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Articles by S. H Lee
Total Records ( 14 ) for S. H Lee
  S. J You , S. H Lee and J. S. Lee

We kinetically analyzed RNA interference (RNAi) for lamin A/C in HeLa cells, assuming suppression and recovery phases of gene expression, and dilution of transfected small interfering RNA (siRNA) by cell divisions. We observed the inhibitory effect of RNAi over a period of 6 days using various siRNA concentrations, and the maximum gene silencing efficiency occurred at Day 2 or 3. The gene silencing efficiency as a function of time and siRNA concentration was further quantitatively evaluated using a kinetic analysis method, demonstrating that RNAi for lamin A/C can be understood as a conventional drug–response system. This work provides potentially important guidelines for future applications using nanomaterials as delivery vehicles of siRNA in RNAi for lamin A/C.

  C. W Lee , T. H Kim , H. M Lee , S. H Lee , J. H Yoo , Y. S Kim and S. H. Lee

Objectives  To investigate the expression levels and distribution patterns of elafin and cystatin C in normal and inflammatory human sinus mucosa and to evaluate their roles in chronic sinusitis.

Design  A controlled, prospective study.

Setting  A tertiary academic institution.

Patients  Normal sinus mucosa was obtained from the ethmoid sinus during surgery in 30 patients with blowout fractures. Inflammatory sinus mucosa was obtained from 30 patients undergoing endoscopic sinus surgery for chronic polypoid sinusitis.

Interventions  Reverse transcription–polymerase chain reaction, immunohistochemical analysis, and Western blotting.

Main Outcome Measures  Expression levels and distribution patterns of elafin and cystatin C in normal and inflammatory mucosa.

Results  Expression of elafin and cystatin C messenger RNAs and proteins analyzed by means of reverse transcription–polymerase chain reaction and Western blot was detected in all normal and inflammatory sinus mucosa tested. Their expression levels were increased in inflammatory vs normal mucosa. Elafin in normal and inflammatory sinus mucosa was distinctly expressed in goblet cells, which are increased in inflammatory sinus mucosa. Elafin in submucosal glands was usually weak in staining intensity, except for a few scattered submucosal glands showing moderate intensity in inflammatory sinus mucosa. Cystatin C was also localized in goblet cells and submucosal glands in normal and inflammatory mucosa. Staining intensity was increased more in inflammatory vs normal sinus mucosa.

Conclusion  Elafin and cystatin C may play an important role in the protection of normal sinus mucosa and further in regulation of the inflammatory condition in chronic sinusitis.

  S. H Lee , K. H Koo , J. W Park , H. J Kim , S. K Ye , J. B Park , B. K Park and Y. N. Kim

The plasma membrane microdomains, lipid rafts, are involved in regulation of cellular functions such as cell survival and adhesion. Cholesterol is a critical component of lipid rafts in terms of their integrity and functions and rafts disruption by cholesterol depletion can induce detachment-induced cell death. Hypoxia inducible factor-1 (HIF-1) is stabilized in hypoxia and transactivates numerous genes required for cellular adaptation to hypoxia. It is also induced by non-hypoxic stimuli and contributes to cell survival. Because hypoxia inhibits cholesterol synthesis and HIF-1 plays a role in this process, we here explored a possible connection between lipid rafts and HIF-1. We investigated whether HIF-1 is regulated during cholesterol depletion/rafts disruption in A431 cells in normoxic conditions. Methyl-beta cyclodextrin (MβCD), which induces cholesterol depletion, upregulated HIF-1 even under normoxic conditions and this upregulation required epidermal growth factor receptor (EGFR) and extracellular signal-regulated kinase 1 and 2 activation, but not Akt activation. MβCD treatment induced HIF-1 upregulation at both the transcriptional and translational levels but not at the posttranslational levels. In addition, MβCD robustly induced vascular endothelial growth factor production and stimulated an hypoxia response element-driven luciferase reporter activity under normoxic conditions, indicating that MβCD-induced HIF-1 is functionally activated. Both EGFR activity and HIF-1 expression were higher in the attached cells than in the detached cells after MβCD treatment. Furthermore, inhibition of HIF-1 by RNA interference accelerated cell detachment, thus increasing cell death, indicating that HIF-1 expression attenuates MβCD-induced anoikis-like cell death. These data suggest that, depending on cholesterol levels, lipid rafts or membrane fluidity are probably to regulate HIF-1 expression in normoxia by modulating rafts protein activities such as EGFR, and this connection between lipid rafts and HIF-1 regulation may provide cell survival under membrane-disturbing stress.

