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Biomedical subjects

N Makino

Publications and source records attributed to N Makino.

At least 19 recordsLinked to original sources

Restored vulnerability of cultured endothelial cells to high glucose by iron replenishment.

High glucose (HG) concentrations are toxic to various cells in vivo, but cells become insensitive to HG toxicity when they are subcultured serially in vitro. Oxidative stress is involved in HG toxicity, and metal ions, especially iron, mediate some oxidative stress. To investigate mechanisms involved in the insensitiveness of cultured cells to HG toxicity, we focused on the level of intracellular iron. Freshly prepared human umbilical vein endothelial cells contained a substantial amount of iron, whereas its level decreased rapidly during the course of culture (to less than 10%). The iron content was restored by incubation of the cells with Fe(III)/8-hydroxyquinoline, and the iron-supplemented cells were more susceptible to both oxidant- and HG-induced injury. Under the HG conditions, the iron-loaded cells were subjected to higher levels of oxidative stress. The enhanced HG toxicity by iron was attenuated by the treatment with several antioxidants including catalase, ascorbic acid, and pyruvate. These data suggested that the insensitiveness of subcultured cells to HG toxicity is, at least in part, due to rapid and dramatic loss of intracellular iron. Supplementation with iron is useful to restore the vulnerability of cultured cells to HG that is normally observed in in vivo situations.

Aerobiosis↗

Intracellular mechanisms of cGMP-mediated regulation of myocardial contraction.

The intracellular mechanisms of cGMP, a major intracellular mediator of nitric oxide that regulates the contractility of cardiac muscle, are still to some extent unknown. To investigate these mechanisms, we observed the effects of 8-bromo-cyclic GMP (8br-cGMP) on myofibrillar Ca2+ sensitivity and Ca2+ handling of the sarcoplasmic reticulum (SR) using beta-escin-skinned preparations from Wistar rat hearts. Both low (1 microM) and high doses (100 microM) of 8br-cGMP significantly decreased the myofibrillar Ca2+ sensitivity obtained from pCa-tension relationships to a similar extent (pCa50; from 6.04 to 5.95 by 1 microM 8br-cGMP and 6.00 to 5.89 by 100 microM 8br-cGMP, respectively, n = 9 each). Whereas this Ca2+ desensitization induced by 100 microM 8br-cGMP was blocked by 1 microM KT5823, a specific inhibitor of cGMP-dependent protein kinase (PKG), not induced by 1 microM 8br-cGMP was not effected by KT5823. When the amount of Ca2+ released from the SR was estimated by the peak amplitude of 25 mM caffeine-induced contractions after constant Ca2+-loading by pCa 6, both doses of 8br-cGMP significantly augmented the caffeine-induced peak force to a similar extent (125 +/- 5.8% by 1 microM 8br-cGMP and 116 +/- 5.1% by 100 microM 8br-cGMP, respectively, n = 6 each). The two observed effects of cGMP (a decrease in myofibrillar Ca2+ sensitivity and an increase in Ca2+ uptake by the SR) may participate in regulating myocardial contraction via nitric oxide. Low and high doses of cGMP seem to work mainly via PKG-independent and PKG-dependent pathways, respectively.

Alkaloids↗

Troglitazone, an antidiabetic drug, improves left ventricular mass and diastolic function in normotensive diabetic patients.

