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Articles by B Kim
Total Records ( 5 ) for B Kim
  J. S Kwon , Y. H Joo , H. J Nam , M Lim , E. Y Cho , M. H Jung , J. S Choi , B Kim , D. H Kang , S Oh , T Park and K. S. Hong
 

Context  Several studies have indicated that atypical antipsychotics (AAP) induce obsessive-compulsive (OC) symptoms. Research exploring the mechanism of this phenomenon, however, has been extremely limited. Considering the indirect evidence of genetic control and difficulties in developing animal models and performing gene expression studies, genetic association studies could be an important approach to understanding the molecular mechanism of AAP-induced OC symptoms. The glutamate transporter gene SLC1A1, which was recently reported to be associated with obsessive-compulsive disorder (OCD), is a promising candidate gene for susceptibility to AAP-induced OC symptoms.

Objective  To determine whether polymorphisms in SLC1A1 are associated with AAP-induced OC symptoms in patients with schizophrenia.

Design  A pharmacogenetic case-control association study.

Setting  Outpatient schizophrenia clinics.

Patients  Clinically stable patients with schizophrenia who were receiving AAP treatment (n = 94; OC group). The OC group consisted of 40 patients with AAP-induced OC symptoms, and the non-OC group consisted of 54 patients who had received AAP for more than 24 months without developing OC symptoms.

Main Outcome Measures  Allele, genotype, and haplotype frequencies. The association was tested with a logistic regression model using age, sex, and medication type as covariates.

Results  Trends of association were observed in rs2228622 and rs3780412 (nominal P = .01; adjusted permutation P = .07) for the dominant model that was the inheritance model that best fit our data. In the haplotype -based analysis, the A/C/G haplotype at rs2228622-rs3780413-rs3780412 showed a significant association with AAP-induced OC symptoms; this association withstood multiple test correction (nominal P = .01; adjusted permutation P = .04; odds ratio, 3.955; 95% confidence interval, 1.366-11.452, for dominant model).

Conclusions  These results suggest that sequence variations in SLC1A1 are associated with susceptibility to AAP-induced OC symptoms. This is the first published pharmacogenetic study on this phenomenon and provides preliminary evidence of the involvement of glutamatergic neurotransmission in the pathogenesis of AAP-induced OC symptoms.

  H. J Jeon , J. H Choi , I. H Jung , J. G Park , M. R Lee , M. N Lee , B Kim , J. Y Yoo , S. J Jeong , D. Y Kim , J. E Park , H. Y Park , K Kwack , B. K Choi , B. S Kwon and G. T. Oh
 

Background— The tumor necrosis factor receptor superfamily, which includes CD40, LIGHT, and OX40, plays important roles in atherosclerosis. CD137 (4-1BB), a member of the tumor necrosis factor receptor superfamily, has been reported to be expressed in human atherosclerotic lesions. However, limited information is available on the precise role of CD137 in atherosclerosis and the effects of blocking CD137/CD137 ligand signaling on lesion formation.

Methods and Results— We generated CD137-deficient apolipoprotein E–knockout mice (ApoE–/– CD137–/–) and LDL-receptor–knockout mice (Ldlr–/–CD137–/–) to investigate the role of CD137 in atherogenesis. The deficiency of CD137 induced a reduction in atherosclerotic plaque lesions in both atherosclerosis mouse models, which was attributed to the downregulation of cytokines such as interferon-, monocyte chemoattractant protein-1, and tumor necrosis factor-. CD137 signaling promoted the production of inflammatory molecules, including monocyte chemoattractant protein-1, interleukin-6, vascular cell adhesion molecule-1, and intercellular adhesion molecule-1, in endothelial cells. Stimulation of CD137 ligand signaling activated monocytes/macrophages and augmented the production of proinflammatory cytokines in atherosclerotic vessels.

Conclusions— CD137/CD137 ligand signaling plays multiple roles in the progression of atherosclerosis, and thus, blockade of this pathway is a promising therapeutic target for the disease.

  B Kim , Y Lee , Y Kim , K. H Lee , S Chun , K Rhee , J. T Seo , S. W Kim and J. S. Paick
  BACKGROUND

DAZ is a male infertility gene located at the AZFc region of the Y chromosome. There are four copies of the DAZ gene that share a strong homology but are not identical to one another. In the present study, we carried out cDNA cloning and immunoblot analyses to determine whether all of the DAZ genes are actively expressed in the human testis.

METHODS

AZFc deletion was detected by sequence-tagged site polymerase chain reaction (PCR) of genomic DNA isolated from blood samples. DAZ cDNAs were cloned with RT–PCR followed by sequence analysis. The expression of DAZ proteins in human testis was determined by immunoblot and compared with DAZ cDNA expression.

