The Experts below are selected from a list of 327 Experts worldwide ranked by ideXlab platform
Masako Osumi - One of the best experts on this subject based on the ideXlab platform.
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Dynamics of Cell Structure by Pressure Stress in the Fission Yeast Schizosaccharomyces pombe
Biological Systems Under Extreme Conditions, 2002Co-Authors: Masako Osumi, Mamiko Sato, Shoji ShimadaAbstract:Study of the effect of hydrostatic Pressure on yeast cells revealed the impact of ultrastructural changes including microtubules and actin cytoskeletons. We also found that the fission yeast Schizosaccharomyces pombe is more sensitive to Pressure Stress than the budding yeast Saccharomyces cerevisiae using conventional electron microscopy (CEM), immunoelectron microscopy (immuno-EM), and fluorescence microscopy (FM). To investigate the influence of Pressure Stress on the cell cycle of S. pombe we used the cells of a cold-sensitive mutant, nda3 KM311, of S. pombe which were arrested highly synchronously at a step similar to mitotic prophase under restrictive temperature at 20°C, for 4 h. We describe here that the morphological changes in actin cytoskeleton were caused by acceleration of Pressure Stress in nda3 mutant cells related to induction of diploidization in S. pombe. When the nda3 cells were incubated at the restrictive temperature of 20°C, large cells (diploid cells) appeared on a dye plate after Pressure Stress of 150 MPa. These cells made up over 40% of the colonies on the plate. Nda3 cells were first aerobically grown at 30°C in YPD liquid medium to mid-exponential phase, transferred to restrictive temperature at 20°C for 4 h, and then shifted to a permissive temperature at 36°C for 15 min. The cells grown at 20°C had an abnormal (‘leaf like’) nucleus profile surrounded by normal nuclear membrane. After Pressure Stress treatment at 100 MPa the nuclear membrane was damaged and the matrix of mitochondria had an electron-dense area. At 150 MPa, other altered features were apparent: the nuclear membrane was broken over a broad area; the vacuoles had fused into large pieces in cells grown at both 20°C and 36°C. The influence of Pressure Stress on actin cytoskeleton in nda3 cells was revealed by FM. In the cells grown at 20°C, actin patches were concentrated in the central region and actin rings were seen. Even at 100 MPa specific actin distribution was lost. Long and fine actin cables were seen all over the cells: large actin patches remained in the center of the cell and covered the actin rings, then they changed into thick and short cables at 150 MPa; they finally decomposed but the actin ring was visible even with faint fluorescence. Immuno-EM also showed this phenomenon. These results confirmed the process of degradation in actin cytoskeleton of nda3 cells by Pressure Stress.
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Response of actin cytoskeleton on Schizosaccharomyces pombe to high Pressure-Stress
Progress in Biotechnology, 2002Co-Authors: Mamiko Sato, R. Kobayashi, S. Shimada, Masako OsumiAbstract:We investigated response to Pressure Stress on the actin cytoskeleton and actin cytoskeleton-related protein Cdc8 tropomyosin of the cells of a cold-sensitive mutant nda3 -KM311 Schizosaccharomyces pombe by rhodamine-conjugated phalloidin and the specific antibodies of the actin cytoskeleton-related protein Cdc8 tropomyosin. At below 100 MPa actin cytoskeleton and tropomyosin were equally distributed. Tropomyosin was localized at the actin ring and cables, and at 100 MPa it was localized in the long and fine actin cable. Above 150 MPa, however, tropomyosin was dispersed throughout the cytoplasm. We were unable to elucidate the relationship between the actin cytoskeleton and tropomyosin on the degradation pattern of the former. Using a cdc8 temperature-sensitive mutant ( cdc8 –110) grown at a permissive temperature we studied response of ultrastructure of the cell to Pressure Stress. At 200 MPa septa of cdc8 cells were drastically changed.