AIMS: Patients with NIDDM have excessive cardiovascular morbidity and mortality, even in the absence of hypertension. Left ventricular hypertrophy (LVH), which is an ominous prognostic sign and an independent risk factor for cardiac events, is often present in NIDDM patients. METHODS AND RESULTS: NIDDM male patients with (n=10) and without (n=12) hypertension, all of whom had been diagnosed over 10 years ago, were examined in the present study. Normotensive NIDDM patients had not received any anti-hypertensive drugs. All patients were classified according to the left ventricular mass (LVM) index by using M-mode echocardiography and were assessed regarding their systolic (fractional shortening) and diastolic function, which included the maximal early flow velocity (MFV), the mitral valve deceleration time (DT), and the isovolumic relaxation time (IRT) as determined by Doppler indices. Troglitazone (TRO), an antidiabetic drug, was administered to both groups at a dose of 400 mg/day for 6 months. After TRO treatment, a reduction in the LVM index and an improvement in the diastolic function were observed in the normotensive but not in the hypertensive patients. CONCLUSION: The TRO treatment was sensitive for cardiac regression in those normotensive patients. These results suggest that LVH and the diastolic function in NIDDM patients without hypertension may be associated with elevated insulin resistance because TRO has a pharmacological function to increase the insulin sensitivity and to decrease insulin resistance.

Blood Flow Velocity↗

Effects of losartan on the collagen degradative enzymes in hypertrophic and congestive types of cardiomyopathic hamsters.

The present study was undertaken to determine the effects of AT1 receptor blockade which occurred in response to losartan, on the extracellular matrix (ECM) degradation process in the Bio 14.6 (n = 12) and Bio 53.58 (n = 12) strains which are referred as models of hypertrophic and dilated cardiomyopathy, respectively. The administration of losartan (30 mg/kg/day) in hamsters from 10-20 weeks of age reduced the accumulation of the left ventricular collagen matrix in both of the Bio 14.6 and the Bio 53.58 strains. According to the RT-PCR, the levels of mRNA for matrix metalloproteinase (MMP) and the tissue inhibitor of MMP (TIMP) were examined. MMP-1, -2, -3, and -9 were more enhanced in both myopathic strains than in the control F1beta, strains. With losartan, the levels of MMP-1, -2, -9, TIMP-1 and -2 decreased in the both strains but those for MMP-3 did not in Bio 14.6 strains. TIMP-3 and -4 mRNA levels did not change in any of the experimental hamsters, whether treated or untreated with losartan. The Western blots also showed similar observations in the both strains as seen in mRNA expressions although MMP-2 in the Bio 53.58 strains did not differ between treated and untreated with losartan. Although losartan has an inhibitory effect on collagen accumulation in the development of cardiomyopathy, MMPs (-1, -2, -9) and TIMPs (-1, -2) seem to be susceptible to responding to losartan in Bio cardiomyopathic hamsters.

Angiotensin Receptor Antagonists↗

Altered expression of heme oxygenase-1 in the livers of patients with portal hypertensive diseases.

This study was designed to determine changes in expression of heme oxygenase (HO)-1, the stress-inducible and carbon monoxide-producing enzyme, in normotensive and portal hypertensive human livers. GTS-1, a monoclonal antibody against rat HO-1 cross-reacted with the human HO-1 and blocked its enzyme activity, allowing us to examine the activity and localization of HO-1. In controls, approximately 50% of the total HO activity was from HO-1 as judged by the sensitivity to GTS-1, while the rest of activity was from other isozymes such as HO-2. HO-1 was expressed mainly in a subpopulation of Kupffer cells, and the expression in hepatic stellate cells, sinusoidal endothelial cells, and hepatocytes was little, if any. The HO-1 expression exhibited quite different pictures in the livers of portal hypertensive diseases. In cirrhotic livers, which undergo portal hypertension through increases in intrasinusoidal resistance and regenerative changes in the parenchyma, HO-1 occurred in a majority of Kupffer cells and was also observed in hepatocytes. Consequently, the total HO-1 activities became significantly greater in these tissues than those from normal individuals. By contrast, livers of idiopathic portal hypertension that are characterized by an increase in presinusoidal resistance displayed a significant decrease in the HO-1 expression in Kupffer cells, and its hepatocellular expression was not detectable. Although factors involved in altered HO-1 expression in these cells remain unknown, the results suggest that Kupffer cells could alter their expression of HO-1 in response to local hemodynamic changes associated with chronic portal hypertension in humans.

Antibodies, Monoclonal↗

The down-regulation of glutathione peroxidase causes bovine luteal cell apoptosis during structural luteolysis.

