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Article ; Online: Interaction between Gtr2p and ribosomal Rps31p affects the incorporation of Rps31p into ribosomes of Saccharomyces cerevisiae.

Sekiguchi, Takeshi / Ishii, Takashi / Funakoshi, Minoru / Kobayashi, Hideki / Furuno, Nobuaki

Biochemical and biophysical research communications

2024 Volume 699, Page(s) 149499

Abstract: In yeast, ras-like small G proteins, Gtr1p and Gtr2p, form heterodimers that affect cell division, detect amino acids, and regulate the activity of TORC1, a protein complex that integrates various signals, including those related to nutrient availability, ...

Abstract	In yeast, ras-like small G proteins, Gtr1p and Gtr2p, form heterodimers that affect cell division, detect amino acids, and regulate the activity of TORC1, a protein complex that integrates various signals, including those related to nutrient availability, growth factors, and stress signals. To explore novel roles of Gtr2p, yeast two-hybrid screening was performed using gtr2S23Np, an active form of Gtr2p, which identified Rps31p and Rpl12p as Gtr2p-interacting proteins. In the present study, we found that Gtr2p, but not Gtr1p, interacts with Rps31p, a 40S ribosomal subunit, and a component of the ubiquitin fusion protein Ubi3p, which is essential for the initiation and elongation of translation. In yeast cells expressing gtr2Q66Lp, an inactive form of Gtr2p, the interaction between Rps31p and gtr2Q66Lp, as well as the level of exogenous expression of Rps31p, was reduced. However, the level of exogenous expression of Rpl12p was unaffected. Introducing a mutation in ubiquitin target lysine residues to arginine (rps31-K5R) restored the level of exogenously expressed Rps31p and rescued the rapamycin and caffeine sensitivity of gtr2Q66L cells. Sucrose density gradient centrifugation of yeast cell lysate expressing Rps31p and gtr2Q66Lp revealed that exogenously expressed Rps31p was poorly incorporated, whereas rps31-K5Rp was efficiently incorporated, into ribosomes. These results suggest that Gtr2p influences incorporation of Rps31p into ribosomes and contributes to drug resistance through its interaction with Rps31p.
MeSH term(s)	Monomeric GTP-Binding Proteins/metabolism ; Ribosomal Proteins/genetics ; Ribosomal Proteins/metabolism ; Ribosomes/metabolism ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae/metabolism ; Saccharomyces cerevisiae Proteins/metabolism ; Ubiquitins/metabolism
Chemical Substances	GTR2 protein, S cerevisiae ; Monomeric GTP-Binding Proteins (EC 3.6.5.2) ; Ribosomal Proteins ; Saccharomyces cerevisiae Proteins ; Ubiquitins ; Rps31 protein, S cerevisiae
Language	English
Publishing date	2024-01-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2024.149499
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Article: Evaluation of hospital pharmacists' activities using additional reimbursement for infection prevention as an indicator in small and medium-sized hospitals.

Tasaka, Yuichi / Uchikura, Takeshi / Hatakeyama, Shiro / Kikuchi, Daisuke / Tsuchiya, Masami / Funakoshi, Ryohkan / Obara, Taku

Journal of pharmaceutical health care and sciences

2024 Volume 10, Issue 1, Page(s) 6

Abstract: Background: Hospitals in Japan established the healthcare delivery system from FY 2018 to 2021 by acquiring an additional reimbursement for infection prevention (ARIP) of category 1 or 2. However, research on outcomes of ARIP applications related to the ...