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Effects of Pressure Stress on the fission yeast Schizosaccharomyces pombe cold‐sensitive mutant nda3
FEMS microbiology letters, 1999Co-Authors: Mamiko Sato, Shoji Shimada, Keiko Hasegawa, Masako OsumiAbstract:To investigate the influence of Pressure Stress on the cell cycle of Schizosaccharomyces pombe, we used a cold-sensitive nda3-KM311 mutant which arrests cell division at a step similar to the mitotic prophase, proposed by Hiraoka and colleagues (Cell 39 (1984) 349–358), under the restrictive temperature, 20°C. The nda3-KM311 cells were first aerobically grown at 30°C, transferred to 20°C for 4 h and shifted to a permissive temperature of 36°C for 15 min. The cells were treated with 100–200 MPa Pressure and studied by electron and fluorescence microscopy. At 100 MPa, the nuclear membrane was damaged and the matrix of mitochondria had an electron-dense area. At 150 MPa, the nuclear membrane was broken over broad areas; numerous small vacuoles had fused into large pieces. Actin patches were concentrated in the central region and actin rings were seen in the 20°C-grown cells. Even at 100 MPa, specific actin distribution was lost. Although at 100 MPa, long and fine actin cables were seen all over the cells, large actin patches and the actin rings remained in the center of the cell. They changed into thick and short cables at 150 MPa and above 200 MPa they decomposed but the actin ring was visible even with faint fluorescence. Immunoelectron microscopic observation confirmed this phenomenon.
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Morphological effects of Pressure Stress on yeasts
High Pressure Bioscience and Biotechnology Proceedings of the International Conference on High Pressure Bioscience and Biotechnology, 1996Co-Authors: Masako Osumi, Mamiko Sato, Hiromi Kobori, Zha Hai Feng, Sanae A. Ishijima, Kazuhiro Hamada, Shoji ShimadaAbstract:Abstract To investigate the induction of polyploidy by Pressure Stress, the ultra- structure and microtubules of Saccharomyces cerevisiae and Schizosaccharomyces pombe were studied by conventional and immunoelectron microscopy. The nuclear membrane was disrupted even at 100 MPa and with increasing Pressure mitochondria had electron-dense areas, the cytoplasmic substances changed dramatically and the cellular organelles could hardly be detected. S. pombe cells were more sensitive to low Pressure Stress than were S. cerevisiae cells. Immunoelectron microscopy confirmed that the microtubules were damaged by Pressure Stress. The damage to spindle pole bodies, microtubules and the nuclear membrane was thought to be followed by breakdown of the nuclear division apparatus and inhibition of nuclear division.
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Changes in microfilaments and microtubules of yeasts induced by Pressure Stress
High Pressure Bioscience and Biotechnology Proceedings of the International Conference on High Pressure Bioscience and Biotechnology, 1996Co-Authors: Hiromi Kobori, Mamiko Sato, Kazuhiro Hamada, Shoji Shimada, Akane Tameike, Masako OsumiAbstract:Abstract Changes in cytoskeletal elements induced by Pressure Stress in a budding yeast Saccharomyces cerevisiae , a dimorphic yeast Candida tropicalis and a fission yeast Schizosaccharomyces pombe were investigated by fluorescence microscopy. The cell cycle-specific organization of microfilaments and microtubules in the three yeasts was altered by exposure to hydrostatic Pressure of 50–150 MPa for 10 min and their complete disassembly was observed at 150–300 MPa. Similar morphological changes in the cytoskeleton were caused in the three yeasts by acceleration of Pressure Stress, although their sensitivity differed from that of yeasts; hyphal-form cells of C. tropicalis and S. pombe cells were sensitive to Pressure Stress.
Hideaki Kawaguchi - One of the best experts on this subject based on the ideXlab platform.
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N-terminal kinase, and c-Src are activated in human aortic smooth muscle cells by Pressure Stress.
