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Articles by J. W. Lee
Total Records ( 3 ) for J. W. Lee
  S. A Lee , Y. M Kim , T. K Kwak , H. J Kim , S Kim , W Ko , S. H Kim , K. H Park , M Cho and J. W. Lee
 

Four-transmembrane L6 family member 5 (TM4SF5) and its homolog L6, a tumor antigen, form a four-transmembrane L6 family. TM4SF5 expression causes uncontrolled cell proliferation and angiogenesis. Although other genuine transmembrane 4 superfamily (TM4SF) members co-operate with integrins for cell migration, roles of TM4SF5 in the cellular spreading and migration are unknown. Using hepatocarcinoma cell clones that ectopically express TM4SF5, we found that cross talks via an extracellular interaction between TM4SF5 and integrin 2 in collagen type I environment inhibited integrin 2 functions such as spreading on and migration toward collagen I, which were recovered by suppression of TM4SF5 or structural disturbance of its second extracellular loop using a peptide or mutagenesis. Altogether, the observations suggest that TM4SF5 in hepatocytes negatively regulates integrin 2 function via an interaction between the extracellular loop 2 of TM4SF5 and integrin 2 during cell spreading on and migration through collagen I environment.

  D. H Kim , J Lee , B Lee and J. W. Lee
 

Activating signal cointegrator-2 (ASC-2), a coactivator of multiple nuclear receptors and transcription factors, belongs to a steady-state complex named ASCOM (for ASC-2 complex), which contains histone H3 lysine 4 (H3K4) methyltransferase MLL3 or its paralog MLL4. ASC-2 binds to many nuclear receptors in a ligand-dependent manner through its two LxxLL motifs. Here we show that the first LxxLL motif of ASC-2 shows relatively weak but specific interaction with the nuclear receptor farnesoid X receptor (FXR) and that ASCOM plays crucial roles in FXR transactivation. Our results reveal that ASC-2, MLL3, and MLL4 are recruited to FXR target genes in a ligand-dependent manner. We further show that the recruitment of MLL3 requires ASC-2 and that FXR ligand induces not only expression of FXR-target genes but also their H3K4 trimethylation in a manner dependent on the presence of ASC-2, MLL3, and MLL4. In addition, MLL3 and MLL4 function redundantly with FXR transactivation. Correspondingly, expression of FXR target genes is partially impaired in mice expressing an enzymatically inactivated mutant form of MLL3, and these mice show disrupted bile acid homeostasis. Overall, these results suggest that ASCOM-MLL3 and ASCOM-MLL4 play redundant but essential roles in FXR transactivation via their H3K4 trimethylation activity.

  W. J Choi , K. K Park , B. S Kim and J. W. Lee
  Background

Identifying factors associated with favorable or unfavorable outcomes would provide patients with accurate expectations of the arthroscopic marrow stimulation techniques.

Purpose

To investigate the prognostic significance and optimal measures of defect size in osteochondral lesion of the talus as treated with arthroscopy.

Hypothesis

A critical, or threshold, defect size may exist at which clinical outcomes become poor in the treatment of osteochondral lesion of the talus.

Study Design

Cohort study; Level of evidence, 3.

Methods

In sum, 120 ankles underwent arthroscopic marrow stimulation treatment for osteochondral lesion of the talus and were evaluated for prognostic factors. Clinical failure was defined as patients’ having osteochondral transplantation or an American Orthopaedic Foot and Ankle Society (AOFAS) Ankle-Hindfoot Scale score less than 80. Linear regression analysis and the Kaplan-Meier method were used to identify optimal cutoff values of defect size.

Results

Eight ankles (6.7%) required osteochondral transplantation, and 22 ankles (18.4%) were considered failures because of AOFAS scores less than 80, which indicated fair or poor results. Linear regression analysis showed a high prognostic significance of defect area and suggested a cutoff defect size of 150 mm2 for the optimum identification of poor clinical outcomes (P < .001). Only 10 of 95 ankles (10.5%) with a defect area <150 mm2 showed clinical failure, whereas in patients with an area ≥150 mm2, the clinical failure rate was significantly higher (80%, 20/25). There was no association between outcome and the patient’s age, duration of symptoms, trauma, associated lesions, and location of lesions (P > .05).

Conclusion

Initial defect size is an important and easily obtainable prognostic factor in osteochondral lesions of the talus and so may serve as a basis for preoperative surgical decisions. A cutoff point exists regarding the risk of clinical failure at a defect area of approximately 150 mm2 as calculated from magnetic resonance imaging.

 
 
 
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