Confocal immunofluorescence localization of collagen types I, III, IV, V and VI and their ultrastructural organization in term human fetal membranes

Malak, T. M.; Ockleford, Colin; Bell, Steven; Dalgleish, Raymond; Bright, Nicholas A.; MacVicar, John

doi:10.1016/s0143-4004(05)80460-6

Cited by 204 publications

(132 citation statements)

References 36 publications

Supporting

Mentioning

129

Contrasting

Unclassified

Order By: Relevance

“…The outermost layer-the intermediate layer, sometimes called the spongy layer, or zona spongiosa, forms the junction between the amnion and chorion, and is comprised type III collagen, proteoglycans and glycoproteins [9]. The junctions between the amniotic and chorionic membranes are very fine and not clearly established ( Figure 1); in some cases it is very difficult to avoid the separation between membranes during the preparation for a microscopoc examination [9]. The chorion is thicker than amnion but has less tensile strength.…”

Section: Etiology Anatomy Of Chorio-amniotic Membranesmentioning

confidence: 99%

Mid-trimester preterm premature rupture of membranes (PPROM): etiology, diagnosis, classification, international recommendations of treatment options and outcome

Tchirikov

Schlabritz‐Loutsevitch

Mäher

et al. 2017

Journal of Perinatal Medicine

194

153

View full text Add to dashboard Cite

Mid-trimester preterm premature rupture of membranes (PPROM), defined as rupture of fetal membranes prior to 28 weeks of gestation, complicates approximately 0.4%-0.7% of all pregnancies. This condition is associated with a very high neonatal mortality rate as well as an increased risk of long-and short-term severe neonatal morbidity. The causes of the mid-trimester PPROM are multifactorial. Altered membrane morphology including marked swelling and disruption of the collagen network which is seen with PPROM can be triggered by bacterial products or/and pro-inflammatory cytokines. Activation of matrix metalloproteinases (MMP) have been implicated in the mechanism of PPROM. The propagation of bacteria is an important contributing factor not only in PPROM, but also in adverse neonatal and maternal outcomes after PPROM. Inflammatory mediators likely play a causative role in both disruption of fetal membrane integrity and activation of uterine contraction. The "classic PPROM" with oligo/anhydramnion is associated with a short latency period and worse neonatal outcome compared to similar gestational aged neonates delivered without antecedent PPROM. The "high PPROM" syndrome is defined as a defect of the chorio-amniotic membranes, which is not located over the internal cervical os. It may be associated with either a normal or reduced amount of amniotic fluid. It may explain why sensitive biochemical tests such as the Amniosure (PAMG-1) or IGFBP-1/alpha fetoprotein test can have a positive result without other signs of overt ROM such as fluid leakage with Valsalva. The membrane defect following fetoscopy also fulfils the criteria for "high PPROM" syndrome. In some cases, the rupture of only one membrane -either the chorionic or amniotic membrane, resulting in "pre-PPROM" could precede "classic PPROM" or "high PPROM". The diagnosis of PPROM is classically established by identification of nitrazine positive, fern positive watery leakage from the cervical canal observed during in specula investigation. Other more recent diagnostic tests include the vaginal swab assay for placental alpha macroglobulin-1 test or AFP and IGFBP1. In some rare cases amniocentesis and infusion of indigo carmine has been used to confirm the diagnosis of PPROM. The management of the PPROM requires balancing the potential neonatal benefits from prolongation of the pregnancy with the risk of intraamniotic infection and its consequences for the mother and infant. Close monitoring for signs of chorioamnionitis (e.g. body temperature, CTG, CRP, leucocytes, IL-6, procalcitonine, amniotic fluid examinations) is necessary to minimize the risk of neonatal and maternal complications. In addition to delayed delivery, broad spectrum antibiotics of penicillin or cephalosporin group and/or macrolide and corticosteroids have been show to improve neonatal outcome [reducing risk of chorioamnionitis (average risk ratio (RR) = 0.66), neonatal infections (RR = 0.67) and abnormal ultrasound scan of neonatal brain (RR = 0.67)]. The positive effect of continuo...

show abstract

Section: Etiology Anatomy Of Chorio-amniotic Membranesmentioning

confidence: 99%

Mid-trimester preterm premature rupture of membranes (PPROM): etiology, diagnosis, classification, international recommendations of treatment options and outcome

Tchirikov

Schlabritz‐Loutsevitch

Mäher

et al. 2017

Journal of Perinatal Medicine

194

153

View full text Add to dashboard Cite

show abstract

“…The goals of this study were to determine if cells of the amnion display characteristic biochemical features of apoptosis at term, including nuclear DNA fragmentation (3) and degradation of ribosomal RNA (4), and if these changes are associated with the activation of collagenolytic enzymes that degrade the primary amnion fibrillar collagen, type I collagen (2,5).…”

Section: Introductionmentioning

confidence: 99%

A program of cell death and extracellular matrix degradation is activated in the amnion before the onset of labor.