Molecular and Cellular Biochemistry, 2004Co-Authors: Noriteru Morita, Kenji Iizuka, Takeshi Murakami, Hideaki KawaguchiAbstract:Mechanical forces related to Pressure and flow are important for cell hypertrophy and proliferation. There are still a few studies that examine responses of human vascular smooth muscle cells to pure Pressure Stress (transmural Pressure). It is unclear as to which mechanisms are involved in cellular responses to Pressure elevation. On the other hand, although the involvement of the local renin-angiotensin system (RAS) in Pressure-induced responses was reported, the results were contradictory. It still remains to be determined whether RAS in human vascular smooth muscle cells is activated by pure Pressure Stress. We studied the upstream signal transduction events of extracellular signal kinase (ERK) in response to atmospheric Pressure Stress and involvement of angiotensin II in Pressure-induced cell proliferation in human aortic smooth muscle cells (HASMC). A Pressure-loading apparatus was set up to examine the effects of atmospheric Pressure on human aortic smooth muscle cells. Pressure application of 160 mmHg for 3 h produced cell proliferation and activated ERK and c-JUN N-terminal kinase (JNK). ACE inhibitor suppressed all of them. ERK kinase (MEK) inhibitor also suppressed cell proliferation stimulated by pure Pressure. The phosphorylated c-Src was increased by pure Pressure Stress. The treatment with c-Src kinase inhibitor suppressed Pressure-induced proliferative response. In summary, our study found that ERK activation mediated pure Pressure-induced proliferative response of HASMC. This activation was partly mediated by c-Src. (Mol Cell Biochem 262: 71–78, 2004)
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Pure Pressure Stress increased monocarboxylate transporter in human aortic smooth muscle cell membrane.
Molecular and cellular biochemistry, 2004Co-Authors: Koji Oikawa, Kenji Iizuka, Takeshi Murakami, Tatsuya Nagai, Koichi Okita, Kazuya Yonezawa, Akira Kitabatake, Hideaki KawaguchiAbstract:Lactate is formed and utilized continuously under fully aerobic conditions. Lactate is oxidized actively at all times, especially during exercise. Family of monocarboxylate transport proteins (MCTs) that are differentially expressed in cells and tissues accomplishes the facilitated transport of lactate across membranes. Previously we reported that there is MCT1 in blood circulation. We also reported the Pressure Stress stimulated cell proliferation in aortic smooth muscle cells (HASMC). In this experiment we attempted to prove the existence of MCT1 in HASMC and to clarify the effect of Pressure Stress on MCT1 localization in HASMC. We determined succinate dehydrogenase (SDH) activity as a marker of energy metabolism in cells. SDH activity was increased by Pressure Stress. Lactate enhanced the SDH activity under Pressure Stress (160 mmHg for 3 h) as dose dependent manner. On the other hand, lactate excretion was suppressed by the addition of lactate. We could detect MCT1 in the cytosolic and the membrane fractions of HASMC. The Pressure Stress increased MCT1 in the membrane fraction in the presence of extracellular lactate. In summary, we proved the existence of MCT1 in HASMC. Pressure Stress changed the localization of MCT1. The increased membranous MCT1 may transport lactate for energy metabolism in cells.
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N-terminal kinase, and c-Src are activated in human aortic smooth muscle cells by Pressure Stress.
Molecular and cellular biochemistry, 2004Co-Authors: Noriteru Morita, Kenji Iizuka, Takeshi Murakami, Hideaki KawaguchiAbstract:Mechanical forces related to Pressure and flow are important for cell hypertrophy and proliferation. There are still a few studies that examine responses of human vascular smooth muscle cells to pure Pressure Stress (transmural Pressure). It is unclear as to which mechanisms are involved in cellular responses to Pressure elevation. On the other hand, although the involvement of the local renin-angiotensin system (RAS) in Pressure-induced responses was reported, the results were contradictory. It still remains to be determined whether RAS in human vascular smooth muscle cells is activated by pure Pressure Stress. We studied the upstream signal transduction events of extracellular signal kinase (ERK) in response to atmospheric Pressure Stress and involvement of angiotensin II in Pressure-induced cell proliferation in human aortic smooth muscle cells (HASMC). A Pressure-loading apparatus was set up to examine the effects of atmospheric Pressure on human aortic smooth muscle cells. Pressure application of 160 mmHg for 3 h produced cell proliferation and activated ERK and c-JUN N-terminal kinase (JNK). ACE inhibitor suppressed all of them. ERK kinase (MEK) inhibitor also suppressed cell proliferation stimulated by pure Pressure. The phosphorylated c-Src was increased by pure Pressure Stress. The treatment with c-Src kinase inhibitor suppressed Pressure-induced proliferative response. In summary, our study found that ERK activation mediated pure Pressure-induced proliferative response of HASMC. This activation was partly mediated by c-Src.