RESULTS

Immunoblot analysis revealed four DAZ protein bands in testis samples that showed no deletions in the AZFc region. No specific bands were observed in samples from AZFc deletion patients. Testis samples from individuals with the partial AZFc deletion, gr/gr, showed two DAZ-specific bands. Interestingly, the sizes of DAZ-specific bands varied among individuals. Analysis of DAZ transcripts in testis samples revealed that the DAZ proteins were translated from the largest of the multiple transcripts originating from each single DAZ gene.

CONCLUSIONS

All four DAZ genes are expressed in the human testis, and their products are highly polymorphic among men.

  M. N Lee , S. N Lee , S. H Kim , B Kim , B. K Jung , J. H Seo , J. H Park , J. H Choi , S. H Yim , M. R Lee , J. G Park , J. Y Yoo , J. H Kim , S. T Lee , H. M Kim , S Ryeom , K. W Kim and G. T. Oh
  Background

Vascular endothelial growth factor A (VEGFA), a critical mediator of tumor angiogenesis, is a well-characterized target of hypoxia-inducible factor 1 (HIF-1). Murine arrest-defective protein 1A (mARD1A225) acetylates HIF-1, triggering its degradation, and thus may play a role in decreased expression of VEGFA.

Methods

We generated ApcMin/+/mARD1A225 transgenic mice and quantified growth of intestinal polyps. Human gastric MKN74 and murine melanoma B16F10 cells overexpressing mARD1A225 were injected into mice, and tumor growth and metastasis were measured. VEGFA expression and microvessel density in tumors were assessed using immunohistochemistry. To evaluate the role of mARD1A225 acetylation of Lys532 in HIF-1, we injected B16F10-mARD1A225 cell lines stably expressing mutant HIF-1/K532R into mice and measured metastasis. All statistical tests were two-sided, and P values less than .05 were considered statistically significant.

Results

ApcMin/+/mARD1A225 transgenic mice (n = 25) had statistically significantly fewer intestinal polyps than ApcMin/+ mice (n = 21) (number of intestinal polyps per mouse: ApcMin/+ mice vs ApcMin/+/mARD1A225 transgenic mice, mean = 83.4 vs 38.0 polyps, difference = 45.4 polyps, 95% confidence interval [CI] = 41.8 to 48.6; P < .001). The growth and metastases of transplanted tumors were also statistically significantly reduced in mice injected with mARD1A225-overexpressing cells than in mice injected with control cells (P < .01). Moreover, overexpression of mARD1A225 decreased VEGFA expression and microvessel density in tumor xenografts (P < .04) and ApcMin/+ intestinal polyps (P = .001). Mutation of lysine 532 of HIF-1 in B16F10-mARD1A225 cells prevented HIF-1 degradation and inhibited the antimetastatic effect of mARD1A225 (P < .001).

Conclusion

mARD1A225 may be a novel upstream target that blocks VEGFA expression and tumor-related angiogenesis.

  H Wessells , C. J Sullivan , Y Tsubota , K. L Engel , B Kim , N. E Olson , D Thorner and K. Chitaley
 

To determine specific molecular features of endothelial cells (ECs) relevant to the physiological process of penile erection we compared gene expression of human EC derived from corpus cavernosum of men with and without erectile dysfunction (HCCEC) to coronary artery (HCAEC) and umbilical vein (HUVEC) using Affymetrix GeneChip microarrays and GeneSifter software. Genes differentially expressed across samples were partitioned around medoids to identify genes with highest expression in HCCEC. A total of 190 genes/transcripts were highly expressed only in HCCEC. Gene Ontology classification indicated cavernosal enrichment in genes related to cell adhesion, extracellular matrix, pattern specification and organogenesis. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed high expression of genes relating to ECM-receptor interaction, focal adhesions, and cytokine-cytokine receptor interaction. Real-time PCR confirmed expression differences in cadherins 2 and 11, claudin 11 (CLDN11), desmoplakin, and versican. CLDN11, a component of tight junctions not previously described in ECs, was highly expressed only in HCCEC and its knockdown by siRNA significantly reduced transendothelial electrical resistance in HCCEC. Overall, cavernosal ECs exhibited a transcriptional profile encoding matrix and adhesion proteins that regulate structural and functional characteristics of blood vessels. Contribution of the tight junction protein CLDN11 to barrier function in endothelial cells is novel and may reflect hemodynamic requirements of the corpus cavernosum.

 
 
 
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