Abstract	Background: Hospitals in Japan established the healthcare delivery system from FY 2018 to 2021 by acquiring an additional reimbursement for infection prevention (ARIP) of category 1 or 2. However, research on outcomes of ARIP applications related to the practice of hospital pharmacists is scarce. Methods: This study assessed the activities performed by hospital pharmacists in hospitals with 100 to 299 beds, using ARIP acquirement as an indicator, using data from an annual questionnaire survey conducted in 2020 by the Japanese Society of Hospital Pharmacists on the status of hospital pharmacy departments. Out of the survey items, this study used those related to hospital functions, number of beds, number of pharmacists, whether the hospital is included in the diagnosis procedure combination (DPC) system, average length of stay, and nature of work being performed in the analysis. The relationship between the number of beds per pharmacist and state of implementation of pharmacist services or the average length of hospital stay was considered uncorrelated when the absolute value of the correlation coefficient was within 0-0.2, whereas the relationship was considered to have a weak, moderate, or strong correlation when the absolute value ranged at 0.2-0.4, 0.4-0.7, or 0.7-1, respectively. Results: Responses were received from 3612 (recovery rate: 43.6%) hospitals. Of these, 210 hospitals meeting the criteria for ARIP 1 with 100-299 beds, and 245 hospitals meeting the criteria for ARIP 2 with 100-299 beds, were included in our analysis. There was a significant difference in the number of pharmacists, with a larger number in ARIP 1 hospitals. For the pharmacist services, significant differences were observed, with a more frequency in ARIP 1 hospitals in pharmaceutical management and guidance to pre-hospitalization patients, sterile drug processing of injection drugs and therapeutic drug monitoring. In DPC hospitals with ARIP 1 (173 hospitals) and 2 (105 hospitals), the average number of beds per pharmacist was 21.7 and 24.7, respectively, while the average length of stay was 14.3 and 15.4 d, respectively. Additionally, a weak negative correlation was observed between the number of pharmacist services with "Fairly well" or "Often" and the number of beds per pharmacist for both ARIP 1 (R = -0.207) and ARIP 2 (R = -0.279) DPC hospitals. Furthermore, a weak correlation (R = 0.322) between the average number of beds per pharmacist and the average length of hospital stay was observed for ARIP 2 hospitals. Conclusions: Our results suggest that lower beds per pharmacist might lead to improved pharmacist services in 100-299 beds DPC hospitals with ARIP 1 or 2. The promotion of proactive efforts in hospital pharmacist services and fewer beds per pharmacist may relate to shorter hospital stays especially in small and medium-sized hospitals with ARIP 2 when ARIP acquisition was used as an indicator. These findings may help to accelerate the involvement of hospital pharmacists in infection control in the future.
Language	English
Publishing date	2024-01-10
Publishing country	England
Document type	Journal Article
ZDB-ID	2809913-8
ISSN	2055-0294
ISSN	2055-0294
DOI	10.1186/s40780-023-00327-5
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Article ; Online: Excessive N-acetylcysteine exaggerates glutathione redox homeostasis and apoptosis during acetaminophen exposure in Huh-7 human hepatoma cells.

Aki, Toshihiko / Tanaka, Hiroki / Funakoshi, Takeshi / Unuma, Kana / Uemura, Koichi

Biochemical and biophysical research communications

2023 Volume 676, Page(s) 66–72

Abstract: Acetaminophen (APAP) hepatotoxicity is one of the biggest drawbacks of this relatively safe and widely used drug. In addition to its hepatotoxicity, APAP also cause comparable levels of toxicity on human hepatoma cells. Here we show activation of the ... ...

Abstract	Acetaminophen (APAP) hepatotoxicity is one of the biggest drawbacks of this relatively safe and widely used drug. In addition to its hepatotoxicity, APAP also cause comparable levels of toxicity on human hepatoma cells. Here we show activation of the intrinsic caspase-9/3 pathway of apoptosis followed by gasdermin E (GSDME) cleavage and subsequent ballooning in APAP (10 mM, 72 h)-treated Huh-7 human hepatocarcinoma cells. N-acetylcysteine (NAC), an antioxidant currently used as an antidote for APAP overdose, does not alleviate APAP toxicity in Huh-7 cells; NAC overdose (10 mM) rather aggravates APAP toxicity. NAC overdose not only aggravates cell death, but also decreases the cellular GSH/GSSG ratio, an indicator of redox homeostasis of glutathione. These results show for the first time that APAP-induced apoptosis in hepatoma cells is followed by secondary necrosis via the caspase-3/GSDME pathway. NAC overdose (10 mM) not only worsens the glutathione redox status, but also accelerates this pathway.
MeSH term(s)	Humans ; Acetylcysteine/metabolism ; Acetaminophen/toxicity ; Carcinoma, Hepatocellular/pathology ; Chemical and Drug Induced Liver Injury/pathology ; Glutathione/metabolism ; Liver Neoplasms/pathology ; Apoptosis ; Oxidation-Reduction ; Homeostasis ; Liver/metabolism
Chemical Substances	Acetylcysteine (WYQ7N0BPYC) ; Acetaminophen (362O9ITL9D) ; Glutathione (GAN16C9B8O)
Language	English
Publishing date	2023-07-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2023.07.023
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Article ; Online: Cocaine induces vascular smooth muscle cells proliferation via DRP1-mediated mitochondrial fission and PI3K/HIF-1α signaling.