Shoji Shimada - One of the best experts on this subject based on the ideXlab platform.
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Dynamics of Cell Structure by Pressure Stress in the Fission Yeast Schizosaccharomyces pombe
Biological Systems Under Extreme Conditions, 2002Co-Authors: Masako Osumi, Mamiko Sato, Shoji ShimadaAbstract:Study of the effect of hydrostatic Pressure on yeast cells revealed the impact of ultrastructural changes including microtubules and actin cytoskeletons. We also found that the fission yeast Schizosaccharomyces pombe is more sensitive to Pressure Stress than the budding yeast Saccharomyces cerevisiae using conventional electron microscopy (CEM), immunoelectron microscopy (immuno-EM), and fluorescence microscopy (FM). To investigate the influence of Pressure Stress on the cell cycle of S. pombe we used the cells of a cold-sensitive mutant, nda3 KM311, of S. pombe which were arrested highly synchronously at a step similar to mitotic prophase under restrictive temperature at 20°C, for 4 h. We describe here that the morphological changes in actin cytoskeleton were caused by acceleration of Pressure Stress in nda3 mutant cells related to induction of diploidization in S. pombe. When the nda3 cells were incubated at the restrictive temperature of 20°C, large cells (diploid cells) appeared on a dye plate after Pressure Stress of 150 MPa. These cells made up over 40% of the colonies on the plate. Nda3 cells were first aerobically grown at 30°C in YPD liquid medium to mid-exponential phase, transferred to restrictive temperature at 20°C for 4 h, and then shifted to a permissive temperature at 36°C for 15 min. The cells grown at 20°C had an abnormal (‘leaf like’) nucleus profile surrounded by normal nuclear membrane. After Pressure Stress treatment at 100 MPa the nuclear membrane was damaged and the matrix of mitochondria had an electron-dense area. At 150 MPa, other altered features were apparent: the nuclear membrane was broken over a broad area; the vacuoles had fused into large pieces in cells grown at both 20°C and 36°C. The influence of Pressure Stress on actin cytoskeleton in nda3 cells was revealed by FM. In the cells grown at 20°C, actin patches were concentrated in the central region and actin rings were seen. Even at 100 MPa specific actin distribution was lost. Long and fine actin cables were seen all over the cells: large actin patches remained in the center of the cell and covered the actin rings, then they changed into thick and short cables at 150 MPa; they finally decomposed but the actin ring was visible even with faint fluorescence. Immuno-EM also showed this phenomenon. These results confirmed the process of degradation in actin cytoskeleton of nda3 cells by Pressure Stress.
