LIVIVO - Search results -

Search results

Result 1 - 10 of total 20

Search options

Article ; Online: Inhibition of mitochondrial calcium transporters alters adp-induced platelet responses.

Shehwar, Durre / Barki, Saima / Aliotta, Alessandro / Veuthey, Lucas / Bertaggia Calderara, Debora / Alberio, Lorenzo / Alam, Muhammad Rizwan

Molecular biology reports

2024 Volume 51, Issue 1, Page(s) 177

Abstract: Introduction: ADP-stimulated elevation of cytosolic Ca: Methods and results: The present study aimed to elucidate the role of mitochondrial Ca: Conclusion: Together, these findings uncover a vital and hitherto poorly characterized role of ... ...

Abstract	Introduction: ADP-stimulated elevation of cytosolic Ca Methods and results: The present study aimed to elucidate the role of mitochondrial Ca Conclusion: Together, these findings uncover a vital and hitherto poorly characterized role of mitochondrial Ca
MeSH term(s)	Humans ; Calcium ; P-Selectin ; Platelet Glycoprotein GPIIb-IIIa Complex ; Blood Platelets ; Mitochondrial Membrane Transport Proteins ; Mitoxantrone
Chemical Substances	Calcium (SY7Q814VUP) ; P-Selectin ; Platelet Glycoprotein GPIIb-IIIa Complex ; Mitochondrial Membrane Transport Proteins ; Mitoxantrone (BZ114NVM5P)
Language	English
Publishing date	2024-01-22
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	186544-4
ISSN	1573-4978 ; 0301-4851
ISSN (online)	1573-4978
ISSN	0301-4851
DOI	10.1007/s11033-023-09116-7
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1140: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾
- See ZB MED holdings
- Order with fees

Article: Lapachol-Induced Upregulation of Sirt1/Sirt3 is linked with Improved Skin Wound Healing in Alloxan-induced Diabetic Mice.

Bibi, Shaheen / Ahmad, Fayyaz / Alam, Muhammad Rizwan / Ansar, Muhammad / Yeou, Kim Sun / Wahedi, Hussain Mustatab

Iranian journal of pharmaceutical research : IJPR

2021 Volume 20, Issue 3, Page(s) 419–430

Abstract: Timely repair of damaged skin is very important to maintain the integrity and homeostasis of skin, but the wound healing process is compromised in diabetic patients due to several extrinsic and intrinsic factors thus lead to leg amputation and death ... ...

Abstract	Timely repair of damaged skin is very important to maintain the integrity and homeostasis of skin, but the wound healing process is compromised in diabetic patients due to several extrinsic and intrinsic factors thus lead to leg amputation and death eventually. Sirtuins, a family of seven conserved proteins are known to be associated with pathophysiological processes of the skin. The most important among them are sirt1and sirt3 involved in cell regeneration and cell survival. Naphthoquinone derivatives have a wide range of therapeutic properties, but the potential diabetic wound healing activity of lapachol has not been identified yet. The present study thus aimed to investigate the wound healing effects of lapachol in a diabetic mouse model. Diabetic wounded mice were divided into 3 groups; vehicle, lapachol 0.05%, and lapachol 0.1%. Skin samples collected from diabetic wounded mice on different time points after treatment for 10 consecutive days were subjected to downstream analysis by western blot, ELISA and histology. Lapachol treatment was found to enhance the expression of sirt1/sirt3 and other proteins involved in cell migration and blood vessel formation. The tissue development rate was increased by lapachol treatment with better collagen deposition. Interestingly, lapachol treatment also gave rise to a high concentration of growth factors resulting in speedy and timely recovery of injured skin. In summary, our findings suggest that lapachol promotes efficient wound healing in a diabetic mouse model by increasing the expression of sirt1 and sirt3 and other proteins related to wound repair and skin regeneration including α-PAK, RAC1/CDC42, VEGF and growth factors viz PDGF and VEGF. This research work finds a novel potential activator of sirtuins in the form of lapachol and depicts the role of activated sirtuins in diabetic wound healing.
Language	English
Publishing date	2021-10-27
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2578271-X
ISSN	1735-0328 ; 1726-6890
ISSN	1735-0328 ; 1726-6890
DOI	10.22037/ijpr.2021.112722.13914
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

Order via subito

Details ▾
- Full text online
- Order with fees

Article: Expression analysis of tumour necrosis factor alpha (TNF-α) and alkaline phosphatase in occupational workers exposed to low dose of X-radiation: A case-control study.