Lei¹,

Furth²,

Kalluri

et al. 1996

J. Clin. Invest.

159

View full text Add to dashboard Cite

Fetal membranes usually rupture during the process of labor. Premature fetal membrane rupture occurs not infrequently and is associated with significant fetal and maternal morbidity. The mechanisms of normal and pathologic fetal membrane rupture are not well understood. We have examined structural and biochemical changes in the rat amnion as labor approaches in order to characterize this process in normal pregnancy. Here we report that before the onset of active labor the amnion epithelial cells undergo apoptotic cell death which encompasses degradation of 28S ribosomal subunit RNA and associated P proteins and fragmentation of nuclear DNA. Concurrent with these cellular changes, the amnion type I collagen matrix is degraded with the accumulation of three-quarter length type I collagen fragments in extraembryonic fluid, characteristic of the cleavage of fibrillar collagen by interstitial collagenase. Western blot and immunohistochemical analyses confirmed that interstitial collagenase protein appears in association with the loss of amnion type I collagen. We conclude that amnion epithelial cells undergo a process of programmed cell death associated with orchestrated extracellular matrix degradation which begins before the onset of active labor. Thus, fetal membrane rupture is likely to be the result of biochemical changes as well as physical forces. ( J. Clin. Invest. 1996.

show abstract

“…The predominant collagens of the chorioamnion extracellular matrix are types I and III, but types IV, V, and VI have been localized to the amnion as well. 1,2 Matrix metalloproteinases (MMP), a family of potent enzymes capable of digesting the extracellular matrix, can be classified according to substrate-specific activity. Three distinct collagenases have been described: MMP-1, interstitial collagenase; MMP-8, neutrophil collagenase; and MMP-13, collagenase-3.…”

mentioning

confidence: 99%

Midtrimester amniotic fluid matrix metalloproteinase-8 (MMP-8) levels above the 90th percentile are a marker for subsequent preterm premature rupture of membranes

Biggio

Ramsey

Cliver

et al. 2005

American Journal of Obstetrics and Gynecology

View full text Add to dashboard Cite

Objective-We sought to determine whether midtrimester amniotic fluid levels of matrix metalloproteinase-8 were associated with subsequent preterm premature rupture of membranes.Study design-We conducted a case-control study examining 57 asymptomatic women who underwent genetic amniocentesis from 14 to 21 weeks' gestation and subsequently had preterm premature rupture of membranes (<35 wk) and 58 women with subsequent term delivery. Measurement of total matrix metalloproteinase-8 level in amniotic fluid was conducted using a commercially available enzyme-linked immunosorbent assay and association with preterm birth due to preterm premature rupture of membranes was assessed.Results-The overall distribution of matrix metalloproteinase-8 concentrations was similar in women who had preterm premature rupture of membranes and term controls (median 2.39 ng/mL, 25th to 75th percentile 1.1-10.1 vs 2.37 ng/mL, 25th to 75th percentile 1.5-4.7, P = .94). However, 26% of women who had preterm premature rupture of membranes had a matrix metalloproteinase-8 concentration above the 90th percentile (8.7 ng/mL), compared with only 10% of term controls (odds ratio 3.1, 95% CI 1.1-8.7; P = .03). Elevated matrix metalloproteinase-8 remained associated with preterm premature rupture of membranes after adjustment for maternal age, race, parity, gestational age, and year of amniocentesis (odds ratio 3.4, 95% CI 1.2-9.9; P = .03).Conclusions-The overall distribution of midtrimester amniotic fluid matrix metalloproteinase-8 levels did not differ between women who had preterm premature rupture of membranes and those delivered at term. However, marked elevations of midtrimester amniotic fluid matrix metalloproteinase-8 were highly associated with subsequent preterm premature rupture of membranes, suggesting that the pathophysiologic processes that contribute to preterm premature rupture of membranes may begin in early pregnancy. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. KeywordsPresented at the 23rd Annual Meeting of the Society for Maternal-Fetal Medicine, San Francisco, Calif, Feb 3-8, 2003 Collagens are a family of proteins responsible for the maintenance of tissue tensile strength. Each collagen molecule is composed of 3 polypeptide chains in a triple helical configuration with the specific composition of the monomeric chains defining the collagen subtype. The predominant collagens of the chorioamnion extracellular matrix are types I and III, but types IV, V, and VI have been localized to the amnion as well. 1,2 Matrix metalloproteinases (MMP), a family of potent enzymes capable of ...

show abstract

Confocal immunofluorescence localization of collagen types I, III, IV, V and VI and their ultrastructural organization in term human fetal membranes

Cited by 204 publications

References 36 publications

Mid-trimester preterm premature rupture of membranes (PPROM): etiology, diagnosis, classification, international recommendations of treatment options and outcome

Mid-trimester preterm premature rupture of membranes (PPROM): etiology, diagnosis, classification, international recommendations of treatment options and outcome

A program of cell death and extracellular matrix degradation is activated in the amnion before the onset of labor.

Midtrimester amniotic fluid matrix metalloproteinase-8 (MMP-8) levels above the 90th percentile are a marker for subsequent preterm premature rupture of membranes

Contact Info

Product

Resources

About