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Lee, Cheol Whan,Hwang, Ilseon,Park, Chan-Sik,Lee, Hyangsin,Park, Duk-Woo,Kang, Soo-Jin,Lee, Seung-Whan,Kim, Young-Hak,Park, Seong-Wook,Park, Seung-Jung BMJ Publishing Group Ltd 2013 Journal of clinical pathology Vol.66 No.9
<P><B>Background</B></P><P>Stanniocalcin-1 (STC1) is involved in fundamental biological processes such as angiogenesis, inflammation and wound healing, but little is known about its expression in human coronary atherosclerotic plaques or its relationship to plaque instability.</P><P><B>Objective</B></P><P>STC1 expression was examined in the culprit coronary plaques of 70 patients with acute myocardial infarction (AMI; n=49) or stable angina (n=21) who underwent directional coronary atherectomy.</P><P><B>Methods</B></P><P>The specimens were stained with H&E, STC1-specific antibodies, and endothelial cells, macrophages and smooth muscle cell markers.</P><P><B>Results</B></P><P>The baseline characteristics of the two groups of patients were largely similar. CD31-immunopositive and CD68-immunopositive areas, indicative of the presence of endothelial cells and macrophages, respectively, were proportionately larger while areas immunopositive for α-actin, as a smooth muscle cell marker, were proportionately smaller in the AMI group than in the stable angina group. The proportion of STC1-immunopositive areas was significantly greater in the AMI group than in the stable angina group (20.0% (8.2–29.0%) vs 8.8% (3.9–19.4%), p=0.022). Areas positive for STC1 were independently correlated with those immunopositive for CD31 (r=0.42, p<0.001) and CD68 (r=0.40, p<0.001). STC1 immunoreactivity co-localised with CD31-immunopositive and CD68-immunopositive cells.</P><P><B>Conclusions</B></P><P>STC1 is differentially expressed in the culprit coronary plaques of patients with AMI versus those with stable angina. STC1 may play a role in plaque instability.</P>
Comparison of ruptured coronary plaques in patients with unstable and stable clinical presentation
Lee, Cheol Whan,Park, Chan-Sik,Hwang, Ilseon,Lee, Hyangsin,Park, Duk-Woo,Kang, Su-Jin,Lee, Seung-Whan,Kim, Young-Hak,Park, Seong-Wook,Park, Seung-Jung Springer-Verlag 2011 Journal of thrombosis and thrombolysis Vol.32 No.2
Gil, Minchan,Pak, Hyo-Kyung,Park, Seo-Jeong,Lee, A-Neum,Park, Young-Soo,Lee, Hyangsin,Lee, Hyunji,Kim, Kyung-Eun,Lee, Kyung Jin,Yoon, Dok Hyun,Chung, Yoo-Sam,Park, Chan-Sik 한국조명·전기설비학회 2015 한국조명·전기설비학회 학술대회논문집 Vol. No.
<P>CD99 signaling is crucial to a diverse range of biological functions including survival and proliferation. CD99 engagement is reported to augment activator protein-1 (AP-1) activity through mitogen-activated protein (MAP) kinase pathways in a T-lymphoblastic lymphoma cell line Jurkat and in breast cancer cell lines. In this study, we report that CD99 differentially regulated AP-1 activity in the human myeloma cell line RPMI8226. CD99 was highly expressed and the CD99 engagement led to activation of the MAP kinases, but suppressed AP-1 activity by inducing the expression of basic leucine zipper transcription factor, ATF-like (BATF), a negative regulator of AP-1 in RPMI8226 cells. By contrast, engagement of CD99 enhanced AP-1 activity and did not change the BATF expression in Jurkat cells. CD99 engagement reduced the proliferation of RPMI8226 cells and expression of cyclin 1 and 3. Overall, these results suggest novel CD99 functions in RPMI8226 cells.</P>
Lim, Dong-Gyun,Park, Youn-Hee,Kim, Sung-Eun,Jung, Eun-Jung,Jeong, Seong-Hee,Lee, Hyangsin,Shin, Su-Jin,Park, Chan-Sik,Han, Duck-Jong,Kim, Song-Cheol Lippincott Williams Wilkins, Inc. 2012 Transplantation Vol.94 No.8
BACKGROUND: The ability to induce tolerance, or at least minimize the need for immunosuppressive therapy, is a high priority in organ transplantation. Accomplishing this goal requires a novel method for determining when a patient has become tolerant to or is rejecting their graft. Here, we sought to develop an efficient monitoring protocol based on gene expression profiles of recipient T cells in murine skin and islet allograft models. METHODS: Unlike previous studies, here, gene expression analysis was focused on donor antigen-reactive T cells, which were prepared by collecting CD69 T cells from cocultures of recipient peripheral T cells and donor antigen-presenting cells. Candidate tolerance and rejection biomarker genes were selected from a CD69 T-cell microarray analysis, and their expression levels were measured in the recipient CD69 T-cell fraction using quantitative reverse transcription polymerase chain reaction. RESULTS: Our new monitoring protocol was capable of precisely detecting the immune status of recipients relative to their graft regardless of the organ received, whether they were taking immunosuppressive drugs, or different strains of origin. CONCLUSIONS: Gene expression analysis focusing on recipient CD69 T cells as the donor antigen-reactive T-cell population could be used as an effective and sensitive method for monitoring transplant patients.