Collagen of umbilical cord arteries and its alterations in EPH-gestosis

Bańkowski, Edward; Romanowicz, Lech; Jaworski, Stefan

doi:10.1515/jpme.1993.21.6.491

Cited by 51 publications

(46 citation statements)

References 20 publications

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“…The enhancement in collagenolytic activity suggested by the increase in MMP-1, the lack of increase in TIMP-1, and the lack of precursor form of COL1A1 synthesis during preeclampsia strongly imply the alteration of the collagen network in the blood vessel wall. This is consistent with a previous report 40 showing that preeclampsia is accompanied by a decrease in collagen type 1 in umbilical cord arteries. Because collagen is found in all three layers of blood vessels and especially around smooth muscle cells of the media, where it provides mechanical strength and maintains the structural integrity of the vasculature, it is reasonable to infer that the damage to this network might increase vascular permeability.…”

Section: Discussionsupporting

confidence: 94%

Increased Expression of Matrix Metalloproteinase-1 in Systemic Vessels of Preeclamptic Women

Estrada-Gutiérrez

Cappello

Mishra

et al. 2011

The American Journal of Pathology

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This study was conducted to determine the following: (1) whether matrix metalloproteinase-1 (MMP-1) is increased in systemic vessels of preeclamptic women, (2) whether this increase might be mediated by neutrophils, and (3) whether MMP-1 could be responsible for vascular dysfunction. Omental arteries and plasma were collected from healthy pregnant and preeclamptic women. Omental arteries were evaluated for gene and protein expression of MMP-1, collagen type 1␣, tissue inhibitor of metalloproteinase-1, and vascular reactivity to MMP-1. Gene and protein expression levels were also evaluated in human vascular smooth muscle cells (VSMCs) co-cultured with activated neutrophils, reactive oxygen species, or tumor necrosis factor ␣. Vessel expression of MMP-1 and circulating MMP-1 levels were increased in preeclamptic women, whereas vascular expression of collagen or tissue inhibitor of metalloproteinase-1 were down-regulated or unchanged. In cultured VSMCs, the imbalance in collagen-regulating genes of preeclamptic vessels was reproduced by treatment with neutrophils, tumor necrosis factor ␣, or reactive oxygen species. Chemotaxis studies with cultured cells revealed that MMP-1 promoted recruitment of neutrophils via vascular smooth muscle release of interleukin-8. Furthermore, MMP-1 induced vasoconstriction via protease-activated receptor-1, whose expression was significantly increased in omental arteries of preeclamptic women and in VSMCs co-cultured with neutrophils. Collectively, these findings disclose a novel role for MMP-1 as a mediator of vasoconstriction and vascular dysfunction in preeclampsia.

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Section: Discussionsupporting

confidence: 94%

Increased Expression of Matrix Metalloproteinase-1 in Systemic Vessels of Preeclamptic Women

Estrada-Gutiérrez

Cappello

Mishra

et al. 2011

The American Journal of Pathology

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“…Arteries isolated from women with preeclampsia show increased collagen content in the umbilical cord artery (2). The L-NAME mUA evaluated in our study echo the literature's description of preclamptic maternal arteries as our vessels also had increased collagen and elastin content and increased wall-to-lumen ratios (2,49).…”

Section: Discussionsupporting

confidence: 79%

“…Collagen is a very stiff protein that does not contribute to the elasticity of the vessel at lower pressures but is a mediator of the passive pressure/diameter relationship of arteries at higher pressures (1). Arteries isolated from women with preeclampsia show increased collagen content in the umbilical cord artery (2). The L-NAME mUA evaluated in our study echo the literature's description of preclamptic maternal arteries as our vessels also had increased collagen and elastin content and increased wall-to-lumen ratios (2,49).…”

Section: Discussionmentioning

confidence: 99%

Reduced NO signaling during pregnancy attenuates outward uterine artery remodeling by altering MMP expression and collagen and elastin deposition