Wen, Shuheng / Unuma, Kana / Funakoshi, Takeshi / Aki, Toshihiko / Uemura, Koichi

Biochemical and biophysical research communications

2023 Volume 676, Page(s) 30–35

Abstract: Long-term cocaine abuse is associated with cardiovascular and pulmonary vascular complications. The vascular toxicity of cocaine can lead to vascular remodeling characterized by excessive proliferation of vascular smooth muscle cells. Though hypoxia- ... ...

Abstract	Long-term cocaine abuse is associated with cardiovascular and pulmonary vascular complications. The vascular toxicity of cocaine can lead to vascular remodeling characterized by excessive proliferation of vascular smooth muscle cells. Though hypoxia-inducible factor (HIF) signaling and mitochondrial fission have been suggested to play essential roles in the pathogenesis of hypoxia-induced vascular remodeling, pathogenetic mechanism for cocaine-related vascular remodeling remains to be elucidated. In this study, we explore the effect of cocaine on the proliferation of vascular smooth muscle cells by in vitro experiments. The findings indicated that the cocaine-induced vascular smooth muscle cell hyperproliferation is achieved by enhancing DRP1-mediated mitochondrial fission and activating PI3K/HIF-1α signaling. Current findings suggested that mitochondrial fission would play a pivotal role in cocaine-related vascular remodeling and would be helpful in understanding the vascular toxicity of cocaine.
MeSH term(s)	Humans ; Phosphatidylinositol 3-Kinases/pharmacology ; Vascular Remodeling ; Cell Proliferation ; Muscle, Smooth, Vascular ; Mitochondrial Dynamics ; Cocaine/toxicity ; Hypoxia/complications ; Hypoxia-Inducible Factor 1, alpha Subunit ; Myocytes, Smooth Muscle ; Cells, Cultured
Chemical Substances	Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Cocaine (I5Y540LHVR) ; Hypoxia-Inducible Factor 1, alpha Subunit
Language	English
Publishing date	2023-07-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2023.07.020
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Zs.A 116: Show issues

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Article ; Online: Aristolochic acid induces an inflammatory response with prostaglandin E2 production and apoptosis in NRK-52E proximal tubular cells.

Komatsu, Miyu / Funakoshi, Takeshi / Aki, Toshihiko / Unuma, Kana / Uemura, Koichi

Toxicology letters

2023 Volume 378, Page(s) 39–50

Abstract: Aristolochic acid nephropathy (AAN) is a type of drug-induced nephropathy in which ingestion of aristolochic acid (AA) causes acute kidney injury, with progressive renal fibrosis and upper urothelial carcinoma. Although the pathological features of AAN ... ...