Rehman, Khurram / Mustafa, Ghulam / Ayub, Hina / Ullah, Irfan / Alam, Muhammad Rizwan / Khan, Muzammil Ahmad

JPMA. The Journal of the Pakistan Medical Association

2020 Volume 70, Issue 11, Page(s) 1887–1896

Abstract: Objectives: To evaluate liver and inflammatory biomarkers in occupationally exposed radiology workers.: Methods: The descriptive study was conducted at Mufti Mehmood Memorial Teaching Hospital and Gomal Centre of Biochemistry and Biotechnology, Gomal ...

Abstract	Objectives: To evaluate liver and inflammatory biomarkers in occupationally exposed radiology workers. Methods: The descriptive study was conducted at Mufti Mehmood Memorial Teaching Hospital and Gomal Centre of Biochemistry and Biotechnology, Gomal University, Dera Ismail Khan, Pakistan, from September 2017 to May 2018, and comprised X-ray technicians working 48-72 hours per week, and a group of age- and gender-matched unexposed healthy controls. The exposed group was divided into three sub-groups based on their radiation work duration. Liver health status involved estimation of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, gamma-glutamyl transferase GGT and bilirubin through automated chemistry analyser, while serum tumour necrosis factor-alpha and interleukin- 6 levels through enzyme-linked immunosorbent assay technique. Relative gene expression analysis of tumour necrosis factor-alpha and alkaline phosphatase was performed through reverse transcription-polymerase chain reaction. Data was analysed using SPSS 20. Results: Of the 70 subjects, 50(71.4%) were cases with a mean age of 36.98±8.07 years and 20(28.6%) were controls with a mean age of 36.80±7.78 years. Serum alanine aminotransferase and alkaline phosphatase levels showed significant elevation in the cases compared to the controls (p<0.0001), although alanine aminotransferase levels were within the normal range. The difference in aspartate aminotransferase, gamma-glutamyl transferase and bilirubin levels was not significant (p>0.05). Tumour necrosis factor-alpha concentration was significantly high in the cases compared to the controls (p<0.0001). In contrast with proteomic analysis, relative gene expression analysis revealed reduced level of alkaline phosphatase and tumour necrosis factor-alpha in the cases compared to the controls (p<0.05). Conclusions: Serum proteomic analysis of X-ray technicians indicated acute inflammatory conditions, while genomic analysis exhibited down-regulation of alkaline phosphatase and tumour necrosis factor-alpha genes.
MeSH term(s)	Adult ; Alanine Transaminase ; Alkaline Phosphatase ; Aspartate Aminotransferases ; Case-Control Studies ; Humans ; Liver ; Middle Aged ; Pakistan ; Proteomics ; Tumor Necrosis Factor-alpha ; X-Rays
Chemical Substances	Tumor Necrosis Factor-alpha ; Aspartate Aminotransferases (EC 2.6.1.1) ; Alanine Transaminase (EC 2.6.1.2) ; Alkaline Phosphatase (EC 3.1.3.1)
Language	English
Publishing date	2020-12-05
Publishing country	Pakistan
Document type	Journal Article
ZDB-ID	603873-6
ISSN	0030-9982
ISSN	0030-9982
DOI	10.5455/JPMA.10644
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.B 845: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: A loss of function variant in AGPAT3 underlies intellectual disability and retinitis pigmentosa (IDRP) syndrome.

Malik, Madiha Amin / Saqib, Muhammad Arif Nadeem / Mientjes, Edwin / Acharya, Anushree / Alam, Muhammad Rizwan / Wallaard, Ilse / Schrauwen, Isabelle / Bamshad, Michael J / Santos-Cortez, Regie Lyn P / Elgersma, Ype / Leal, Suzanne M / Ansar, Muhammad

European journal of human genetics : EJHG

2023 Volume 31, Issue 12, Page(s) 1447–1454

Abstract: Intellectual disability (ID) and retinal dystrophy (RD) are the frequently found features of multiple syndromes involving additional systemic manifestations. Here, we studied a family with four members presenting severe ID and retinitis pigmentosa (RP). ... ...