Prostaglandin (PG) F(2)a is known to initiate luteal cell apoptosis in the bovine corpus luteum (CL) via its specific receptor (FP) on the luteal membrane by inducing intracellular Ca(2+) mobilization and the activation of PKC. In order to identify the signaling components involved in cell apoptosis, mRNA levels and activities of antioxidative enzymes were analyzed using bovine CL at different stages of the estrous cycle. Northern blot analysis revealed that the levels of two isozymes of superoxide dismutase (SOD), the Mn and Cu/Zn types, and catalase are highly enriched in the middle estrous phase, whereas glutathione peroxidase (GPx) levels gradually decrease as the estrous cycle progresses. The incubation of bovine luteal cells with H(2)O(2) and mercaptosuccinate (MS), a specific inhibitor of GPx, resulted in an increase in chromatin DNA condensation and apoptotic DNA fragmentation. Analyses of the enzymatic activities of GPx and catalase support the RNA data, indicating that H(2)O(2) produced due to the lack of GPx is a potent inducer of luteal cell apoptosis.

Animals↗

Alpha1-adrenoceptor-Gq-RhoA signaling is upregulated to increase myofibrillar Ca2+ sensitivity in failing hearts.

Alpha1-adrenergic stimulation, coupled to Gq, has been shown to promote heart failure. However, the role of alpha1-adrenergic signaling in the regulation of myocardial contractility in failing myocardium is still poorly understood. To investigate this, we observed 1) the effect of phenylephrine on myofibrillar Ca2+ sensitivity in alpha-toxin-skinned cardiomyocytes, and 2) protein expression of Gq, RhoA, and myosin light chain phosphorylation using tachypacing-induced canine failing hearts. Phenylephrine significantly increased myofibrillar Ca2+ sensitivity in failing but not in normal cardiomyocytes. Whereas Y-27632 (Rho kinase inhibitor) blocked the phenylephrine-induced Ca2+ sensitization in the failing myocytes, calphostin C (protein kinase C inhibitor) had no effect on Ca2+ sensitization. The protein expression of Galpha(q) and RhoA and the phosphorylation level of regulatory myosin light chain significantly increased in the failing myocardium. Our results suggest that alpha1-adrenoceptor-Gq signaling is upregulated in the failing myocardium to increase the myofibrillar Ca2+ sensitivity mainly through the RhoA-Rho kinase pathway rather than through the protein kinase C pathway.

Amides↗

Isolation and characterization of the human gene homologous to the Drosophila headcase (hdc) gene in chromosome bands 6q23-q24, a region of common deletion in human pancreatic cancer.

Deletions of the long arm of chromosome 6 (6q) are one of the most common chromosomal abnormalities in multiple human malignancies. Previously, we have identified three commonly deleted regions on 6q (6q21, 6q23-q24, and 6q26) in pancreatic cancer by loss of heterozygosity studies, suggesting the presence of one or more tumor suppressor genes on this chromosome arm. Using a combination of database search and cDNA library screening, we successfully isolated a transcript from 6q24. This mRNA encodes a protein consisting of 543 amino acids with homology to the Drosophila headcase (hdc) gene and, thus, is designated as hHDC. Northern analysis identified a ubiquitously expressed 5.6-kb transcript. Seventeen (81%) of 21 pancreatic cancer cell lines and four (80%) of five renal cell carcinoma cell lines showed low level expression, suggesting that the hHDC gene may play an important role in some human cancers.

Amino Acid Sequence↗

Status of myocardial antioxidants in ischemia-reperfusion injury.

