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Peripheral Blood NK Cells Reflect Changes in Decidual NK Cells in Women With Recurrent Miscarriages
Park, Dong Wook,Lee, Hyun Joo,Park, Chan Woo,Hong, Sung Ran,Kwak-Kim, Joanne,Yang, Kwang Moon Blackwell Publishing Ltd 2010 American journal of reproductive immunology Vol.63 No.2
<P><B>Citation</B> Park DW, Lee HJ, Park CW, Hong SR, Kwak-Kim J, Yang KM. Peripheral blood NK cells reflect changes in decidual NK cells in women with recurrent miscarriages. Am J Reprod Immunol 2010; 63: 173–180</P><P>Problem </P><P>We aimed to investigate if peripheral blood natural killer (pNK) cell levels are correlated with decidual NK (dNK) cell levels, and if chemokine expression has any role in dNK cell regulation.</P><P>Method of study </P><P>Decidual tissues of women having two or more miscarriages with normal karyotype were collected after miscarriage and an immuno-histochemisty study was made. pNK cells were evaluated using flow cytometric analysis.</P><P>Results </P><P>The %CD3<SUP>−</SUP>/56<SUP>+</SUP> and %CD3<SUP>−</SUP>/56<SUP>+</SUP>/16<SUP>+</SUP> pNK cells showed a significant correlation with mean number of CD56<SUP>+</SUP> dNK cells. The number of decidual CD16<SUP>+</SUP> cells was significantly higher in women with elevated pNK (≥15%) than that of normal pNK (<15%). The %CD3<SUP>−</SUP>/56<SUP>+</SUP> and %CD3<SUP>−</SUP>/56<SUP>+</SUP>/16<SUP>+</SUP> pNK cells showed an inverse correlation with duration of gestation. The CCL3<SUP>+</SUP> and CXCL12<SUP>+</SUP> cells were present in the decidua; however, staining intensity was not correlated with number of dNK cells.</P><P>Conclusion </P><P>The pNK cell levels reflect changes in dNK cell levels. This implicates that pNK cell level is a clinically useful marker to predict pregnancy outcome. Further study is needed to examine if elevated pNK cells enhance recruitment of dNK cells in the decidua.</P>
Park, Chan-Woo,Han, Ae-Ra,Kim, Joanne-Kwak,Park, So-Yeon,Han, Jung-Yeol,Koong, Mi-Kyoung,Song, In-Ok,Yang, Kwang-Moon The Korean Society for Reproductive Medicine 2011 Clinical and Experimental Reproductive Medicine Vol.38 No.3
Objective: To examine the association between methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism and hyperhomocysteinemia in women with unexplained recurrent miscarriages (RM) and to investigate the association between MTHFR genotype variants and alloimmune activation, proportion of peripheral blood natural killer (pbNK) cells. Methods: A total of 39 patients with a history of two or more unexplained miscarriages were recruited to this study. The controls were women who had a live birth without a history of RM (n=50). The proportion of pbNK cells was measured by flow cytometry. Plasma homocysteine levels and the incidence of the MTHFR variant of the RM and control groups were compared. The proportion of pbNK cells was compared to the MTHFR variants in the RM group. Results: No differences were found between the two groups' mean plasma homocysteine levels ($7.6{\pm}1.5{\mu}mol$/L vs. $7.1{\pm}2.1{\mu}mol$/L) or incidence of the MTHFR genotype variant (CC, 35% vs. 33%; CT, 40% vs. 53%; and TT, 25% vs. 14%). In the RM group, individuals with the TT variant ($7.7{\pm}1.1{\mu}mol$/L) had higher homocysteine levels than those with the CC and CT variants ($7.4{\pm}1.9{\mu}mol$/L and $7.4{\pm}1.2{\mu}mol$/L) and those with the CT variant ($19.2{\pm}8.1%$) had a higher proportion of CD3-/CD56+ pbNK cells than those with the CC and TT variants ($17.7{\pm}6.6%$ and $17.9{\pm}7.0%$), but the results of both comparisons were statistically insignificant. Conclusion: These preliminary results show no difference in plasma homocysteine levels between the RM and control groups or among MTHFR genotype variants in the RM group, which may suggest that the plasma homocysteine level is difficult to use as a predictive marker of RM in the Korean population. A study of a larger number of patients is needed.
Directed migration of cancer cells guided by the graded texture of the underlying matrix
Park, JinSeok,Kim, Deok-Ho,Kim, Hong-Nam,Wang, Chiaochun Joanne,Kwak, Moon Kyu,Hur, Eunmi,Suh, Kahp-Yang,An, Steven S.,Levchenko, Andre Nature Publishing Group, a division of Macmillan P 2016 Nature materials Vol.15 No.7
<P>Living cells and the extracellular matrix (ECM) can exhibit complex interactions that define key developmental, physiological and pathological processes. Here, we report a new type of directed migration-which we term 'topotaxis'-guided by the gradient of the nanoscale topographic features in the cells' ECM environment. We show that the direction of topotaxis is reflective of the effective cell stiffness, and that it depends on the balance of the ECM-triggered signalling pathways PI(3)K-Akt and ROCK-MLCK. In melanoma cancer cells, this balance can be altered by different ECM inputs, pharmacological perturbations or genetic alterations, particularly a loss of PTEN in aggressive melanoma cells. We conclude that topotaxis is a product of the material properties of cells and the surrounding ECM, and propose that the invasive capacity of many cancers may depend broadly on topotactic responses, providing a potentially attractive mechanism for controlling invasive and metastatic behaviour.</P>
Park, JinSeok,Holmes, William R.,Lee, Sung Hoon,Kim, Hong-Nam,Kim, Deok-Ho,Kwak, Moon Kyu,Wang, Chiaochun Joanne,Edelstein-Keshet, Leah,Levchenko, Andre National Academy of Sciences 2017 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.114 No.28
<P>Cell polarization and directional cell migration can display random, persistent, and oscillatory dynamic patterns. However, it is not clear whether these polarity patterns can be explained by the same underlying regulatory mechanism. Here, we show that random, persistent, and oscillatory migration accompanied by polarization can simultaneously occur in populations of melanoma cells derived from tumors with different degrees of aggressiveness. We demonstrate that all of these patterns and the probabilities of their occurrence are quantitatively accounted for by a simple mechanism involving a spatially distributed, mechanochemical feedback coupling the dynamically changing extracellular matrix (ECM)-cell contacts to the activation of signaling downstream of the Rho-family small GTPases. This mechanism is supported by a predictive mathematical model and extensive experimental validation, and can explain previously reported results for diverse cell types. In melanoma, this mechanism also accounts for the effects of genetic and environmental perturbations, including mutations linked to invasive cell spread. The resulting mechanistic understanding of cell polarity quantitatively captures the relationship between population variability and phenotypic plasticity, with the potential to account for a wide variety of cell migration states in diverse pathological and physiological conditions.</P>