endothelium.…”

Section: Conclusion/discussionmentioning

confidence: 93%

Serum levels of matrix metalloproteinases MMP-2 and MMP-9 and their inhibitors in women with glucose intolerance in pregnancy and normal controls

Stojanovic

Lewandowski²,

Salata

et al. 2010

Gynecological Endocrinology

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Increased matrix metalloproteinases 2 and 9 in placenta of diabetic rats at midgestation

Cited by 32 publications

References 67 publications

Fractalkine (CX3CL1) and Its Receptor CX3CR1 May Contribute to Increased Angiogenesis in Diabetic Placenta

Fractalkine (CX3CL1) and Its Receptor CX3CR1 May Contribute to Increased Angiogenesis in Diabetic Placenta

Matrix Metalloproteinases in Normal Pregnancy and Preeclampsia

Serum levels of matrix metalloproteinases MMP-2 and MMP-9 and their inhibitors in women with glucose intolerance in pregnancy and normal controls

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