Hale

Weger

Mandalà

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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Hale SA, Weger L, Mandala M, Osol G. Reduced NO signaling during pregnancy attenuates outward uterine artery remodeling by altering MMP expression and collagen and elastin deposition. Am J Physiol Heart Circ Physiol 301: H1266 -H1275, 2011. First published August 19, 2011 doi:10.1152/ajpheart.00519.2011.-Recent findings indicate that endothelial nitric oxide (NO) plays a key role in uterine artery outward circumferential remodeling during pregnancy. Although the underlying mechanisms are not known, they likely involve matrix metalloproteinases (MMPs). The goal of this study was to examine the linkage among NO inhibition, expansive remodeling, and MMP expression within the uterine vascular wall. Adult female rats were treated with N G -nitro-L-arginine methyl ester [L-NAME (LPLN)] beginning on day 10 of pregnancy and until death at day 20 and compared with age-matched controls [late pregnant (LP)]. Mean arterial pressure of LPLN rats was significantly higher than controls. LPLN fetal and placental weights were significantly reduced compared with controls. Main uterine arteries (mUA) were collected to determine dimensional properties (lumen area and wall thickness), collagen and elastin content, and levels of endothelial nitric oxide synthase (eNOS) and MMP expression. Circumferential remodeling was attenuated, as evidenced by significantly smaller lumen diameters. eNOS RNA and protein were significantly (Ͼ90%) decreased in the LPLN mUA compared with LP. Collagen and elastin contents were significantly increased in LPLN rats by ϳ10 and 25%, respectively, compared with LP (P Ͻ 0.05). Both MMP-2 and tissue inhibitors of metalloproteinase-2 as assessed by immunofluorescence were lower in the endothelium (reduction of 60%) and adventitia (reduction of 50%) of LPLN compared with LP mUA. Membrane bound MMP-1 (MT1-MMP) as assessed by immunoblot was significantly decreased in LPLN. These data suggest a novel contribution of MMPs to gestational uterine vascular remodeling and substantiate the linkage between NO signaling and gestational remodeling of the uterine circulation via altered MMP, TIMP-2, and MT1-MMP expression and activity. matrix metalloproteinase; extracellular matrix; hypertension; pregnancy; nitric oxide DURING PREGNANCY, THE UTERINE vasculature undergoes significant expansive remodeling to accommodate the dramatic increase in uteroplacental blood flow that is requisite for normal pregnancy outcome. Studies from our and other laboratories (40,41,44,46,50,61) have established that nitric oxide (NO) is a key molecule involved in vascular remodeling during pregnancy and that expression of endothelial nitric oxide synthase (eNOS) is increased during pregnancy, leading to increased synthesis and release of NO from the endothelium.The importance of NO and NO signaling during pregnancy is underscored by the vascular and reproductive implications evident in mouse knockouts for endothelial NO synthase and in rats treated with the NO inhibitor N G -nitro-L-arginine methyl ester (L-NAME) during pregnancy (50, 64). Tre...

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“…We found in previous studies that the umbilical cord contains significant amounts of extracellular matrix components, mainly collagen [9,10] and GAGs [10,11]. It is known that extracellular matrix compounds serve as a storage site to concentrate and stabilize growth factors in the vicinity of cells [12].…”

Section: Introductionmentioning

confidence: 97%

“…It is accompanied by a significant increase in collagen content [9] in the umbilical cord arteries and early replacement of hyaluronic acid by sulfated GAGs both in the umbilical cord arteries and in Wharton's jelly [11]. One may expect that a growth factor(s) may be responsible for EPH gestosis-associated remodeling of the umbilical cord tissue.…”

Section: Introductionmentioning

confidence: 99%

Stimulation of Glycosaminoglycan Biosynthesis by Umbilical Cord Serum of Newborns Delivered by Mothers with EPH Gestosis (Preeclampsia)

Romanowicz¹,

Bańkowski²,

Jaworski

2000

Pathobiology

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Objective: Edema, proteinuria, hypertension (EPH) gestosis, also known as preeclampsia, is the most common, pregnancy-associated pathological syndrome. It is accompanied by a significant increase in collagen content in the umbilical cord arteries and early replacement of hyaluronic acid by sulfated glycosaminoglycans (GAGs) both in these arteries and in Wharton’s jelly. Such a remodelling of the umbilical cord tissues is accompanied by an increase in insulin-like growth factor-I (IGF-I) concentration in the umbilical cord serum. Methods: Contact-inhibited human fibroblasts were incubated in Dulbecco culture medium containing control or EPH umbilical cord serum and supplemented with ¹⁴C-glucosamine or ³⁵S-sulfate. Radioactive GAGs were isolated, submitted to electrophoretic fractionation and quantified. Results: The presence of umbilical cord serum in culture medium strongly stimulated the incorporation of ¹⁴C-glucosamine and ³⁵S-sulfate into GAGs synthesized by these cells. EPH serum was much more active in stimulation of sulfated GAGs biosynthesis than control serum, whereas the biosynthesis of hyaluronic acid was stimulated by both sera to a similar degree. Conclusion: Since IGF-I is known as a stimulator of collagen and sulfated GAG biosynthesis, the high concentration of this growth factor in the umbilical cord plasma may be responsible for preeclampsia-associated remodeling of the umbilical cord.

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Collagen of umbilical cord arteries and its alterations in EPH-gestosis

Cited by 51 publications

References 20 publications

Increased Expression of Matrix Metalloproteinase-1 in Systemic Vessels of Preeclamptic Women

Increased Expression of Matrix Metalloproteinase-1 in Systemic Vessels of Preeclamptic Women

Reduced NO signaling during pregnancy attenuates outward uterine artery remodeling by altering MMP expression and collagen and elastin deposition

Stimulation of Glycosaminoglycan Biosynthesis by Umbilical Cord Serum of Newborns Delivered by Mothers with EPH Gestosis (Preeclampsia)

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