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Articles by H. K Lee
Total Records ( 6 ) for H. K Lee
  W. T Wong , X. Y Tian , Y Chen , F. P Leung , L Liu , H. K Lee , C. F Ng , A Xu , X Yao , P. M Vanhoutte , G. L Tipoe and Y. Huang
  Rationale:

Bone morphogenic protein (BMP)4 can stimulate superoxide production and exert proinflammatory effects on the endothelium. The underlying mechanisms of how BMP4 mediates endothelial dysfunction and hypertension remain elusive.

Objective:

To elucidate the cellular pathways by which BMP4-induced endothelial dysfunction is mediated through oxidative stress–dependent upregulation of cyclooxygenase (COX)-2.

Methods and Results:

Impaired endothelium-dependent relaxations, exaggerated endothelium-dependent contractions, and reactive oxygen species (ROS) production were observed in BMP4-treated mouse aortae, which were prevented by the BMP4 antagonist noggin. Pharmacological inhibition with thromboxane prostanoid receptor antagonist or COX-2 but not COX-1 inhibitor prevented BMP4-induced endothelial dysfunction, which was further confirmed with the use of COX-1–/– or COX-2–/– mice. Noggin and knockdown of BMP receptor 1A abolished endothelium-dependent contractions and COX-2 upregulation in BMP4-treated aortae. Apocynin and tempol treatment were effective in restoring endothelium-dependent relaxations, preventing endothelium-dependent contractions and eliminating ROS overproduction and COX-2 overexpression in BMP4-treated aortae. BMP4 increased p38 mitogen-activated protein kinase (MAPK) activity through a ROS-sensitive mechanism and p38 MAPK inhibitor prevented BMP4-induced endothelial dysfunction. COX-2 inhibition blocked the effect of BMP4 without affecting BMP4-induced ROS overproduction and COX-2 upregulation. Importantly, renal arteries from hypertensive rats and humans showed higher levels of COX-2 and BMP4 accompanied by endothelial dysfunction.

Conclusions:

We show for the first time that ROS serve as a pathological link between BMP4 stimulation and the downstream COX-2 upregulation in endothelial cells, leading to endothelial dysfunction through ROS-dependent p38 MAPK activation. This BMP4/ROS/COX-2 cascade is important in the maintenance of endothelial dysfunction in hypertension.

  G. H Kim , K Park , S. Y Yeom , K. J Lee , G Kim , J Ko , D. K Rhee , Y. H Kim , H. K Lee , H. W Kim , G. T Oh , K. U Lee , J. W Lee and S. W. Kim
 

Activating signal cointegrator-2 (ASC-2) functions as a transcriptional coactivator of many nuclear receptors and also plays important roles in the physiology of the liver and pancreas by interacting with liver X receptors (LXRs), which antagonize the development of atherosclerosis. This study was undertaken to establish the specific function of ASC-2 in macrophages and atherogenesis. Intriguingly, ASC-2 was more highly expressed in macrophages than in the liver and pancreas. To inhibit LXR-specific activity of ASC-2, we used DN2, which contains the C-terminal LXXLL motif of ASC-2 and thereby acts as an LXR-specific, dominant-negative mutant of ASC-2. In DN2-overexpressing transgenic macrophages, cellular cholesterol content was higher and cholesterol efflux lower than in control macrophages. DN2 reduced LXR ligand-dependent increases in the levels of ABCA1, ABCG1, and apolipoprotein E (apoE) transcripts as well as the activity of luciferase reporters driven by the LXR response elements (LXREs) of ABCA1, ABCG1, and apoE genes. These inhibitory effects of DN2 were reversed by overexpression of ASC-2. Chromatin immunoprecipitation analysis demonstrated that ASC-2 was recruited to the LXREs of the ABCA1, ABCG1, and apoE genes in a ligand-dependent manner and that DN2 interfered with the recruitment of ASC-2 to these LXREs. Furthermore, low-density lipoprotein receptor (LDLR)-null mice receiving bone marrow transplantation from DN2-transgenic mice showed accelerated atherogenesis when administered a high-fat diet. Taken together, these results indicate that suppression of the LXR-specific activity of ASC-2 results in both defective cholesterol metabolism in macrophages and accelerated atherogenesis, suggesting that ASC-2 is an antiatherogenic coactivator of LXRs in macrophages.

  A. Y Kim , Y. S Lee , K. H Kim , J. H Lee , H. K Lee , S. H Jang , S. E Kim , G. Y Lee , J. W Lee , S. A Jung , H. Y Chung , S Jeong and J. B. Kim
 

In obesity, dysregulation of adipocytokines is involved in several pathological conditions including diabetes and certain cancers. As a member of the adipocytokines, adiponectin plays crucial roles in whole-body energy homeostasis. Recently, it has been reported that the level of plasma adiponectin is reduced in several types of cancer patients. However, it is largely unknown whether and how adiponectin affects colon cancer cell growth. Here, we show that adiponectin suppresses the proliferation of colon cancer cells including HCT116, HT29, and LoVo. In colon cancer cells, adiponectin attenuated cell cycle progression at the G1/S boundary and concurrently increased expression of cyclin-dependent kinase inhibitors such as p21 and p27. Adiponectin stimulated AMP-activated protein kinase (AMPK) phosphorylation whereas inhibition of AMPK activity blunted the effect of adiponectin on the proliferation of colon cancer cells. Furthermore, knockdown of adiponectin receptors such as AdipoR1 and AdipoR2 relieved the suppressive effect of adiponectin on the growth of colon cancer cells. In addition, adiponectin repressed the expression of sterol regulatory element binding protein-1c, which is a key lipogenic transcription factor associated with colon cancers. These results suggest that adiponectin could inhibit the growth of colon cancer cells through stimulating AMPK activity.