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Effects of Pressure Stress on the fission yeast Schizosaccharomyces pombe cold‐sensitive mutant nda3
FEMS microbiology letters, 1999Co-Authors: Mamiko Sato, Shoji Shimada, Keiko Hasegawa, Masako OsumiAbstract:To investigate the influence of Pressure Stress on the cell cycle of Schizosaccharomyces pombe, we used a cold-sensitive nda3-KM311 mutant which arrests cell division at a step similar to the mitotic prophase, proposed by Hiraoka and colleagues (Cell 39 (1984) 349–358), under the restrictive temperature, 20°C. The nda3-KM311 cells were first aerobically grown at 30°C, transferred to 20°C for 4 h and shifted to a permissive temperature of 36°C for 15 min. The cells were treated with 100–200 MPa Pressure and studied by electron and fluorescence microscopy. At 100 MPa, the nuclear membrane was damaged and the matrix of mitochondria had an electron-dense area. At 150 MPa, the nuclear membrane was broken over broad areas; numerous small vacuoles had fused into large pieces. Actin patches were concentrated in the central region and actin rings were seen in the 20°C-grown cells. Even at 100 MPa, specific actin distribution was lost. Although at 100 MPa, long and fine actin cables were seen all over the cells, large actin patches and the actin rings remained in the center of the cell. They changed into thick and short cables at 150 MPa and above 200 MPa they decomposed but the actin ring was visible even with faint fluorescence. Immunoelectron microscopic observation confirmed this phenomenon.
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Morphological effects of Pressure Stress on yeasts
High Pressure Bioscience and Biotechnology Proceedings of the International Conference on High Pressure Bioscience and Biotechnology, 1996Co-Authors: Masako Osumi, Mamiko Sato, Hiromi Kobori, Zha Hai Feng, Sanae A. Ishijima, Kazuhiro Hamada, Shoji ShimadaAbstract:Abstract To investigate the induction of polyploidy by Pressure Stress, the ultra- structure and microtubules of Saccharomyces cerevisiae and Schizosaccharomyces pombe were studied by conventional and immunoelectron microscopy. The nuclear membrane was disrupted even at 100 MPa and with increasing Pressure mitochondria had electron-dense areas, the cytoplasmic substances changed dramatically and the cellular organelles could hardly be detected. S. pombe cells were more sensitive to low Pressure Stress than were S. cerevisiae cells. Immunoelectron microscopy confirmed that the microtubules were damaged by Pressure Stress. The damage to spindle pole bodies, microtubules and the nuclear membrane was thought to be followed by breakdown of the nuclear division apparatus and inhibition of nuclear division.
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Changes in microfilaments and microtubules of yeasts induced by Pressure Stress
High Pressure Bioscience and Biotechnology Proceedings of the International Conference on High Pressure Bioscience and Biotechnology, 1996Co-Authors: Hiromi Kobori, Mamiko Sato, Kazuhiro Hamada, Shoji Shimada, Akane Tameike, Masako OsumiAbstract:Abstract Changes in cytoskeletal elements induced by Pressure Stress in a budding yeast Saccharomyces cerevisiae , a dimorphic yeast Candida tropicalis and a fission yeast Schizosaccharomyces pombe were investigated by fluorescence microscopy. The cell cycle-specific organization of microfilaments and microtubules in the three yeasts was altered by exposure to hydrostatic Pressure of 50–150 MPa for 10 min and their complete disassembly was observed at 150–300 MPa. Similar morphological changes in the cytoskeleton were caused in the three yeasts by acceleration of Pressure Stress, although their sensitivity differed from that of yeasts; hyphal-form cells of C. tropicalis and S. pombe cells were sensitive to Pressure Stress.
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Direct induction of homozygous diploidization in the fission yeast Schizosaccharomyces pombe by Pressure Stress
FEMS Microbiology Letters, 1996Co-Authors: Kazuhiro Hamada, Masako Osumi, Yasuo Nakatomi, Shoji ShimadaAbstract:Hydrostatic Pressure Stress and a dye plate method were first used to investigate the direct induction of homozygous diploids from the haploid yeast Schizosaccharomyces pombe. Above 100 MPa at 25 °C for 10 min, Pressure Stress greatly inactivated the haploid strains of JY1 (L972 h−) JY3 (L975 h90) and JY334 (ade6-M216 leul h+). At the same time, when Pressure Stressed cells of these strains at more than 100–200 MPa were spread on a dye plate, some Pressure-effected visible colonies were stained violet (variant colonies); the rest were stained pink, similar to colonies originating from haploid cells that were not Pressure-Stressed. Based on the cell size, DNA content, crosses, and random spore analyses for the segregation of mating types or auxotrophic markers, variant cells originating from color changed colonies of JY1 after Pressure Stress were very stable and found to be homozygous diploid with an h−h− genotype at the mating-type locus. From these results we conclude that Pressure Stress in combination with a dye plate is a simple and useful method for direct induction of homozygous diploid cells with very high stability.
