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Articles by K Otsui
Total Records ( 3 ) for K Otsui
  M Terashima , Y Ohashi , H Azumi , K Otsui , H Kaneda , K Awano , S Kobayashi , T Honjo , T Suzuki , K Maeda , M Yokoyama and N. Inoue
 

Background— Coronary arterial remodeling, which is a response to the growth of atherosclerotic plaques, is associated with plaque vulnerability. Oxidative stress induced by reactive oxygen species (ROS) via NAD(P)H oxidase in the vasculature also plays a crucial role in the pathogenesis of atherosclerosis-based cardiovascular disease. In this study, the relationship between coronary arterial remodeling and ROS generation was examined by comparing preinterventional intravascular ultrasound findings of atherosclerotic lesions to the histochemical findings of corresponding specimens obtained by directional coronary atherectomy.

Methods and Results— Predirectional coronary atherectomy intravascular ultrasound images of 49 patients were analyzed. The remodeling index was calculated by dividing the target-lesion external elastic membrane cross-sectional area by the reference-segment external elastic membrane cross-sectional area. Expansive remodeling was defined as a remodeling index of >1.0. ROS generation and NAD(P)H oxidase p22phox expression in directional coronary atherectomy specimens were evaluated using the dihydroethidium staining method and immunohistochemistry as the ratio of the positive area to the total surface area in each specimen, respectively. ROS generation and p22phox expression were significantly greater in lesions with expansive remodeling than in lesions without remodeling (0.18±0.12 versus 0.03±0.02, P<0.0001, 0.10±0.08 versus 0.04±0.05, P=0.0039, respectively). Both ROS generation and p22phox expression significantly correlated with the intravascular ultrasound-derived remodeling index (r=0.77, P<0.0001, r=0.53, P<0.0001, respectively).

Conclusions— Simultaneous examination with intravascular ultrasound and immunohistochemistry analyses suggests that NAD(P)H oxidase-derived ROS is related to the coronary arterial remodeling process associated with plaque vulnerability.

  Y Fujita , A Kakino , M Harada Shiba , Y Sato , K Otsui , R Yoshimoto and T. Sawamura
 

Background: C-reactive protein (CRP) increases in response to inflammation and is purported to be a risk factor for atherogenesis. We recently demonstrated that a scavenger receptor, lectin-like oxidized LDL receptor (LOX-1), is a receptor for CRP. In light of the overlapping ligand spectrum of scavenger receptors such as modified LDL, bacteria, and advanced glycation end products, we examined whether other scavenger receptors recognize CRP.

Methods: We analyzed the uptake of fluorescently labeled CRP in COS-7 cells expressing a series of scavenger receptors and in a monocytic cell line, THP-1, differentiated into macrophage with phorbol 12-myristate 13-acetate (PMA). We applied small interfering RNA (siRNA) against class-A scavenger receptor (SR-A) to THP-1 cells to suppress the expression of SR-A. We also analyzed the binding of nonlabeled CRP to immobilized recombinant LOX-1 and SR-A in vitro using anti-CRP antibody.

Results: COS-7 cells expressing LOX-1 and SR-A internalized fluorescently labeled CRP in a dose-dependent manner, but cells expressing CD36, SR-BI, or CD68 did not. The recombinant LOX-1 and SR-A proteins recognized nonlabeled purified CRP and native CRP in serum in vitro. THP-1 cells differentiated into macrophage-like cells by treatment with PMA-internalized fluorescently labeled CRP. siRNA against SR-A significantly and concomitantly inhibited the expression of SR-A (P < 0.01) and CRP uptake (P < 0.01), whereas control siRNA did not.

Conclusions: CRP is recognized by SR-A as well as LOX-1 and taken up via SR-A in a macrophage-like cell line. This process might be of significance in the pathogenesis of atherosclerotic disease.

  N Inoue , T Okamura , Y Kokubo , Y Fujita , Y Sato , M Nakanishi , K Yanagida , A Kakino , S Iwamoto , M Watanabe , S Ogura , K Otsui , H Matsuda , K Uchida , R Yoshimoto and T. Sawamura
 

Background: Lectin-like oxidized LDL receptor 1 (LOX-1) is implicated in atherothrombotic diseases. Activation of LOX-1 in humans can be evaluated by use of the LOX index, obtained by multiplying the circulating concentration of LOX-1 ligands containing apolipoprotein B (LAB) times that of the soluble form of LOX-1 (sLOX-1) [LOX index = LAB x sLOX-1]. This study aimed to establish the prognostic value of the LOX index for coronary heart disease (CHD) and stroke in a community-based cohort.

Methods: An 11-year cohort study of 2437 residents age 30–79 years was performed in an urban area located in Japan. Of these, we included in the analysis 1094 men and 1201 women without history of stroke and CHD. We measured LAB and sLOX-1 using ELISAs with recombinant LOX-1 and monoclonal anti–apolipoprotein B antibody and with 2 monoclonal antibodies against LOX-1, respectively.

Results: During the follow-up period, there were 68 incident cases of CHD and 91 cases of stroke (with 60 ischemic strokes). Compared with the bottom quartile, the hazard ratio (HR) of the top quartile of LOX index was 1.74 (95% CI 0.92–3.30) for stroke and 2.09 (1.00–4.35) for CHD after adjusting for sex, age, body mass index, drinking, smoking, hypertension, diabetes, non-HDL cholesterol, and use of lipid-lowering agents. Compared with the bottom quartile of LOX index, the fully adjusted HRs for ischemic stroke were consistently high from the second to the top quartile: 3.39 (95% CI 1.34–8.53), 3.15 (1.22–8.13) and 3.23 (1.24–8.37), respectively.

Conclusions: Higher LOX index values were associated with an increased risk of CHD. Low LOX index values may be protective against ischemic stroke.

 
 
 
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