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Articles by Y Morikawa
Total Records ( 3 ) for Y Morikawa
  K Onoue , S Uemura , Y Takeda , S Somekawa , H Iwama , K Imagawa , T Nishida , Y Morikawa , Y Takemoto , O Asai , T Soeda , S Okayama , K Ishigami , K Nakatani , H Kawata , M Horii , T Nakajima , Y Akai , M Iwano and Y. Saito
 

Background— Renal dysfunction is commonly accompanied by a worsening of atherosclerosis; however, the underlying molecular mechanism is not fully understood. We examined the role played by soluble fms-like tyrosine kinase-1 (sFlt-1), an endogenous antagonist of the proatherogenic cytokine placental growth factor (PlGF), in the worsening of atherosclerosis in patients with renal dysfunction and in an animal model of renal failure.

Methods and Results— In this study, 329 patients who received cardiac catheterization and 76 patients who underwent renal biopsy were enrolled. Both plasma sFlt-1 levels and renal sFlt-1 mRNA expression were positively correlated with estimated glomerular filtration rate (P<0.01). The PlGF/sFlt-1 ratio was negatively correlated with estimated glomerular filtration rate (P<0.01), whereas plasma PlGF levels were not affected by it. The PlGF/sFlt-1 ratio was significantly higher in patients with multivessel coronary artery disease than in patients with single-vessel or no coronary artery disease. The reduction of circulating sFlt-1 and renal sFlt-1 mRNA levels was confirmed in five-sixths (5/6)–nephrectomized apolipoprotein E–deficient mice that developed experimental renal dysfunction. Atherosclerotic plaque area and macrophage infiltration into the plaque were significantly higher in 5/6–nephrectomized apolipoprotein E–deficient mice than in control mice, but replacement therapy with recombinant sFlt-1 significantly reduced both plaque formation and macrophage infiltration.

Conclusions— The present study demonstrates that a reduction in the circulating levels of sFlt-1 is associated with the worsening of atherosclerosis that accompanies renal dysfunction.

  H Nakagawa , Y Morikawa , Y Mizuno , E Harada , T Ito , K Matsui , Y Saito and H. Yasue
 

Background— Coronary spasm plays an important role in the pathogenesis of ischemic heart disease. However, similarities and differences between coronary spasm and atherosclerosis are not known. We examined the angiographic characteristics of coronary spasm in comparison with those of atherosclerosis.

Methods and Results— Thirty-two left anterior descending arteries, 11 left circumflex arteries, and 23 right coronary arteries with spasm and atherosclerotic plaque were analyzed for the localization of spasm in comparison with that of plaque in 47 patients (38 men and 9 women, mean age 66.8±10.3 yrs). Spasm predominantly occurred at the branch point as compared with plaque in each of the 3 arteries (76.7% versus 23.3%, P<0.0001; 72.7% versus 9.1%, P<0.039; and 60.0% versus 10.0%, P=0.002, in the left anterior descending, left circumflex, and right coronary arteries, respectively). Spasm involved the proximal segment less frequently as compared with plaque in each of the 3 arteries (56.7% versus 93.3%, P<0.0001; 18.2% versus 81.8%, P=0.016; and 15.0% versus 75.0%, P<0.0001 in the left anterior descending, left circumflex, and right coronary arteries, respectively). Most spasms occurred at the nonplaque site in each of the 3 arteries (73.3%, P=0.018; 100%, P<0.0001; and 75.0%, P=0.041 in the left anterior descending, left circumflex, and right coronary arteries, respectively).

Conclusion— Coronary spasm preferentially occurred at branch points and nonplaque sites, whereas the atherosclerotic lesion was predominantly localized at the nonbranch points of the curved proximal segments. Coronary spasm may thus be a manifestation of a distinct type of arteriosclerosis different from the lipid-laden coronary atherosclerosis.

  Y Yamanishi , J Kitaura , K Izawa , A Kaitani , Y Komeno , M Nakamura , S Yamazaki , Y Enomoto , T Oki , H Akiba , T Abe , T Komori , Y Morikawa , H Kiyonari , T Takai , K Okumura and T. Kitamura
 

Leukocyte mono-immunoglobulin (Ig)–like receptor 5 (LMIR5)/CD300b is a DAP12-coupled activating receptor predominantly expressed in myeloid cells. The ligands for LMIR have not been reported. We have identified T cell Ig mucin 1 (TIM1) as a possible ligand for LMIR5 by retrovirus-mediated expression cloning. TIM1 interacted only with LMIR5 among the LMIR family, whereas LMIR5 interacted with TIM4 as well as TIM1. The Ig-like domain of LMIR5 bound to TIM1 in the vicinity of the phosphatidylserine (PS)-binding site within the Ig-like domain of TIM1. Unlike its binding to TIM1 or TIM4, LMIR5 failed to bind to PS. LMIR5 binding did not affect TIM1- or TIM4-mediated phagocytosis of apoptotic cells, and stimulation with TIM1 or TIM4 induced LMIR5-mediated activation of mast cells. Notably, LMIR5 deficiency suppressed TIM1-Fc–induced recruitment of neutrophils in the dorsal air pouch, and LMIR5 deficiency attenuated neutrophil accumulation in a model of ischemia/reperfusion injury in the kidneys in which TIM1 expression is up-regulated. In that model, LMIR5 deficiency resulted in ameliorated tubular necrosis and cast formation in the acute phase. Collectively, our results indicate that TIM1 is an endogenous ligand for LMIR5 and that the TIM1–LMIR5 interaction plays a physiological role in immune regulation by myeloid cells.

 
 
 
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