Effects of Tumor Necrosis Factor‐Alpha on Human Trophoblast Cell Adhesion and Motility

Todt, Jill C.; Yang, Yan; Lei, Jun; Lauria, Michele R.; Sorokin, Yoram; Cotton, David B.; Yelian, Frank D.

doi:10.1111/j.1600-0897.1996.tb00141.x

Cited by 76 publications

(36 citation statements)

References 31 publications

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“…In vitro studies confirm the ability of activated immune cells, mainly of a Th1-profile, to attack trophoblast cells expressing "foreign" paternal antigens [41]. Many authors have pointed out TNF- § as a key player in the etiology of PE [4, 12,42]; this is supported by our data on very high amounts of TNF- § at the feto--maternal interface of mice with PE-like symptoms.…”

Section: Discussionsupporting

confidence: 77%

Introducing a mouse model for pre‐eclampsia: adoptive transfer of activated Th1 cells leads to pre‐eclampsia‐like symptoms exclusively in pregnant mice

et al. 2004

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Pre-eclampsia (PE) is the most severe pregnancy-related disease, leading to high maternal and fetal morbidity/mortality. Immunological imbalances associated with endothelial cell dysfunction have been hypothesized as a cause for the onset and perpetuation of PE. Valid and reliable animal models are urgently required to test this hypothesis and to better understand the mechanisms underlying PE. We developed a novel PE-model by adoptively transferring activated BALB/c Th1-like splenocytes into allogeneically pregnant BALB/c female mice during late gestation; the model mimicked the symptoms of PE, i.e. increased blood pressure and glomerulonephritis accompanied by proteinuria. Interestingly, these PE-like symptoms were not detectable in non-pregnant recipients of activated Th1-like cells. Adoptive cell transfer adversely affected the outcome of pregnancy by increasing fetal rejection, with uterine immune cells showing an inflammatory profile. In conclusion, we have established a valid and reliable PE mouse model, which opens vast opportunities for therapeutic interventions.

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Section: Discussionsupporting

confidence: 77%

Introducing a mouse model for pre‐eclampsia: adoptive transfer of activated Th1 cells leads to pre‐eclampsia‐like symptoms exclusively in pregnant mice

et al. 2004

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“…44 Several cytokines, such as interleukin-2, interferon-γ, and TNF-α, are well-known mediators of immune maladaptation in preeclampsia. 30,45 TNF-α has been shown to decrease the motility of HTR-8/SVneo cells in vitro 31 and to negatively affect the migration and invasion of trophoblasts. It has been reported that TNF-α stimulates reactive oxygen species production by several mechanisms, including direct toxicity and its effects on mitochondrial function.…”

Section: Discussionmentioning

confidence: 99%

“…[30][31][32][33][34] We treated HTR8/SVneo cells with recombinant human TNF-α and examined miR-210 and KCMF1 levels after 24 hours. As shown in Figure 6, TNF-α significantly increased the expression of miR-210 by ≈1.8-fold over the control ( Figure 6A), whereas it decreased KCMF1 mRNA and protein levels to 60% to 70% of the control ( Figure 6B and 6C).…”

Section: Tnf-α Increases Mir-210 Expression But Downregulates Kcmf1mentioning

confidence: 99%

MicroRNA-210 Contributes to Preeclampsia by Downregulating Potassium Channel Modulatory Factor 1

Luo

Shao

et al. 2014

Hypertension

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C omplicating 7% to 10% of pregnancies, 1 preeclampsia, along with other hypertensive disorders of pregnancy, is a major contributor to maternal morbidity worldwide. 2,3Although abnormal placentation is thought to play a major role in the development of preeclampsia, the pathogenesis of this disorder is not clearly understood. 4 Defects of trophoblast cell function, such as reduced proliferation, 5 excessive apoptosis, 6 aberrant differentiation, 7 limited migration and invasion of the uterus, and poor remodeling of spiral arteries, 8,9 have been considered to be associated with preeclampsia. Nevertheless, the molecular mechanisms underlying the onset and progression of preeclampsia remain largely unknown.MicroRNAs are 22-to 24-nucleotide noncoding RNAs that regulate gene expression by seed sequence pairing with the 3′-untranslated region (UTR) of target mRNAs, leading to repressed translation or induced mRNA cleavage of the target genes. 10,11 MicroRNAs have been identified as essential mediators of numerous cellular processes, 12 potentially including the response to hypoxia. In particular, microRNA-210 (miR-210) is specifically induced by hypoxia-inducible factor-1α during hypoxia 13 and regulates many hypoxia response pathways, including cell survival, 14 angiogenesis, mitochondrial metabolism, 15 and DNA repair. 16 miR-210 can target and suppress a large number of genes, including the cell cycle regulator E2F transcription factor 3, 17 the receptor tyrosine kinase ligand ephrinA3, 18 the DNA repair protein RAD52, 19 and the iron-sulfur cluster assembly proteins 1/2. 15 Recent studies revealed that miR-210 was upregulated in patients with preeclampsia [20][21][22][23][24] and demonstrated that hypoxia-inducible miR-210 might participate in the occurrence of preeclampsia via the downregulation of ephrin-A3 and homeobox-A9. 24 The repressive effect of miR-210 on primary trophoblast cell invasion was also reported. 23 In addition, the study by us and others revealed that miR-210 could be a potential serum biomarker Abstract-Preeclampsia is a pregnancy-specific syndrome manifested by the onset of hypertension and proteinuria after the 20th week of gestation. Abnormal placenta development has been generally accepted as the initial cause of the disorder. Recently, microRNA-210 (miR-210) has been found to be upregulated in preeclamptic placentas compared with normal placentas, indicating a possible association of this small molecule with the placental pathology of preeclampsia. However, the function of miR-210 in the development of the placenta remains elusive. The aim of this study was to characterize the molecular mechanism of preeclampsia development by examining the role of miR-210. In this study, miR-210 and potassium channel modulatory factor 1 (KCMF1) expressions were compared in placentas from healthy pregnant individuals and patients with preeclampsia, and the role of miR-210 in trophoblast cell invasion via the downregulation of KCMF1 was investigated in the immortal trophoblast cell line HTR8/SVneo. Th...