Abstract	Aristolochic acid nephropathy (AAN) is a type of drug-induced nephropathy in which ingestion of aristolochic acid (AA) causes acute kidney injury, with progressive renal fibrosis and upper urothelial carcinoma. Although the pathological features of AAN have been reported to involve significant cell degeneration and loss in the proximal tubules, the details of the toxic mechanism in the acute phase of the disease remain unclear. This study investigates the cell death pathway and intracellular metabolic kinetics of AA exposure in rat NRK-52E proximal tubular cells. AA exposure induces dose- and time-dependent apoptotic cell death in NRK-52E cells. We examined the inflammatory response to further investigate the mechanism of AA-induced toxicity. AA exposure increased the gene expression of inflammatory cytokines IL-6 and TNF-α, suggesting that AA exposure induces inflammation. Furthermore, analysis of lipid mediators by LC-MS revealed increases in intra- and extra-cellular arachidonic acid and prostaglandin E2 (PGE2). To investigate the relationship between the AA-induced increase in PGE2 production and cell death, celecoxib, an inhibitor of cyclooxygenase-2 (COX-2), which is involved in the production of PGE2, was administered, and a marked inhibition of AA-induced cell death was observed. These results suggest that exposure to AA induces concentration- and time-dependent apoptosis in NRK-52E cells, which is attributed to inflammatory responses mediated by COX-2 and PGE2.
MeSH term(s)	Rats ; Animals ; Dinoprostone/metabolism ; Kidney Tubules/metabolism ; Cell Line ; Cyclooxygenase 2/genetics ; Cyclooxygenase 2/metabolism ; Carcinoma, Transitional Cell/metabolism ; Carcinoma, Transitional Cell/pathology ; Urinary Bladder Neoplasms/pathology ; Apoptosis/physiology ; Aristolochic Acids/toxicity ; Kidney Diseases/chemically induced
Chemical Substances	Dinoprostone (K7Q1JQR04M) ; aristolochic acid I (94218WFP5T) ; Cyclooxygenase 2 (EC 1.14.99.1) ; Aristolochic Acids
Language	English
Publishing date	2023-03-01
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	433788-8
ISSN	1879-3169 ; 0378-4274
ISSN (online)	1879-3169
ISSN	0378-4274
DOI	10.1016/j.toxlet.2023.02.009
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Zs.A 1367: Show issues

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Article ; Online: Early mobilization in spinal cord injury promotes changes in microglial dynamics and recovery of motor function.

Asano, Kohta / Nakamura, Takeshi / Funakoshi, Kengo

IBRO neuroscience reports

2022 Volume 12, Page(s) 366–376

Abstract: In the acute phase of spinal cord injury, the initial injury triggers secondary damage due to neuroinflammation, leading to the formation of cavities and glial scars that impair nerve regeneration. Following injuries to the central nervous system, early ... ...

Abstract	In the acute phase of spinal cord injury, the initial injury triggers secondary damage due to neuroinflammation, leading to the formation of cavities and glial scars that impair nerve regeneration. Following injuries to the central nervous system, early mobilization promotes the recovery of physical function. Therefore, in the present study, we investigated the effects of early mobilization on motor function recovery and neuroinflammation in rats. Early mobilization of rats with complete spinal cord transection resulted in good recovery of hindlimb motor function after 3 weeks. At 1 week after spinal cord injury, the early-mobilized rats expressed fewer inflammatory M1 microglia/macrophages and more anti-inflammatory M2 microglia. In addition, significantly more matrix metalloproteinase 2 (MMP2)-positive cells were observed at the lesion site 1 week after injury in the early-mobilized rats. Multiple labeling studies suggested that many MMP2-positive cells were M2 microglia. MMP9-positive cells that highly co-expressed GFAP were also observed more frequently in the early-mobilized rats. The density of growth-associated protein-positive structures in the lesion center was significantly higher in the early-mobilized rats at 3 weeks after spinal cord injury. The present results suggest that early mobilization after spinal cord injury reduced the production of M1 microglia/macrophages while increasing the production of M2 microglia at the lesion site. Early mobilization might also activate the expression of MMP2 in M2 microglia and MMP9 in astrocytes. These cellular dynamics might suppress neuroinflammation at the lesion site, thereby inhibiting the progression of tissue destruction and promoting nerve regeneration to recover motor function.
Language	English
Publishing date	2022-04-14
Publishing country	Netherlands
Document type	Journal Article
ISSN	2667-2421
ISSN (online)	2667-2421
DOI	10.1016/j.ibneur.2022.04.002
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Article ; Online: Aggregation-prone A53T mutant of α-synuclein exaggerates methamphetamine neurotoxicity in SH-SY5Y cells: Protective role of cellular cholesterol.