Kenji Iizuka - One of the best experts on this subject based on the ideXlab platform.
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Docosahexaenoic acid suppresses angiotensin II-induced A7r5 vascular smooth muscle cell proliferation and migration under pulsatile Pressure Stress.
Biomedical research (Tokyo Japan), 2018Co-Authors: Takuji Machida, Kenji Iizuka, Mikiko Yutani, Akihiro Goto, Saaya Nishimura, Ayaka Kawamura, Masahiko HirafujiAbstract:Elevated mechanical Stress applied to vascular walls is well known to modulate vascular remodeling and plays a part in the pathogenesis of atherosclerosis. On the other hand, docosahexaenoic acid (DHA), an n-3 polyunsaturated fatty acid, has been shown to protect against several types of cardiovascular diseases including atherosclerosis and hypertension. The aim of this study was to clarify the effect of pulsatile Pressure Stress and DHA on angiotensin II-induced proliferation and migration in A7r5 vascular smooth muscle cells (VSMCs). Pulsatile Pressure of between 80 and 160 mmHg was repeatedly applied to VSMCs at a frequency of 4 cycles per min using an apparatus that we developed. Cell proliferation and migration were evaluated using a live cell movie analyzer. Application of pulsatile Pressure Stress for 24 h significantly increased cell proliferation. Angiotensin II also significantly increased cell proliferation in the presence or absence of Pressure Stress. DHA significantly inhibited angiotensin II-induced cell proliferation regardless of the Pressure load. Angiotensin II significantly induced cell migration regardless of the pulsatile Pressure load. Pulsatile Pressure Stress alone slightly, but not significantly, induced cell migration. DHA inhibited angiotensin II-induced VSMC proliferation and migration under abnormal Pressure conditions. Pressure Stress tended to induce extracellular signal-regulated kinase (ERK) phosphorylation in the absence of angiotensin II, whereas it significantly induced ERK phosphorylation in the presence of angiotensin II. However, the Pressure-induced ERK phosphorylation was not observed in the DHA-treated VSMCs. Our findings may contribute to the understanding of the beneficial effect of DHA on various cardiovascular disorders.
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Pressure Stress reduces inducible NO synthase expression by interleukin-1β stimulation in cultured rat vascular smooth muscle cells.
European journal of pharmacology, 2014Co-Authors: Takuji Machida, Kenji Iizuka, Kosaku Shinohara, Nanae Hatakeyama, Keita Nakano, Yuta Kubo, Masahiko HirafujiAbstract:Abstract Elevated mechanical Stress applied to vascular walls is well known to modulate vascular remodeling. We investigated the effect of pulsatile Pressure Stress on nitric oxide (NO) production and inducible NO synthase (iNOS) expression by interleukin-1β (IL-1β) stimulation in rat vascular smooth muscle cells (VSMCs). VSMCs were enzymatically isolated from aortic media of Wistar rats. Pulsatile Pressure applied to VSMCs was repeatedly given between 80 and 160 mmHg at a frequency of 4 cycles per min using an original apparatus. Protein expression and activation were evaluated by Western blot analysis. mRNA expression was evaluated by real-time reverse transcription-polymerase chain reaction. The pulsatile Pressure reduced IL-1β-induced NO production, iNOS protein, and mRNA expression. The Pressure also reduced GTP cyclohydrolase I mRNA expression. Furthermore, the Pressure reduced phosphorylation of IL-1β-induced extracellular signal-regulated kinase (ERK), nuclear factor-κB (NF-κB) p65, and I-κBα. The Pressure had no effect on I-κBβ degradation by IL-1β stimulation. The present study shows for the first time that Pressure Stress reduces IL-1β-induced iNOS expression via a mechanism involving the ERK-NF-κB signaling pathway.