  S. H Lee , C Krisanapun and S. J. Baek

Capsaicin, a natural product of the Capsicum species of red peppers, is known to induce apoptosis and suppress growth. Non-steroidal anti-inflammatory drug-activated gene-1 (NAG-1) is a cytokine associated with pro-apoptotic and antitumorigenic property in colorectal and lung cancer. Our data demonstrate that capsaicin leads to induction of apoptosis and up-regulates NAG-1 gene expression at the transcriptional level. Overexpression of CCAAT/enhancer binding protein β (C/EBPβ) caused a significant increase of basal and capsaicin-induced NAG-1 promoter activity. We subsequently identified C/EBPβ binding sites in the NAG-1 promoter responsible for capsaicin-induced NAG-1 transactivation. Electrophoretic mobility shift assay and chromatin immunoprecipitation assay confirmed binding of C/EBPβ to the NAG-1 promoter. Capsaicin treatment resulted in an increase of phosphorylated serine/threonine residues on C/EBPβ, and the immunoprecipitation study showed that capsaicin enhanced binding of C/EBPβ with glycogen synthase kinase 3β (GSK3β) and activating transcription factor 3 (ATF3). The phosphorylation and interaction of C/EBPβ with GSK3β and ATF3 are decreased by the inhibition of the GSK3β and Protein Kinase C pathways. Knockdown of C/EBPβ, GSK3β or ATF3 ameliorates NAG-1 expression induced by capsaicin treatment. These data indicate that C/EBPβ phosphorylation through GSK3β may mediate capsaicin-induced expression of NAG-1 and apoptosis through cooperation with ATF3 in human colorectal cancer cells.

  T. H Lee , S. H Song , K. L Kim , J. Y Yi , G. H Shin , J. Y Kim , J Kim , Y. M Han , S. H Lee , S. H Shim and W. Suh

Rationale: Generation of induced pluripotent stem (iPS) cells has been intensively studied by a variety of reprogramming methods, but the molecular and functional properties of the cells differentiated from iPS cells have not been well characterized.

Objective: To address this issue, we generated iPS cells from human aortic vascular smooth muscle cells (HASMCs) using lentiviral transduction of defined transcription factors and differentiated these iPS cells back into smooth muscle cells (SMCs).

Methods and Results: Established iPS cells were shown to possess properties equivalent to human embryonic stem cells, in terms of the cell surface markers, global mRNA and microRNA expression patterns, epigenetic status of OCT4, REX1, and NANOG promoters, and in vitro/in vivo pluripotency. The cells were differentiated into SMCs to enable a direct, comparative analysis with HASMCs, from which the iPS cells originated. We observed that iPS cell–derived SMCs were very similar to parental HASMCs in gene expression patterns, epigenetic modifications of pluripotency-related genes, and in vitro functional properties. However, the iPS cells still expressed a significant amount of lentiviral transgenes (OCT4 and LIN28) because of partial gene silencing.

Conclusions: Our study reports, for the first time, the generation of iPS cells from HASMCs and their differentiation into SMCs. Moreover, a parallel comparative analysis of human iPS cell–derived SMCs and parental HASMCs revealed that iPS-derived cells possessed representative molecular and in vitro functional characteristics of parental HASMCs, suggesting that iPS cells hold great promise as an autologous cell source for patient-specific cell therapy.

  M. N Ismail , E. L Stone , M Panico , S. H Lee , Y Luu , K Ramirez , S. B Ho , M Fukuda , J. D Marth , S. M Haslam and A. Dell

Core 2 β1,6-N-acetylglucosaminyltransferase (C2GnT), which exists in three isoforms, C2GnT1, C2GnT2 and C2GnT3, is one of the key enzymes in the O-glycan biosynthetic pathway. These isoenzymes produce core 2 O-glycans and have been correlated with the biosynthesis of core 4 O-glycans and I-branches. Previously, we have reported mice with single and multiple deficiencies of C2GnT isoenzyme(s) and have evaluated the biological and structural consequences of the loss of core 2 function. We now present more comprehensive O-glycomic analyses of neutral and sialylated glycans expressed in the colon, small intestine, stomach, kidney, thyroid/trachea and thymus of wild-type, C2GnT2 and C2GnT3 single knockouts and the C2GnT1–3 triple knockout mice. Very high-quality data have emerged from our mass spectrometry techniques with the capability of detecting O-glycans up to at least 3500 Da. We were able to unambiguously elucidate the types of O-glycan core, branching location and residue linkages, which allowed us to exhaustively characterize structural changes in the knockout tissues. The C2GnT2 knockout mice suffered a major loss of core 2 O-glycans as well as glycans with I-branches on core 1 antennae especially in the stomach and the colon. In contrast, core 2 O-glycans still dominated the O-glycomic profile of most tissues in the C2GnT3 knockout mice. Analysis of the C2GnT triple knockout mice revealed a complete loss of both core 2 O-glycans and branched core 1 antennae, confirming that the three known isoenzymes are entirely responsible for producing these structures. Unexpectedly, O-linked mannosyl glycans are upregulated in the triple deficient stomach. In addition, our studies have revealed an interesting terminal structure detected on O-glycans of the colon tissues that is similar to the RM2 antigen from glycolipids.

