scholarly journals Corrigendum to “Decidua basalis and acute atherosis: Expression of atherosclerotic foam cell associated proteins” [Placenta 107 (2021) 1–7]

Placenta ◽  
2022 ◽  
Vol 117 ◽  
pp. 28
Author(s):  
Ingrid Knutsdotter Fosheim ◽  
Guro Mørk Johnsen ◽  
Patji Alnaes-Katjavivi ◽  
Gitta Turowski ◽  
Meryam Sugulle ◽  
...  
Placenta ◽  
2021 ◽  
Author(s):  
I.K. Fosheim ◽  
G.M. Johnsen ◽  
P. Alnaes-Katjavivi ◽  
G. Turowski ◽  
M. Sugulle ◽  
...  

Placenta ◽  
2016 ◽  
Vol 37 ◽  
pp. 26-33 ◽  
Author(s):  
Patji Alnaes-Katjavivi ◽  
Fiona Lyall ◽  
Borghild Roald ◽  
Christopher W.G. Redman ◽  
Anne Cathrine Staff

2016 ◽  
Vol 115 ◽  
pp. 28
Author(s):  
Guro M. Johnsen ◽  
Gro L. Størvold ◽  
Jos J.M. Drabbels ◽  
Geert W. Haasnoot ◽  
Michael Eikmans ◽  
...  

2016 ◽  
Vol 115 ◽  
pp. 63-64
Author(s):  
Guro M. Johnsen ◽  
Gro L. Størvold ◽  
Jos J.M. Drabbels ◽  
Geert W. Haasnoot ◽  
Michael Eikmans ◽  
...  

Placenta ◽  
2017 ◽  
Vol 52 ◽  
pp. 114-115
Author(s):  
Patji Alnaes-Katjavivi ◽  
Fiona Lyall ◽  
Borghild Roald ◽  
Christopher W.G. Redman ◽  
Anne Cathrine Staff

2013 ◽  
Vol 2013 ◽  
pp. 1-17 ◽  
Author(s):  
Hayley J. Dawson ◽  
Andrew P. Hibbert ◽  
Peter D. Chantler ◽  
Kathleen M. Botham

Myosin VI (Myo6) functions in endocytosis in conjunction with binding partners including adaptor protein (AP)-2, disabled 2 (Dab2), and GAIP interacting protein C terminus 1 (GIPC1). This study aimed to investigate the expression and function of Myo6 in macrophages and its possible role in the endocytosis of lipoproteins during the induction of foam cell formation. Expression of Myo6, AP-2 (α2 subunit), and Dab2 in THP-1 macrophages and primary human monocyte-derived macrophages was demonstrated at the mRNA and protein level, but GIPC1 was only detected at the mRNA level. Immunofluorescence showed that Myo6 was distributed similarly to F-actin in both macrophage types. AP-2α2 was found to have a similar subcellular distribution to Myo6 and Dab2 in THP-1 cells. Myo6 was located within membrane ruffles and protrusions of the plasma membrane. These results suggest that in macrophages Myo6 is required for several functions including cell adhesion, cell progression, and macropinocytosis. Low-density lipoprotein (LDL) and oxidised LDL (oxLDL) decreased Myo6 and GIPC1 mRNA expression in THP-1 cells, but uptake of the fluorescence-labelled lipoproteins was unaffected by knockdown of the expression of Myo6 or associated proteins with siRNA. Our findings, therefore, do not support the idea that Myo6 plays a major role in foam cell formation.


Placenta ◽  
2019 ◽  
Vol 82 ◽  
pp. 10-16 ◽  
Author(s):  
Ingrid Knutsdotter Fosheim ◽  
Patji Alnaes-Katjavivi ◽  
Christopher Redman ◽  
Borghild Roald ◽  
Anne Cathrine Staff ◽  
...  

2018 ◽  
Vol 129 ◽  
pp. 23-29 ◽  
Author(s):  
Guro M. Johnsen ◽  
Gro L. Størvold ◽  
Jos J.M. Drabbels ◽  
Geert W. Haasnoot ◽  
Michael Eikmans ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Daniel Pitz Jacobsen ◽  
Heidi Elisabeth Fjeldstad ◽  
Guro Mørk Johnsen ◽  
Ingrid Knutsdotter Fosheim ◽  
Kjartan Moe ◽  
...  

Decidua basalis, the endometrium of pregnancy, is an important interface between maternal and fetal tissues, made up of both maternal and fetal cells. Acute atherosis is a uteroplacental spiral artery lesion. These patchy arterial wall lesions containing foam cells are predominantly found in the decidua basalis, at the tips of the maternal arteries, where they feed into the placental intervillous space. Acute atherosis is prevalent in preeclampsia and other obstetric syndromes such as fetal growth restriction. Causal factors and effects of acute atherosis remain uncertain. This is in part because decidua basalis is challenging to sample systematically and in large amounts following delivery. We summarize our decidua basalis vacuum suction method, which facilitates tissue-based studies of acute atherosis. We also describe our evidence-based research definition of acute atherosis. Here, we comprehensively review the existing literature on acute atherosis, its underlying mechanisms and possible short- and long-term effects. We propose that multiple pathways leading to decidual vascular inflammation may promote acute atherosis formation, with or without poor spiral artery remodeling and/or preeclampsia. These include maternal alloreactivity, ischemia-reperfusion injury, preexisting systemic inflammation, and microbial infection. The concept of acute atherosis as an inflammatory lesion is not novel. The lesions themselves have an inflammatory phenotype and resemble other arterial lesions of more extensively studied etiology. We discuss findings of concurrently dysregulated proteins involved in immune regulation and cardiovascular function in women with acute atherosis. We also propose a novel hypothesis linking cellular fetal microchimerism, which is prevalent in women with preeclampsia, with acute atherosis in pregnancy and future cardiovascular and neurovascular disease. Finally, women with a history of preeclampsia have an increased risk of premature cardiovascular disease. We review whether presence of acute atherosis may identify women at especially high risk for premature cardiovascular disease.


Placenta ◽  
2017 ◽  
Vol 57 ◽  
pp. 311
Author(s):  
Ingrid Knutsdotter Fosheim ◽  
Patji Alnaes-Katjavivi ◽  
Christopher Redman ◽  
Anne Cathrine Staff ◽  
Gro Leite Størvold

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