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Articles by T Kita
Total Records ( 5 ) for T Kita
  Y Inuzuka , J Okuda , T Kawashima , T Kato , S Niizuma , Y Tamaki , Y Iwanaga , Y Yoshida , R Kosugi , K Watanabe Maeda , Y Machida , S Tsuji , H Aburatani , T Izumi , T Kita and T. Shioi
 

Background— Heart failure is a typical age-associated disease. Although age-related changes of heart are likely to predispose aged people to heart failure, little is known about the molecular mechanism of cardiac aging.

Methods and Results— We analyzed age-associated changes in murine heart and the manner in which suppression of the p110 isoform of phosphoinositide 3-kinase activity modified cardiac aging. Cardiac function declined in old mice associated with the expression of senescence markers. Accumulation of ubiquitinated protein and lipofuscin, as well as comprehensive gene expression profiling, indicated that dysregulation of protein quality control was a characteristic of cardiac aging. Inhibition of phosphoinositide 3-kinase preserved cardiac function and attenuated expression of the senescence markers associated with enhanced autophagy. Suppression of target of rapamycin, a downstream effector of phosphoinositide 3-kinase, also prevented lipofuscin accumulation in the heart.

Conclusions— Suppression of phosphoinositide 3-kinase prevented many age-associated changes in the heart and preserved cardiac function of aged mice.

  T Kato , S Niizuma , Y Inuzuka , T Kawashima , J Okuda , Y Tamaki , Y Iwanaga , M Narazaki , T Matsuda , T Soga , T Kita , T Kimura and T. Shioi
  Background—

Congestive heart failure (CHF) is associated with a change in cardiac energy metabolism. However, the mechanism by which this change is induced and causes the progression of CHF is unclear.

Methods and Results—

We analyzed the cardiac energy metabolism of Dahl salt-sensitive rats fed a high-salt diet, which showed a distinct transition from compensated left ventricular hypertrophy to CHF. Glucose uptake increased at the left ventricular hypertrophy stage, and glucose uptake further increased and fatty acid uptake decreased at the CHF stage. The gene expression related to glycolysis, fatty acid oxidation, and mitochondrial function was preserved at the left ventricular hypertrophy stage but decreased at the CHF stage and was associated with decreases in levels of transcriptional regulators. In a comprehensive metabolome analysis, the pentose phosphate pathway that regulates the cellular redox state was found to be activated at the CHF stage. Dichloroacetate (DCA), a compound known to enhance glucose oxidation, increased energy reserves and glucose uptake. DCA improved cardiac function and the survival of the animals. DCA activated the pentose phosphate pathway in the rat heart. DCA activated the pentose phosphate pathway, decreased oxidative stress, and prevented cell death of cultured cardiomyocytes.

Conclusions—

Left ventricular hypertrophy or CHF is associated with a distinct change in the metabolic profile of the heart. DCA attenuated the transition associated with increased energy reserves, activation of the pentose phosphate pathway, and reduced oxidative stress.

  M Kinoshita , K Ono , T Horie , K Nagao , H Nishi , Y Kuwabara , R Takanabe Mori , K Hasegawa , T Kita and T. Kimura
 