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N-terminal kinase, and c-Src are activated in human aortic smooth muscle cells by Pressure Stress.
Molecular and Cellular Biochemistry, 2004Co-Authors: Noriteru Morita, Kenji Iizuka, Takeshi Murakami, Hideaki KawaguchiAbstract:Mechanical forces related to Pressure and flow are important for cell hypertrophy and proliferation. There are still a few studies that examine responses of human vascular smooth muscle cells to pure Pressure Stress (transmural Pressure). It is unclear as to which mechanisms are involved in cellular responses to Pressure elevation. On the other hand, although the involvement of the local renin-angiotensin system (RAS) in Pressure-induced responses was reported, the results were contradictory. It still remains to be determined whether RAS in human vascular smooth muscle cells is activated by pure Pressure Stress. We studied the upstream signal transduction events of extracellular signal kinase (ERK) in response to atmospheric Pressure Stress and involvement of angiotensin II in Pressure-induced cell proliferation in human aortic smooth muscle cells (HASMC). A Pressure-loading apparatus was set up to examine the effects of atmospheric Pressure on human aortic smooth muscle cells. Pressure application of 160 mmHg for 3 h produced cell proliferation and activated ERK and c-JUN N-terminal kinase (JNK). ACE inhibitor suppressed all of them. ERK kinase (MEK) inhibitor also suppressed cell proliferation stimulated by pure Pressure. The phosphorylated c-Src was increased by pure Pressure Stress. The treatment with c-Src kinase inhibitor suppressed Pressure-induced proliferative response. In summary, our study found that ERK activation mediated pure Pressure-induced proliferative response of HASMC. This activation was partly mediated by c-Src. (Mol Cell Biochem 262: 71–78, 2004)
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Pure Pressure Stress increased monocarboxylate transporter in human aortic smooth muscle cell membrane.
Molecular and cellular biochemistry, 2004Co-Authors: Koji Oikawa, Kenji Iizuka, Takeshi Murakami, Tatsuya Nagai, Koichi Okita, Kazuya Yonezawa, Akira Kitabatake, Hideaki KawaguchiAbstract:Lactate is formed and utilized continuously under fully aerobic conditions. Lactate is oxidized actively at all times, especially during exercise. Family of monocarboxylate transport proteins (MCTs) that are differentially expressed in cells and tissues accomplishes the facilitated transport of lactate across membranes. Previously we reported that there is MCT1 in blood circulation. We also reported the Pressure Stress stimulated cell proliferation in aortic smooth muscle cells (HASMC). In this experiment we attempted to prove the existence of MCT1 in HASMC and to clarify the effect of Pressure Stress on MCT1 localization in HASMC. We determined succinate dehydrogenase (SDH) activity as a marker of energy metabolism in cells. SDH activity was increased by Pressure Stress. Lactate enhanced the SDH activity under Pressure Stress (160 mmHg for 3 h) as dose dependent manner. On the other hand, lactate excretion was suppressed by the addition of lactate. We could detect MCT1 in the cytosolic and the membrane fractions of HASMC. The Pressure Stress increased MCT1 in the membrane fraction in the presence of extracellular lactate. In summary, we proved the existence of MCT1 in HASMC. Pressure Stress changed the localization of MCT1. The increased membranous MCT1 may transport lactate for energy metabolism in cells.
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N-terminal kinase, and c-Src are activated in human aortic smooth muscle cells by Pressure Stress.