Aoki, Sho / Funakoshi, Takeshi / Aki, Toshihiko / Uemura, Koichi

Toxicology reports

2022 Volume 9, Page(s) 2020–2029

Abstract: The aim of this study is to examine the effects of wild type as well as a mutant (A53T) form of α-synuclein (α-syn) on neuronal cells exposed to methamphetamine (METH). SH-SY5Y human dopaminergic neuronal cells stably expressing exogenously added wild ... ...

Abstract	The aim of this study is to examine the effects of wild type as well as a mutant (A53T) form of α-synuclein (α-syn) on neuronal cells exposed to methamphetamine (METH). SH-SY5Y human dopaminergic neuronal cells stably expressing exogenously added wild type (WT) or A53T α-syn were established for this purpose. Among the three types of cells, parental, WT α-syn-overexpressing, and A53T α-syn overexpressing SH-SY5Y cells (hereafter referred to as SH-SY5Y, WT SH-SY5Y, and A53T SH-SY5Y, respectively), only A53T SH-SY5Y cells showed significant loss of cell viability after exposure to 2 mM METH for 24 h. Transcriptome analysis using DNA microarray showed that METH induced genes for cholesterol biosynthesis in all of these three cell lines, suggesting that METH upregulates cellular cholesterol biosynthesis independently from cellular α-syn levels. Visualization of the cellular localization of free cholesterol showed that METH induces an aberrant intracellular accumulation of free cholesterol in all three cell lines. In addition, we observed the aggregation of α-syn into cytoplasmic granules, which was more apparent with A53T α-syn than WT α-syn, in cells exposed to METH. Furthermore, the cell death observed in METH-treated A53T SH-SY5Y cells was exaggerated by the addition of 2-hydroxypropyl-β-cyclodextrin (CD), a substance used to extract cholesterol from cells. These results suggest that the aggregation of A53T α-syn in METH-treated cells should be involved in cell death. The upregulation of cellular biosynthesis and cholesterol accumulation by METH should play a protective role against A53T α-syn neurotoxicity in METH-treated SH-SY5Y cells.
Language	English
Publishing date	2022-11-21
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	2805786-7
ISSN	2214-7500 ; 2214-7500
ISSN (online)	2214-7500
ISSN	2214-7500
DOI	10.1016/j.toxrep.2022.11.006
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Article ; Online: Inverse regulation of GSDMD and GSDME gene expression during LPS-induced pyroptosis in RAW264.7 macrophage cells.

Aki, Toshihiko / Funakoshi, Takeshi / Unuma, Kana / Uemura, Koichi

Apoptosis : an international journal on programmed cell death

2022 Volume 27, Issue 1-2, Page(s) 14–21

Abstract: GSDMD and GSDME, members of the gasdermin protein family, are involved in the formation of plasma membrane channels contributing to cell rupture during a certain type of necrosis called pyroptosis. GSDMD is activated in response to immunological ... ...

Abstract	GSDMD and GSDME, members of the gasdermin protein family, are involved in the formation of plasma membrane channels contributing to cell rupture during a certain type of necrosis called pyroptosis. GSDMD is activated in response to immunological stimulation such as lipopolysaccharides (LPS) treatment while GSDME is mainly involved in drug-induced tumor cell death. Here we show that the expression of the GSDMD gene increases significantly during LPS-induced pyroptosis in RAW264.7 murine macrophage cells. In contrast, GSDME expression is decreased in the same cells. The increasing effect of LPS on GSDMD expression was observed only when the cells were cultured in high glucose (4.5 g/l) medium, suggesting that glucose availability is important for this effect. The effect of LPS on GSDMD expression is abolished by 2-deoxyglucose (2DG), confirming that glycolysis plays crucial roles in the increasing effect of LPS. Small interference RNA-mediated knock down of GSDMD or overexpression of GSDME causes LPS-induced pyroptosis to take place through GSDME rather than through GSDMD. Taken together, LPS regulates GSDMD and GSDME expression in opposite directions through, at least in part, its effect on glycolysis. This transcriptional regulation may contribute to the execution of pyroptosis in a GSDMD-dependent manner.
MeSH term(s)	Animals ; Apoptosis ; Gene Expression ; Lipopolysaccharides/pharmacology ; Macrophages/metabolism ; Mice ; Pyroptosis/genetics
Chemical Substances	Lipopolysaccharides
Language	English
Publishing date	2022-01-10
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1452360-7
ISSN	1573-675X ; 1360-8185
ISSN (online)	1573-675X
ISSN	1360-8185
DOI	10.1007/s10495-022-01708-1
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Zs.A 5178: Show issues