  K Yang , N Jeong , J. K Moon , Y. H Lee , S. H Lee , H. M Kim , C. H Hwang , K Back , R. G Palmer and S. C. Jeong

Soybean exhibits natural variation in flower and seed coat colors via the deposition of various anthocyanin pigments in the respective tissues. Although pigmentation in seeds or flowers has been well dissected at molecular level in several plant species, the genes controlling natural variation in anthocyanin traits in the soybean are not completely understood. To evaluate the genetic correlation between genetic loci and genes, 8 enzyme-encoding gene families and a transcription factor were localized in a soybean genome-wide genetic map. Among the seed coat color–controlling loci, the genetic location of the gene encoding for W1 was substantiated in the context of the current soybean molecular genetic map and O was postulated to correspond to anthocyanidin reductase. Among the genetic loci that regulate flower pigmentation, the genetic locations of the genes encoding for W1, W4, and Wp were identified, W3 was mapped on soybean linkage group B2 (chromosome 14), and W2 was postulated to correspond to an MYB transcription factor. Correlation studies between the developed markers and 3 color-controlling loci provided important empirical data that should prove useful in the design of marker-assisted breeding schemes as well as future association studies involving soybean.

  S. C Wang , S. H Lee , M. C Lee and L. Wang

This study aimed to examine the associations between aboriginality, age, demographic and socioeconomic factors of the mother and the risk of low birth weight (LBW) in mountain townships of Taiwan.


We analyzed the LBW proportion of single live babies born to 2032 first-time mothers between 2004 and 2005. Data were analyzed using the chi-square test, analysis of variance, the Scheffe test and logistic regression.


About 14.8% of Aboriginal mothers and 18.7% of Aboriginal teen mothers gave birth to infants of LBW. Aboriginal mothers were found to be at higher risk of delivering LBW infants; however, after controlling for marital status and education, the influence of aboriginality and age was no longer significant.


Marital status and education are more important determinants of LBW than aboriginality and age in mountain townships of Taiwan.

  S. H Lee , K. S Kim , K. C Moon , Y Choi and H. I. Cheong

When compared to medullary nephrocalcinosis, cortical nephrocalcinosis is a rare and usually secondary to acute cortical necrosis or chronic glomerulonephritis. Here, we report two paediatric cases in which cortical nephrocalcinosis developed during the course of persistent nephrotic syndrome due to focal segmental glomerulosclerosis associated with an intronic mutation in the WT1 gene. The cause of development of cortical nephrocalcinosis was uncertain in both patients. This is the first case report of WT1 mutation-related glomerulopathy associated with cortical nephrocalcinosis, although it is currently unclear if the association is coincidental or causally related.

  S. H Lee , M. H Kim and H. J. Han

Recent investigations suggest that hypoxia increases the release of fatty acids, which participate in the regulation of cytokine synthesis and cell growth. Therefore, in this study, we examined the effect of arachidonic acid (AA) on hypoxia-induced vascular endothelial growth factor (VEGF) expression and its related signaling pathways in mouse embryonic stem (ES) cells. Hypoxia increased the level of [3H]AA release and VEGF expression. AA treatment concurrent with hypoxia further increased the PGE2 production and VEGF expression level, which was inhibited by the suppression of cPLA2 and cyclooxygenase 2 (COX-2) pathways. Hypoxia increased the level of Notch-1 and Wnt-1/β-catenin expression, which was blocked by the inhibition of COX-2, and inhibition of Notch-1 by -secretase inhibitor blocked Wnt-1 activation. Moreover, the hypoxia-induced increase of hypoxia-inducible factor 1 (HIF-1) expression induced Notch-1 activation and was regulated by Wnt-1 activation. The expression of each signaling molecule induced an increase in VEGF expression that was greater in hypoxia with AA than in hypoxia alone. The inhibition of VEGF expression using VEGF-targeted small interfering RNA decreased the hypoxia-induced increase in cell cycle regulatory protein expression, DNA synthesis, and cell number, suggesting that hypoxia-induced VEGF expression stimulates proliferation of mouse ES cells. In conclusion, AA potentiates hypoxia-induced VEGF expression in mouse ES cells through the Notch-1, Wnt-1, and HIF-1 pathways.