Molecular and cellular biochemistry, 2004Co-Authors: Noriteru Morita, Kenji Iizuka, Takeshi Murakami, Hideaki KawaguchiAbstract:Mechanical forces related to Pressure and flow are important for cell hypertrophy and proliferation. There are still a few studies that examine responses of human vascular smooth muscle cells to pure Pressure Stress (transmural Pressure). It is unclear as to which mechanisms are involved in cellular responses to Pressure elevation. On the other hand, although the involvement of the local renin-angiotensin system (RAS) in Pressure-induced responses was reported, the results were contradictory. It still remains to be determined whether RAS in human vascular smooth muscle cells is activated by pure Pressure Stress. We studied the upstream signal transduction events of extracellular signal kinase (ERK) in response to atmospheric Pressure Stress and involvement of angiotensin II in Pressure-induced cell proliferation in human aortic smooth muscle cells (HASMC). A Pressure-loading apparatus was set up to examine the effects of atmospheric Pressure on human aortic smooth muscle cells. Pressure application of 160 mmHg for 3 h produced cell proliferation and activated ERK and c-JUN N-terminal kinase (JNK). ACE inhibitor suppressed all of them. ERK kinase (MEK) inhibitor also suppressed cell proliferation stimulated by pure Pressure. The phosphorylated c-Src was increased by pure Pressure Stress. The treatment with c-Src kinase inhibitor suppressed Pressure-induced proliferative response. In summary, our study found that ERK activation mediated pure Pressure-induced proliferative response of HASMC. This activation was partly mediated by c-Src.
Martin G. Keane - One of the best experts on this subject based on the ideXlab platform.
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time varying myocardial Stress and systolic Pressure Stress relationship role in myocardial arterial coupling in hypertension
Circulation, 2009Co-Authors: Julio A. Chirinos, Patrick Segers, Amit K. Gupta, Abigail Swillens, Ernst Rietzschel, Marc De Buyzere, James N. Kirkpatrick, Thierry C. Gillebert, Yan Wang, Martin G. KeaneAbstract:Background— Myocardial afterload depends on left ventricular (LV) cavity size, Pressure, and wall thickness, all of which change markedly throughout ejection. We assessed the relationship between instantaneous ejection-phase Pressure and myocardial Stress and the effect of arterial wave reflections on myocardial Stress in hypertensive and normotensive adults. Methods and Results— We studied 42 untreated hypertensive, 42 treated hypertensive, and 42 normotensive adults with normal LV ejection fraction. Time-resolved central Pressure, flow, and LV geometry were measured with carotid tonometry, Doppler, and speckle-tracking echocardiography for computation of arterial load and time-varying circumferential and longitudinal myocardial Stress. In all 3 groups, peak myocardial Stress typically occurred in early systole (within the first 100 milliseconds of ejection), followed by a marked midsystolic shift in the Pressure-Stress relationship, which favored lower late systolic Stress values (P<0.001) relative to p...
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Time-Varying Myocardial Stress and Systolic Pressure-Stress Relationship Role in Myocardial-Arterial Coupling in Hypertension
Circulation, 2009Co-Authors: Julio A. Chirinos, Patrick Segers, Amit K. Gupta, Abigail Swillens, Ernst Rietzschel, Marc De Buyzere, James N. Kirkpatrick, Thierry C. Gillebert, Yan Wang, Martin G. KeaneAbstract:Background— Myocardial afterload depends on left ventricular (LV) cavity size, Pressure, and wall thickness, all of which change markedly throughout ejection. We assessed the relationship between instantaneous ejection-phase Pressure and myocardial Stress and the effect of arterial wave reflections on myocardial Stress in hypertensive and normotensive adults. Methods and Results— We studied 42 untreated hypertensive, 42 treated hypertensive, and 42 normotensive adults with normal LV ejection fraction. Time-resolved central Pressure, flow, and LV geometry were measured with carotid tonometry, Doppler, and speckle-tracking echocardiography for computation of arterial load and time-varying circumferential and longitudinal myocardial Stress. In all 3 groups, peak myocardial Stress typically occurred in early systole (within the first 100 milliseconds of ejection), followed by a marked midsystolic shift in the Pressure-Stress relationship, which favored lower late systolic Stress values (P