Abstract	Intellectual disability (ID) and retinal dystrophy (RD) are the frequently found features of multiple syndromes involving additional systemic manifestations. Here, we studied a family with four members presenting severe ID and retinitis pigmentosa (RP). Using genome wide genotyping and exome sequencing, we identified a nonsense variant c.747 C > A (p.Tyr249Ter) in exon 7 of AGPAT3 which co-segregates with the disease phenotype. Western blot analysis of overexpressed WT and mutant AGPAT3 in HEK293T cells showed the absence of AGPAT3, suggesting instability of the truncated protein. Knockdown of Agpat3 in the embryonic mouse brain caused marked deficits in neuronal migration, strongly suggesting that reduced expression of AGPAT3 affects neuronal function. Altogether, our data indicates that AGPAT3 activity is essential for neuronal functioning and loss of its activity probably causes intellectual disability and retinitis pigmentosa (IDRP) syndrome.
MeSH term(s)	Animals ; Humans ; Mice ; Exome ; HEK293 Cells ; Intellectual Disability/genetics ; Mutation ; Pedigree ; Retinitis Pigmentosa/genetics
Chemical Substances	2-acylglycerophosphate acyltransferase (EC 2.3.1.52) ; Lpaat3 protein, mouse (EC 2.3.1.-)
Language	English
Publishing date	2023-10-11
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1141470-4
ISSN	1476-5438 ; 1018-4813
ISSN (online)	1476-5438
ISSN	1018-4813
DOI	10.1038/s41431-023-01475-w
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 3589: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Hepatitis C virus replication requires integrity of mitochondria-associated ER membranes.

Duponchel, Sarah / Monnier, Lea / Molle, Jennifer / Bendridi, Nadia / Alam, Muhammad Rizwan / Gaballah, Ahmed / Grigorov, Boyan / Ivanov, Alexander / Schmiel, Marcel / Odenthal, Margarete / Ovize, Michel / Rieusset, Jennifer / Zoulim, Fabien / Bartosch, Birke

JHEP reports : innovation in hepatology

2022 Volume 5, Issue 3, Page(s) 100647

Abstract: Background & aims: Chronic HCV infection causes cellular stress, fibrosis and predisposes to hepatocarcinogenesis. Mitochondria play key roles in orchestrating stress responses by regulating bioenergetics, inflammation and apoptosis. To better ... ...

Abstract	Background & aims: Chronic HCV infection causes cellular stress, fibrosis and predisposes to hepatocarcinogenesis. Mitochondria play key roles in orchestrating stress responses by regulating bioenergetics, inflammation and apoptosis. To better understand the role of mitochondria in the viral life cycle and disease progression of chronic hepatitis C, we studied morphological and functional mitochondrial alterations induced by HCV using productively infected hepatoma cells and patient livers. Methods: Biochemical and imaging assays were used to assess localization of cellular and viral proteins and mitochondrial functions in cell cultures and liver biopsies. Cyclophilin D (CypD) knockout was performed using CRISPR/Cas9 technology. Viral replication was quantified by quantitative reverse-transcription PCR and western blotting. Results: Several HCV proteins were found to associate with mitochondria-associated endoplasmic reticulum (ER) membranes (MAMs), the points of contact between the ER and mitochondria. Downregulation of CypD, which is known to disrupt MAM integrity, reduced viral replication, suggesting that MAMs play an important role in the viral life cycle. This process was rescued by ectopic CypD expression. Furthermore, HCV proteins were found to associate with voltage dependent anion channel 1 (VDAC1) at MAMs and to reduce VDAC1 protein levels at MAMs Conclusions: HCV proteins associate specifically with MAMs and MAMs play an important role in viral replication. The association between viral proteins and MAMs did not impact Ca Impact and implications: Hepatitis C virus infects the liver, where it causes inflammation, cell damage and increases the long-term risk of liver cancer. We show that several HCV proteins interact with mitochondria in liver cells and alter the composition of mitochondrial subdomains. Importantly, HCV requires the architecture of these mitochondrial subdomains to remain intact for efficient viral replication.
Language	English
Publishing date	2022-12-09
Publishing country	Netherlands
Document type	Journal Article
ISSN	2589-5559
ISSN (online)	2589-5559
DOI	10.1016/j.jhepr.2022.100647
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article: Naphthoquinones from