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Article ; Online: Role of Mitochondrial Dynamics in Cocaine's Neurotoxicity.

Wen, Shuheng / Aki, Toshihiko / Funakoshi, Takeshi / Unuma, Kana / Uemura, Koichi

International journal of molecular sciences

2022 Volume 23, Issue 10

Abstract: The dynamic balance of mitochondrial fission and fusion maintains mitochondrial homeostasis and optimal function. It is indispensable for cells such as neurons, which rely on the finely tuned mitochondria to carry out their normal physiological ... ...

Abstract	The dynamic balance of mitochondrial fission and fusion maintains mitochondrial homeostasis and optimal function. It is indispensable for cells such as neurons, which rely on the finely tuned mitochondria to carry out their normal physiological activities. The potent psychostimulant cocaine impairs mitochondria as one way it exerts its neurotoxicity, wherein the disturbances in mitochondrial dynamics have been suggested to play an essential role. In this review, we summarize the neurotoxicity of cocaine and the role of mitochondrial dynamics in cellular physiology. Subsequently, we introduce current findings that link disturbed neuronal mitochondrial dynamics with cocaine exposure. Finally, the possible role and potential therapeutic value of mitochondrial dynamics in cocaine neurotoxicity are discussed.
MeSH term(s)	Cocaine/metabolism ; Cocaine/toxicity ; Homeostasis ; Mitochondria ; Mitochondrial Dynamics/physiology ; Neurons/metabolism
Chemical Substances	Cocaine (I5Y540LHVR)
Language	English
Publishing date	2022-05-12
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23105418
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Article ; Online: Increased fatty acid synthesis and disturbed lipid metabolism in Neuro2a cells after repeated cocaine exposure: A preliminary study.

Nomura, Moeka / Wen, Shuheng / Unuma, Kana / Funakoshi, Takeshi / Aki, Toshihiko / Uemura, Koichi

Biochemical and biophysical research communications

2023 Volume 695, Page(s) 149438

Abstract: Chronic use of cocaine prompts neurodegeneration and neuroinflammation. Lipids play pivotal roles in neuronal function and pathology. Although evidence correlates cocaine use with the alteration of lipid metabolism in blood and brain, the precise ... ...

Abstract	Chronic use of cocaine prompts neurodegeneration and neuroinflammation. Lipids play pivotal roles in neuronal function and pathology. Although evidence correlates cocaine use with the alteration of lipid metabolism in blood and brain, the precise mechanism remains to be elucidated. In this study, we explore the effect of cocaine on neuronal fatty acid profiles in vitro. Neuro2a cells following seven days of repeated exposure to cocaine (0, 600, 800, 1000 μM) showed apoptosis-irrelevant cell death, dysregulated autophagy, activation of atypical endoplasmic reticulum stress response, increased saturated and unsaturated fatty acid synthesis, and disrupted lipid metabolism. These preliminary findings indicated the association between lipid metabolism and cocaine-induced neurotoxicity, which should be beneficial for understanding the neurotoxicity of cocaine.
MeSH term(s)	Lipid Metabolism ; Fatty Acids/metabolism ; Apoptosis ; Lipogenesis ; Cocaine/toxicity ; Endoplasmic Reticulum Stress
Chemical Substances	Fatty Acids ; Cocaine (I5Y540LHVR)
Language	English
Publishing date	2023-12-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2023.149438
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