  S. H Lee , Y. J Lee , C. H Song , Y. K Ahn and H. J. Han

Here we show that the effect of hypoxia on human umbilical cord blood mesenchymal stem cell (hMSC) migration is via the modulation of focal adhesion kinase (FAK) and its related signaling pathways. Hypoxia increased hMSC migration and cell viability, whereas lactate dehydrogenase (LDH) release was not affected for up to 48 h (data not shown). In addition, hypoxia increased the level of reactive oxygen species (ROS) generation in a time-dependent manner. Hypoxia-induced phosphorylation of p38 mitogen-activated protein kinase (MAPK) and stress-activated protein kinase/c-Jun NH2-terminal kinase (SAPK/JNK) were inhibited by the antioxidant (N-acetylcysteine, NAC, 10–6 M) and (taurine, 4x10–6 M). Hypoxia-induced endothelial nitric oxide synthase (eNOS) phosphorylation was regulated by p38 MAPK and SAPK/JNK activation. In addition, hypoxia increased the level of hypoxia inducible factor (HIF)-1 expression, which was blocked by inhibition of eNOS. Also, hypoxia-induced expression of Flk-1, vascular endothelial growth factor (VEGF), and its secreted form were inhibited by HIF-1 small interfering RNA (siRNA). In this hypoxic condition, FAK and Src phosphorylation were increased in a time-dependent manner. Inhibition of Src with specific inhibitor (PP2, 10–8 M) blocked hypoxia-induced FAK activation. Subsequently, hypoxia-induced FAK phosphorylation was blocked by VEGF siRNA. Finally, hypoxia-induced increase of hMSC migration was inhibited by FAK siRNA. The results indicate that hypoxia increases migration of hMSCs via VEGF-mediated FAK phospholylation and involves the cooperative activity of the ROS, MAPK, eNOS and HIF-1 pathways.

  J. C Yoo , J. H Ahn , S. H Lee and Y. C. Yoon

No consensus has been reached with regard to the ideal timing of anterior cruciate ligament reconstruction in terms of reducing secondary meniscal tears in anterior cruciate ligament–deficient knees.


Delay in anterior cruciate ligament reconstruction increases the incidence and severity of medial meniscal tears.

Study Design

Case series; Level of evidence, 4.


Thirty-one patients were evaluated with arthroscopic all-inside suturing of medial meniscal tears with concurrent anterior cruciate ligament reconstruction who had at least 2 preoperative magnetic resonance imaging studies. Patients were evaluated during the acute phase of injury, but anterior cruciate ligament reconstruction surgery was delayed at least 6 months. Mean interval between first and second imaging studies was 36.8 months. Subsequent medial meniscal tears were identified as longitudinal or bucket-handle types. Relationships between medial meniscal lesions and patient age, time interval between the date of initial injury and surgery, repetitive injury, and patient activity level were evaluated.


During the first preoperative magnetic resonance imaging studies, 14 knees had no medial meniscal tear, 15 a longitudinal tear, and 2 a bucket-handle–type tear; during the second preoperative imaging studies, 5 knees had no medial meniscal tear, 19 a longitudinal tear, and 7 a bucket-handle–type tear. The incidence of medial meniscal tears increased from 55% in first studies to 84% in second studies for chronic anterior cruciate ligament–insufficient knees (P = .0054). Eight knees without a tear during first studies had a longitudinal tear during second studies, 1 knee without a tear and 4 with a longitudinal tear in first studies had a bucket-handle–type tear in second studies. Thirteen knees (42%) had a worse meniscal status during the second studies.


Delayed anterior cruciate ligament reconstruction increases the likelihood of a medial meniscal tear, suggesting that early anterior cruciate ligament reconstruction should reduce or prevent additional medial meniscal injury. The findings show that further medial meniscal damage is common if surgery is delayed by 6 months or more.

  S. H Lee , K. S Kim , N Fodil Cornu , S. M Vidal and C. A. Biron

Natural killer (NK) cells have the potential to deliver both direct antimicrobial effects and regulate adaptive immune responses, but NK cell yields have been reported to vary greatly during different viral infections. Activating receptors, including the Ly49H molecule recognizing mouse cytomegalovirus (MCMV), can stimulate NK cell expansion. To define Ly49H's role in supporting NK cell proliferation and maintenance under conditions of uncontrolled viral infection, experiments were performed in Ly49h–/–, perforin 1 (Prf1)–/–, and wild-type (wt) B6 mice. NK cell numbers were similar in uninfected mice, but relative to responses in MCMV-infected wt mice, NK cell yields declined in the absence of Ly49h and increased in the absence of Prf1, with high rates of proliferation and Ly49H expression on nearly all cells. The expansion was abolished in mice deficient for both Ly49h and Prf1 (Ly49h–/–Prf1–/–), and negative consequences for survival were revealed. The Ly49H-dependent protection mechanism delivered in the absence of Prf1 was a result of interleukin 10 production, by the sustained NK cells, to regulate the magnitude of CD8 T cell responses. Thus, the studies demonstrate a previously unappreciated critical role for activating receptors in keeping NK cells present during viral infection to regulate adaptive immune responses.

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