  H. K Lee , M. H Song , M Kang , J. T Lee , K. A Kong , S. J Choi , K. Y Lee , H Venselaar , G Vriend , W. S Lee , H. J Park , T. K Kwon , J Bok and U. K. Kim
 

X-linked deafness type 3 (DFN3), the most prevalent X-linked form of hereditary deafness, is caused by mutations in the POU3F4 locus, which encodes a member of the POU family of transcription factors. Despite numerous reports on clinical evaluations and genetic analyses describing novel POU3F4 mutations, little is known about how such mutations affect normal functions of the POU3F4 protein and cause inner ear malformations and deafness. Here we describe three novel mutations of the POU3F4 gene and their clinical characterizations in three Korean families carrying deafness segregating at the DFN3 locus. The three mutations cause a substitution (p.Arg329Pro) or a deletion (p.Ser310del) of highly conserved amino acid residues in the POU homeodomain or a truncation that eliminates both DNA-binding domains (p.Ala116fs). In an attempt to better understand the molecular mechanisms underlying their inner ear defects, we examined the behavior of the normal and mutant forms of the POU3F4 protein in C3H/10T1/2 mesodermal cells. Protein modeling as well as in vitro assays demonstrated that these mutations are detrimental to the tertiary structure of the POU3F4 protein and severely affect its ability to bind DNA. All three mutated POU3F4 proteins failed to transactivate expression of a reporter gene. In addition, all three failed to inhibit the transcriptional activity of wild-type proteins when both wild-type and mutant proteins were coexpressed. Since most of the mutations reported for DFN3 thus far are associated with regions that encode the DNA binding domains of POU3F4, our results strongly suggest that the deafness in DFN3 patients is largely due to the null function of POU3F4.

  W. J Lee , E. S Cha , M Ha , Y. W Jin , S. S Hwang , K. A Kong , S. W Lee , H. K Lee , K. Y Lee and H. J. Kim
 

This study details the distribution and trends of doses of occupational radiation among diagnostic radiation workers by using the national dose registry between 1996 and 2006 by the Korea Food and Drug Administration. Dose measurements were collected quarterly by the use of thermoluminescent dosemeter personal monitors. A total of 61 732 workers were monitored, including 18 376 radiologic technologists (30 %), 13 762 physicians (22 %), 9858 dentists (16 %) and 6114 dental hygienists (9.9 %). The average annual effective doses of all monitored workers decreased from 1.75 to 0.80 mSv over the study period. Among all diagnostic radiation workers, radiologic technologists received both the highest effective and collective doses. Male radiologic technologists aged 30–49 y composed the majority of workers receiving more than 5 mSv in a quarter. More intensive monitoring of occupational radiation exposure and investigation into its health effects on diagnostic radiation workers are required in South Korea.

  J. H Oh , H. K Lee , J. Y Kim , S. H Kim and H. S. Gong
  Background

Although arthroscopic glenoid labrum repair using the BioKnotless anchor is common, the benefits and efficacy have not been fully evaluated.

Hypothesis

BioKnotless suture anchor is a clinically and radiologically suitable material for arthroscopic labral repair.

Study Design

Case series; Level of evidence, 4.

Methods

Ninety-seven patients underwent arthroscopic glenoid labrum repair with BioKnotless anchor between July 2004 and December 2005. Thirty-seven patients had traumatic anterior instability and 60 patients had an isolated superior labrum, anterior-posterior (SLAP) lesion. The mean age at surgery was 36.0 years (range, 15–66); the average follow-up was 34.1 months (range, 24–54). Clinical outcomes were evaluated using range of motion and various functional evaluation scores including sports activity. Pain and patient satisfaction were measured using a visual analog scale (VAS). Computed tomography arthrography was conducted in 73 patients at least 1 year after surgery for radiologic evaluation.

Results

In patients with instability, the Western Ontario Shoulder Instability index and Rowe score improved from 53.2 to 85.9 and from 68.7 to 92.7, respectively. Return to normal recreation and sports were possible in 30 patients (81.1%); the mean satisfaction VAS was 9.2. There was 1 postoperative dislocation, and the apprehension test was positive in 1 case. Postoperative range of motion including external rotation was not different. In patients with a SLAP lesion, the American Shoulder and Elbow Surgeons score and Constant score improved from 67.3 to 96.0 and 79.1 to 96.8, respectively. Pain VAS decreased from 6.0 to 0.4, and the mean satisfaction VAS was 9.4. Return to normal recreation and sports were possible in 50 patients (83.3%). All labra were found to have firmly healed to bony glenoid rim without anchor-related osteolysis in postoperative CT arthrography.

Conclusion

Clinically and radiologically, the BioKnotless anchor appears to be an acceptable alternative for arthroscopic labrum repair, and a suitable material allowing the avoidance of certain troublesome drawbacks of the conventional knot-tying suture anchor.

 
 
 
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