Retrovirus insertion-mediated random mutagenesis was applied in 3T3-L1 preadipocyte cells to better understand the molecular basis of obesity (the expansion of individual adipocytes). We found that tryptophan hydroxylase-1, a rate-limiting enzyme for the synthesis of serotonin (5-HT), is expressed in adipocytes and is required for their differentiation. A 5-HT type 2A receptor (5-HT2AR) antagonist, ketanserin, and a 5-HT2cR antagonist, SB-242084, inhibited adipocyte differentiation. Because 5-HT2cR mRNA levels are up-regulated during adipocyte differentiation and micro-RNA (miR)-448 is located in the fourth intron of Htr2c, we also studied the role of miR-448 in 3T3-L1 cells. Through a bioinformatics approach, Krüppel-like factor 5 (KLF5) was identified as a potential target of miR-448. Using a luciferase reporter assay, we confirmed that miR-448 targets the Klf5 3'-intranslated region. Overexpression of miR-448 reduced the expression of Klf5 and adipocyte differentiation, which was confirmed by the reduced expression of adipogenic genes and triglyceride accumulation. To examine the loss of miR-448 function, we constructed a decoy gene that had tandem complementary sequences for miR-448 in the 3'-untranslated region of a luciferase gene under the control of a cytomegalovirus promoter. When the miR-448 decoy gene was introduced into 3T3-L1 preadipocytes, KLF5 was up-regulated and triglyceride concentration was increased. In this study, we identified the regulation of adipocyte differentiation by 5-HT, 5-HT2AR, and 5-HT2CR. miR-448-mediated repression of KLF5 was identified as a negative regulator for adipocyte differentiation.

  K Nishiyama , M Horiguchi , S Shizuta , T Doi , N Ehara , R Tanuguchi , Y Haruna , Y Nakagawa , Y Furukawa , M Fukushima , T Kita and T. Kimura
  Background

The incidence of strokes has not decreased after coronary artery bypass graft surgery (CABG). The purpose of this study is to identify incidence, risk factors, and temporal pattern of strokes after on-pump and off-pump CABG.

Methods

We analyzed 2,516 consecutive patients who underwent first elective isolated CABG. The primary endpoint was strokes within 30 days. The temporal onset of the deficits was classified by consensus as either an "early stroke," which is present just after emergence from anesthesia, or a "delayed stroke," which is present after first awaking from surgery without a neurologic deficit.

Results

More than half of strokes (29 of 46; 63%) were delayed strokes. Patients undergoing off-pump CABG had significantly lower risk of early stroke (0.1% versus 1.1%, p = 0.0009), whereas the incidence of delayed strokes was not different significantly (0.9% versus 1.4%, p = 0.3484) between patients undergoing on-pump and off-pump CABG. In multivariate analyses, undergoing off-pump CABG was an independent protective factor for all strokes (relative risk 0.29, 95% confidence interval: 0.14 to 0.56, p = 0.0005) and early strokes (relative risk 0.05, 95% confidence interval: 0.003 to 0.24, p < 0.0001), but it was not an independent protective factor for delayed strokes (relative risk 0.54, 95% confidence interval: 0.24 to 1.17, p = 0.1210).

Conclusions

Undergoing off-pump CABG reduces the incidence of perioperative stroke mainly by minimizing early strokes; however, the risk of delayed strokes is not different between patients undergoing on-pump and off-pump CABG.

  T Kita , H Nishida , H Shibata , S Niimi , T Higuti and N. Arakaki
 

Mitochondrial fusion and fission processes play a role in a variety of cell functions, including energy metabolism, cell differentiation and programmed cell death. Still, it is not clear how these processes contribute to the cell functions. Here, we investigated the role of mitochondrial remodelling on lipid metabolism in adipocytes. In 3T3-L1 pre-adipocytes, the morphology of mitochondria is organized as a continuous reticulum. Upon differentiation of adipocytes manifested by cellular triacylglycerol (TG) accumulation, mitochondrial morphology altered from filamentous to fragmented and/or punctate structures. When the mitochondrial fusion was induced in adipocytes by silencing of mitochondrial fission proteins including Fis1 and Drp1, the cellular TG content was decreased. In contrast, the silencing of mitochondrial fusion proteins including mitofusin 2 and Opa1 increased the cellular TG content followed by fragmentation of mitochondria. It also appears that polyphenolic phytochemicals, negative regulators of lipid accumulation, have mitochondrial fusion activity and that there is a good correlation between mitochondrial fusion activity and the cellular TG accumulation-reducing activity of the phytochemicals. These results suggest that cellular TG accumulation is regulated, at least in part, via mitochondrial fusion and fission processes.

 
 
 
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