Ahmad, Fayyaz / Bibi, Shaheen / Kang, Mincheol / Anees, Mariam / Ansar, Muhammad / Alam, Muhammad Rizwan / Kim, Sun Yeou / Wahedi, Hussain Mustatab

Iranian journal of basic medical sciences

2020 Volume 23, Issue 9, Page(s) 1139–1145

Abstract: Objectives: Lapachone is a natural naphthoquinone-derived compound found in : Materials and methods: Expression of Sirt3, migration-related proteins (Rac1, Cdc42, α-Pak) and angiogenesis-related protein of vascular endothelial growth factor (VEGF) ... ...

Abstract	Objectives: Lapachone is a natural naphthoquinone-derived compound found in Materials and methods: Expression of Sirt3, migration-related proteins (Rac1, Cdc42, α-Pak) and angiogenesis-related protein of vascular endothelial growth factor (VEGF) was monitored using western blot analysis. Blood vessel formation and tissue development were monitored by angiogenesis assay and hematoxylin & eosin (H & E) staining, respectively on mouse skin tissue samples. Both α-lapachone and β-lapachone increased Sirt3 expression Results: Both the compounds accelerated wound healing in cultured skin cells as well as mouse skin; however, β-lapachone was more effective at lower concentrations. Both of the compounds increased the expression of migration-related proteins both Conclusion: These findings indicated that α-lapachone and β-lapachone are novel Sirt3 activators, and Sirt3 has a role in wound healing. Thus, Sirt3 and its regulators come out as a novel target and potential drug candidates, respectively in the important field of cutaneous wound healing.
Language	English
Publishing date	2020-05-01
Publishing country	Iran
Document type	Journal Article
ZDB-ID	2500485-2
ISSN	2008-3874 ; 2008-3866
ISSN (online)	2008-3874
ISSN	2008-3866
DOI	10.22038/ijbms.2020.43706.10275
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: Metabolism-secretion coupling and mitochondrial calcium activities in clonal pancreatic β-cells.

Groschner, Lukas N / Alam, Muhammad Rizwan / Graier, Wolfgang F

Vitamins and hormones

2014 Volume 95, Page(s) 63–86

Abstract: Pancreatic β-cells are the only cells capable of lowering blood glucose by secreting insulin. The β-cell continuously adjusts its secretory activity to substrate availability in order to keep blood glucose levels within the physiological range--a process ...

Abstract	Pancreatic β-cells are the only cells capable of lowering blood glucose by secreting insulin. The β-cell continuously adjusts its secretory activity to substrate availability in order to keep blood glucose levels within the physiological range--a process called metabolism-secretion coupling. Glucose is readily taken up by the β-cell and broken down into intermediates that fuel oxidative metabolism inside the mitochondria to generate ATP. The resulting increase in the ATP/ADP ratio causes closure of plasma membrane KATP channels, thereby depolarizing the cell and triggering the opening of voltage-gated Ca²⁺ channels. Consequential oscillations of cytosolic Ca²⁺ not only mediate the exocytosis of insulin granules but are also relayed to other subcellular compartments including the mitochondria, where Ca²⁺ is required to accelerate mitochondrial metabolism in response to nutrient stimulation. The mitochondrial Ca²⁺ uptake machinery plays a fundamental role in this feed-forward mechanism that guarantees sustained insulin secretion and, thus, represents a promising therapeutic target for type 2 diabetes.
MeSH term(s)	Animals ; Calcium Signaling ; Clone Cells ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/pathology ; Diabetes Mellitus, Type 2/physiopathology ; Energy Metabolism ; Humans ; Insulin/metabolism ; Insulin Secretion ; Insulin-Secreting Cells/cytology ; Insulin-Secreting Cells/metabolism ; Insulin-Secreting Cells/pathology ; Mitochondria/metabolism ; Models, Biological ; Pancreas/cytology ; Pancreas/pathology ; Pancreas/physiology ; Pancreas/physiopathology ; Up-Regulation
Chemical Substances	Insulin
Language	English
Publishing date	2014-02-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	201161-x
ISSN	2162-2620 ; 0083-6729
ISSN (online)	2162-2620
ISSN	0083-6729
DOI	10.1016/B978-0-12-800174-5.00003-X
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.238: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Cyclophilin D and myocardial ischemia-reperfusion injury: a fresh perspective.

