Fibrin Enhances Differentiation, but not Apoptosis, and Limits Hypoxic Injury of Cultured Term Human Trophoblasts

Humphrey, Rachel; Smith, Steven D.; Pang, Liyi; Sadovsky, Yoel; Nelson, D. Michael

doi:10.1016/j.placenta.2004.08.011

Cited by 16 publications

(5 citation statements)

References 28 publications

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“…The affected chorionic villi in our study also showed more roughened fibrillar skeleton with increased fibrin deposition (Figure 21). The same results were reported by Guller Seth [20] and Salafia et al [25] who revealed that there were aberrantly high levels of intervillous fibrin which is a critical component of physiological repair and differentiation of the placental villi [26].…”

Section: Disscussionsupporting

confidence: 81%

Electron and Scanning Microscopic Observations on the Syncytiotrophoblast Microvillous Membrane Contribution to Preeclampsia in Early Placental Rats

Selim¹,

Elshmry²,

Rashed³

2013

J Blood Disord Transfus

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Section: Disscussionsupporting

confidence: 81%

Electron and Scanning Microscopic Observations on the Syncytiotrophoblast Microvillous Membrane Contribution to Preeclampsia in Early Placental Rats

Selim¹,

Elshmry²,

Rashed³

2013

J Blood Disord Transfus

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“…In the present study, a trend to lower risk of mortality was predicted by rs1333049 (similar to the protective effect of the risk allele for MI noted in an earlier study [17]). The findings herein of a 9p21.3 association with CAD onset but not with subsequently higher mortality risk is supported by other recent literature reports [19,29].…”

Section: Discussionsupporting

confidence: 92%

Association of Chromosome 9p21.3 with Disease Location, Including the Number of Diseased Vessels, but not with Greater Burden of Coronary Disease

Horne¹

2013

J Clin Exp Cardiolog

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Introduction: Single nucleotide polymorphisms (SNPs) at chromosome 9p21.3 do not influence myocardial infarction, but their role in coronary artery disease (CAD) progression, burden, and outcomes is controversial. This study evaluated whether rs1333049 impacts CAD burden.Methods: Non-diabetic CAD patients enrolled in the Intermountain Heart Collaborative Study (N=1,757) were evaluated for association of rs1333049 with the Duke CAD Index (primary endpoint) and other CAD measures. Multivariable regression adjusted for potential confounders. Statistical significance of secondary endpoints was corrected for multiple comparisons. Results:No association of rs1333049 with Duke CAD Index was found for 0, 1, and 2 C alleles: 42. 4 ± 16.1, 44.0 ± 17.4, 47.4 ± 17.6, respectively (p-trend=0.12, adjusted p-trend=0.11). It also did not predict the number of CAD lesions (adjusted p-trend=0.11) or the maximum CAD stenosis (adjusted p-trend=0.89). The SNP did predict the number of major vessels with proximal or left main lesions (0.56 ± 0.69, 0.62 ± 0.74, and 0.71 ± 0.77 for 0, 1, and 2 C alleles, respectively; adjusted p-trend=0.0056) and another location parameter: the number of major vessels with at least one significant stenosis (p-trend=0.0017). Rs1333049 was not associated with future events, but association with CAD presence was confirmed (p-trend<0.0001). Conclusion:Rs1333049 was not associated with CAD burden, lesion number or severity, or cardiovascular events. The SNP did strongly predict CAD presence and was associated with lesion location. These findings reaffirm that a primary role of 9p21.3 may be related to the presence of CAD rather than the clinical severity of obstructive lesions. Because follow-up angiography was not systematically performed, CAD progression could not be evaluated. [6][7][8]. These SNPs are located at CDKN2BAS, an antisense noncoding RNA (i.e., ANRIL) [9]. Deletion of an orthologous region in a murine model showed a higher mortality rate during both development and adult life than normal mice [10]. That mortality risk was linked to primary cultures of smooth muscle cells having markedly increased proliferation, which may indicate decreased expression of Cdkn1a and Cdkn2b (products of the two closest genes), [10] or may indicate ANRIL regulation of some unknown gene or pathway [11].In humans, 9p21.3 SNPs are associated with various complex, overlapping coronary heart disease (CHD) phenotypes [6][7][8][12][13][14][15][16]. CHD is a complex disease that may evolve through several distinct stages, including disease initiation, progression to obstructive lesions, and (for some but not all patients) acute coronary syndrome precipitation, each of which may involve distinct pathophysiological mechanisms [15]. A refined understanding of the role of 9p21.3 in CHD requires an analysis of its impact on each of these stages. Chromosome 9p21.3 was shown to not increase the risk of myocardial infarction (MI), [16][17][18][19][20] and to not predispose to restenosis [18]. In patients with prevalent...

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“…Fibrin-type fibrinoid is more prevalent in PE placentas [347], and is associated with apoptosis in trophoblast cells in PE [348]. In cultured primary term trophoblasts fibrin protects against hypoxic injury [349].…”

Section: Fibrinoid Tissuementioning

confidence: 99%

Long-chain Polyunsaturated Fatty Acid Transport across Human Placental Choriocarcinoma (BeWo) Cells

et al. 2009

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Fibrin Enhances Differentiation, but not Apoptosis, and Limits Hypoxic Injury of Cultured Term Human Trophoblasts

Cited by 16 publications

References 28 publications

Electron and Scanning Microscopic Observations on the Syncytiotrophoblast Microvillous Membrane Contribution to Preeclampsia in Early Placental Rats

Electron and Scanning Microscopic Observations on the Syncytiotrophoblast Microvillous Membrane Contribution to Preeclampsia in Early Placental Rats

Association of Chromosome 9p21.3 with Disease Location, Including the Number of Diseased Vessels, but not with Greater Burden of Coronary Disease

Long-chain Polyunsaturated Fatty Acid Transport across Human Placental Choriocarcinoma (BeWo) Cells

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