BACKGROUND: Myocardial ischemia-reperfusion represents a clinically relevant problem associated with thrombolysis, angioplasty and coronary bypass surgery. Injury of myocardium due to ischemia-reperfusion includes cardiac contractile dysfunction, arrhythmias as well as irreversible myocyte damage. These changes are considered to be the consequence of imbalance between the formation of oxidants and the availability of endogenous antioxidants in the heart. OBSERVATIONS: An increase in the formation of reactive oxygen species during ischemia-reperfusion and the adverse effects of oxyradicals on myocardium have now been well established by both direct and indirect measurements. Although several experimental studies as well as clinical trials have demonstrated the cardioprotective effects of antioxidants, some studies have failed to substantiate the results. Nonetheless, it is becoming evident that some of the endogenous antioxidants such as glutathione peroxidase, superoxide dismutase, and catalase act as a primary defense mechanism whereas the others including vitamin E may play a secondary role for attenuating the ischemia-reperfusion injury. The importance of various endogenous antioxidants in suppressing oxidative stress is evident from the depression in their activities and the inhibition of cardiac alterations which they produce during ischemia-reperfusion injury. The effects of an antioxidant thiol containing compound, N-acetylcysteine, and ischemic preconditioning were shown to be similar in preventing changes in the ischemic-reperfused hearts. CONCLUSIONS: The available evidence support the role of oxidative stress in ischemia-reperfusion injury and emphasize the importance of antioxidant mechanisms in cardioprotection.

Acetylcysteine↗

High-density lipoproteins protect endothelial cells from tumor necrosis factor-alpha-induced apoptosis.

High-density lipoproteins (HDL) levels have been shown to be inversely correlated with coronary heart disease, but the mechanisms of the direct protective effect of HDL on endothelial cells are not fully understood. The apoptosis of endothelial cells induced by cytokines and/or oxidized low-density lipoproteins, etc. may provide a mechanistic clue to the "response-to-injury" hypothesis of atherogenesis. Here we report that HDL prevent the apoptosis of human umbilical venous endothelial cells (HUVECs) induced by tumor necrosis factor-alpha (TNF-alpha) via an inhibition of CPP32-like protease activity. The incubation of HUVECs with TNF-alpha significantly increased the CPP32-like protease activity, and induced apoptosis. Preincubation of HUVECs with HDL before incubation with TNF-alpha significantly suppressed the increase in the CPP32-like protease activity, preventing apoptosis in a concentration-dependent manner. These results suggest that HDL prevent the suicide pathway leading to apoptosis of endothelial cells by decreasing the CPP32-like protease activity and that HDL thus play a protective role against the "response-to-injury" hypothesis of atherogenesis.

Apolipoprotein A-I↗

Pacing-induced palmar sweating evaluated by unique hygrometer: possible implications of sympathetic activation during tachycardia.

Although reflex sympathetic activation is a major determinant of the haemodynamic tolerability of ventricular tachycardia (VT), the methods for evaluating this aspect during on-going VT remain invasive and complicated. Palmar sweating as an indirect but non-invasive measure of sympathetic activity was estimated by means of a unique hygrometer under right ventricular (RV) rapid pacing (up to 150 beats min-1) replicating VT, and concurrent monitoring of aortic blood pressure in five patients with various kinds of cardiac arrhythmias in our electrophysiological laboratory. The peak palmar sweating rate in arbitrary units was augmented as the RV pacing rate increased and was proportional to the pacing-induced fall in systolic blood pressure (SBP), with a correlation coefficient of more than 0.903 (P<0.006). The slope of linearity between the sweating rate and the fall in SBP varied among individual patients, with greater sweating amplitude in the younger patients even with the same extent of fall in SBP. This preliminary study suggests sympathetic acceleration caused by haemodynamic deterioration under simulated VT, and therefore this protocol may be able to predict the haemodynamic tolerability of sustained monomorphic VT.

Adult↗

Does high-resolution MR imaging have better accuracy than standard MR imaging for evaluation of the triangular fibrocartilage complex?