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“…With the use of freely available software, multiple tracks can be evaluated for each treatment to accomplish statistical requirements. The assay can be utilized to assess motility of many cell types, such as cancer cells 11,12 , fibroblasts 9 , neutrophils 13 , skeletal muscle cells 14 , keratinocytes 15 , trophoblasts 16 , endothelial cells 17 , and monocytes 10,[18][19][20][21][22] . The protocol involves the creation of slides coated with gold nanoparticles (Au°) that are generated by a reduction of chloroauric acid (Au 3+ ) by sodium citrate.…”

mentioning

confidence: 99%

A Quantitative Evaluation of Cell Migration by the Phagokinetic Track Motility Assay

Nogalski

Chan

Stevenson

et al. 2012

JoVE

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Cellular motility is an important biological process for both unicellular and multicellular organisms. It is essential for movement of unicellular organisms towards a source of nutrients or away from unsuitable conditions, as well as in multicellular organisms for tissue development, immune surveillance and wound healing, just to mention a few roles 1,2,3 . Deregulation of this process can lead to serious neurological, cardiovascular and immunological diseases, as well as exacerbated tumor formation and spread 4,5 . Molecularly, actin polymerization and receptor recycling have been shown to play important roles in creating cellular extensions (lamellipodia), that drive the forward movement of the cell 6,7,8 . However, many biological questions about cell migration remain unanswered.The central role for cellular motility in human health and disease underlines the importance of understanding the specific mechanisms involved in this process and makes accurate methods for evaluating cell motility particularly important. Microscopes are usually used to visualize the movement of cells. However, cells move rather slowly, making the quantitative measurement of cell migration a resource-consuming process requiring expensive cameras and software to create quantitative time-lapsed movies of motile cells. Therefore, the ability to perform a quantitative measurement of cell migration that is cost-effective, non-laborious, and that utilizes common laboratory equipment is a great need for many researchers.The phagokinetic track motility assay utilizes the ability of a moving cell to clear gold particles from its path to create a measurable track on a colloidal gold-coated glass coverslip 9,10 . With the use of freely available software, multiple tracks can be evaluated for each treatment to accomplish statistical requirements. The assay can be utilized to assess motility of many cell types, such as cancer cells 11,12 10,[18][19][20][21][22] . The protocol involves the creation of slides coated with gold nanoparticles (Au°) that are generated by a reduction of chloroauric acid (Au 3+ ) by sodium citrate. This method was developed by Turkevich et al. in 1951 23 and then improved in the 1970s by Frens et al. 24,25 . As a result of this chemical reduction step, gold particles (10-20 nm in diameter) precipitate from the reaction mixture and can be applied to glass coverslips, which are then ready for use in cellular migration analyses 9,26,27 . In general, the phagokinetic track motility assay is a quick, quantitative and easy measure of cellular motility. In addition, it can be utilized as a simple high-throughput assay, for use with cell types that are not amenable to time-lapsed imaging, as well as other uses depending on the needs of the researcher. Together, the ability to quantitatively measure cellular motility of multiple cell types without the need for expensive microscopes and software, along with the use of common laboratory equipment and chemicals, make the phagokinetic track motility assay a solid choice for sc...

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Effects of Tumor Necrosis Factor‐Alpha on Human Trophoblast Cell Adhesion and Motility

Cited by 76 publications

References 31 publications

Introducing a mouse model for pre‐eclampsia: adoptive transfer of activated Th1 cells leads to pre‐eclampsia‐like symptoms exclusively in pregnant mice

Introducing a mouse model for pre‐eclampsia: adoptive transfer of activated Th1 cells leads to pre‐eclampsia‐like symptoms exclusively in pregnant mice

MicroRNA-210 Contributes to Preeclampsia by Downregulating Potassium Channel Modulatory Factor 1

A Quantitative Evaluation of Cell Migration by the Phagokinetic Track Motility Assay

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