We compared the findings of high-resolution MR imaging and standard MR imaging in the detection of tears of the triangular fibrocartilage in 33 patients with chronic wrist pain on the ulnar side. With arthroscopy as the standard of reference, sensitivity was 100%, specificity 53%, and accuracy 79% with the high-resolution MR imaging, against 83%, 67%, and 76% with the standard MR imaging. High-resolution MR imaging showed a higher sensitivity, but a decreased specificity in the assessment of the triangular fibrocartilage. The results showed that diagnosis of tears in the triangular fibrocartilage by MR imaging, even high-resolution MR imaging, is unsatisfactory, although further technological advances may well improve the accuracy.

Adult↗

Interactions of nitric oxide and oxygen in cytotoxicity: proliferation and antioxidant enzyme activities of endothelial cells in culture.

Nitric oxide (NO) shows cytotoxicity, and its reaction products with reactive oxygen species, such as peroxynitrite, are potentially more toxic. To examine the role of O2 in the NO toxicity, we have examined the proliferation of cultured human umbilical vein endothelial cells in the presence or absence of NO donor, ((Z)-1-[N-(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-++ +ium-1,2-diolate) (DETA-NONOate) (100-500 microM), under normoxia (air), hypoxia (< 0.04% O2) or hyperoxia (88-94% O2). It was found that the dose dependency on NONOate was little affected by the ambient O2 concentration, showing no apparent synergism between the two treatments. We have also examined the effects of exogenous NO under normoxia and hyperoxia on the cellular activities of antioxidant enzymes involved in the H2O2 elimination, since many of them are known to be inhibited by NO or peroxynitrite in vitro. Under normoxia DETA-NONOate (500 microM) caused 25% decrease in catalase activity and 30% increases in glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase activities in 24h. Under hyperoxia NO caused about 25% decreases in activities of catalase, glutathione reductase and glucose-6-phosphate dehydrogenase. The H2O2 removal rate by NO-treated cells was computed on the mathematical model for the enzyme system. It was concluded that the cellular antioxidant function is little affected by NO under normoxia but that it is partially impaired when the cells are exposed to NO under hyperoxia.

Catalase↗

Reduction of plasma angiotensin II to normal levels by antisense oligodeoxynucleotides against liver angiotensinogen cannot completely attenuate vascular remodeling in spontaneously hypertensive rats.

OBJECTIVE: The exact role of angiotensinogen (AGT) in vascular remodeling has yet to be determined. In the present study, we examined the effects of reducing plasma AGT by intravenous injections with antisense oligodeoxynucleotides (ODNs) against AGT targeted to the liver on vascular remodeling in spontaneously hypertensive rats (SHRs). DESIGN AND METHODS: The ODNs against rat AGT were coupled to asialoglycoprotein (ASOR) carrier molecules, which serve as an important method for regulating liver gene expression. Male SHRs (n = 18) and age-matched male Wistar- Kyoto (WKY) rats (n = 4) were used for this study. All animals were fed a standard rat diet throughout the experiment At 10 weeks of age, the SHRs were divided into three groups (n = 6); systolic blood pressure (SBP) was similar in each group. The control group received saline, the sense group was injected with the sense ODN complex and the antisense group was injected with the antisense ODN complex. WKY rats were fed for the same period of time. The ASOR-poly(L)lysine-ODN complex was injected into the tail veins twice a week. RESULTS: At the end of the treatment, a reduction in AGT mRNA levels in the liver and plasma AGT was observed only in the animals injected with antisense ODNs. Antisense ODNs significantly reduced the plasma angiotensin II (Ang II) concentrations to levels similar to those observed in WKY rats. Antisense ODNs significantly reduced the SBP (180.7 +/- 4.4 mmHg) and media cross-sectional areas of the aorta (1.11 +/- 0.02 mm2), which were still larger than those seen in WKY rats (140.3 +/- 2.1 mmHg, 0.84 +/- 0.02 mm2), compared with the SHRs injected with sense ODNs (225.2 +/- 4.4 mmHg, 1.24 +/- 0.02 mm2) and control SHRs (223.7 +/- 4.8 mmHg, 1.25 +/- 0.02 mm2). The aortic angiotensin-converting enzyme (ACE) activity and collagen concentrations, which were significantly higher than those seen in WKY rats, did not significantly change among the SHR groups. The aortic AGT, ACE, angiotensin II type 1 (AT1) receptor and angiotensin II type 2 (AT2) receptor mRNA also did not significantly change among the SHR groups. CONCLUSION: On the basis of these findings, plasma AGT is thus considered to play a role in the development of hypertrophy of smooth muscle in the aorta of SHRs, it is thought to have only a slight effect, however, on the remodeling of the matrix tissue when the suppression of hypertension is insufficient.

Angiotensin II↗

Determination of left ventricular mass by echocardiography in normotensive diabetic patients.

Patients with Type 2 diabetes mellitus (DM) have excessive cardiovascular morbidity and mortality, even in the absence of hypertension. Left ventricular hypertrophy (LVH), which is an ominous prognostic sign and an independent risk factor for cardiac events, is often present in Type 2 DM patients. Forty-two Type 2 DM patients without hypertension, all of whom had been diagnosed more than 10 years ago, were examined in the present study. They had no evidence of renal dysfunction and had not received any anti-hypertensive drugs. Age-matched healthy normal subjects (n=47) were recruited as controls. All participants were classified according to the left ventricular mass index (LVMI) using M-mode echocardiography and their systolic function (fractional shortening) was examined. The systolic function was not significantly different between the Type 2 DM and control groups. LVH can be seen even in the normotensive Type 2 DM patients, with these patients still having a higher LVMI than the normal control subjects. Although the plasma insulin levels were not significantly increased in the Type 2 DM patients, the LVMI significantly correlated with plasma insulin levels. However, the LVMI did not significantly correlate with plasma fasting glucose and hemoglobin A1c in the Type 2 DM patients. These results suggest that LVH in Type 2 DM patients without hypertension may be associated with elevated plasma insulin levels.

Age Factors↗

Low density lipoproteins develop resistance to oxidative modification due to inhibition of cholesteryl ester transfer protein by a monoclonal antibody.

Although numerous studies have investigated the relationship between cholesteryl ester transfer protein (CETP) and high density lipoprotein (HDL) remodeling, the relationship between CETP and low density lipoproteins (LDL) is still not fully understood. In the present study, we examined the effect of the inhibition of CETP on both LDL oxidation and the uptake of the oxidized LDL, which were made from LDL under condition of CETP inhibition, by macrophages using a monoclonal antibody (mAb) to CETP in incubated plasma. The 6-h incubation of plasma derived from healthy, fasting human subjects led to the transfer of cholesteryl ester (CE) from HDL to VLDL and LDL, and of triglycerides (TG) from VLDL to HDL and LDL. These net mass transfers of neutral lipids among the lipoproteins were eliminated by the mAb. The incubation of plasma either with or without the mAb did not affect the phospholipid compositions in any lipoproteins. As a result, the LDL fractionated from the plasma incubated with the mAb contained significantly less CE and TG in comparison to the LDL fractionated from the plasma incubated without the mAb. The percentage of fatty acid composition of LDL did not differ among the unincubated plasma, the plasma incubated with the mAb, and that incubated without the mAb. When LDL were oxidized with CuSO4, the LDL fractionated from the plasma incubated with the mAb were significantly resistant to the oxidative modification determined by measuring the amount of TBARS and by continuously monitoring the formation of the conjugated dienes, in comparison to the LDL fractionated from the plasma incubated without the mAb. The accumulation of cholesteryl ester of oxidized LDL, which had been oxidized for 2 h with CuSO4, in J774.1 cells also decreased significantly in the LDL fractionated from the plasma incubated with mAb in comparison to the LDL fractionated from the plasma incubated without the mAb. These results indicate that CETP inhibition reduces the composition of CE and TG in LDL and makes the LDL resistant to oxidation. In addition, the uptake of the oxidized LDL, which was made from the LDL under condition of CETP inhibition, by macrophages also decreased.

Antibodies, Monoclonal↗