Alam, Muhammad Rizwan / Baetz, Delphine / Ovize, Michel

Journal of molecular and cellular cardiology

2014 Volume 78, Page(s) 80–89

Abstract: Reperfusion is characterized by a deregulation of ion homeostasis and generation of reactive oxygen species that enhance the ischemia-related tissue damage culminating in cell death. The mitochondrial permeability transition pore (mPTP) has been ... ...

Abstract	Reperfusion is characterized by a deregulation of ion homeostasis and generation of reactive oxygen species that enhance the ischemia-related tissue damage culminating in cell death. The mitochondrial permeability transition pore (mPTP) has been established as an important mediator of ischemia-reperfusion (IR)-induced necrotic cell death. Although a handful of proteins have been proposed to contribute in mPTP induction, cyclophilin D (CypD) remains its only bona fide regulatory component. In this review we summarize existing knowledge on the involvement of CypD in mPTP formation in general and its relevance to cardiac IR injury in specific. Moreover, we provide insights of recent advancements on additional functions of CypD depending on its interaction partners and post-translational modifications. Finally we emphasize the therapeutic strategies targeting CypD in myocardial IR injury. This article is part of a Special Issue entitled "Mitochondria: From Basic Mitochondrial Biology to Cardiovascular Disease".
MeSH term(s)	Animals ; Calcium/metabolism ; Carrier Proteins/metabolism ; Cell Death ; Peptidyl-Prolyl Isomerase F ; Cyclophilins/metabolism ; Humans ; Mitochondria, Heart/metabolism ; Mitochondrial Membrane Transport Proteins/metabolism ; Mitochondrial Permeability Transition Pore ; Myocardial Reperfusion Injury/metabolism ; Protein Binding ; Protein Processing, Post-Translational ; Signal Transduction
Chemical Substances	Carrier Proteins ; Peptidyl-Prolyl Isomerase F ; Mitochondrial Membrane Transport Proteins ; Mitochondrial Permeability Transition Pore ; Cyclophilins (EC 5.2.1.-) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2014-10-02
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	80157-4
ISSN	1095-8584 ; 0022-2828
ISSN (online)	1095-8584
ISSN	0022-2828
DOI	10.1016/j.yjmcc.2014.09.026
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 426: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: ANT2-Mediated ATP Import into Mitochondria Protects against Hypoxia Lethal Injury.

Gouriou, Yves / Alam, Muhammad Rizwan / Harhous, Zeina / Crola Da Silva, Claire / Baetz, Delphine Baetz / Badawi, Sally / Lefai, Etienne / Rieusset, Jennifer / Durand, Annie / Harisseh, Rania / Gharib, Abdallah / Ovize, Michel / Bidaux, Gabriel

Cells

2020 Volume 9, Issue 12

Abstract: Following a prolonged exposure to hypoxia-reoxygenation, a partial disruption of the ER-mitochondria tethering by mitofusin 2 (MFN2) knock-down decreases the ... ...

Abstract	Following a prolonged exposure to hypoxia-reoxygenation, a partial disruption of the ER-mitochondria tethering by mitofusin 2 (MFN2) knock-down decreases the Ca
MeSH term(s)	Adenine Nucleotide Translocator 2/metabolism ; Adenosine Triphosphate/metabolism ; Animals ; Calcium/metabolism ; Cell Death/physiology ; Cell Line ; Hypoxia/metabolism ; Membrane Potential, Mitochondrial/physiology ; Mitochondria/metabolism ; Mitochondrial Membrane Transport Proteins/metabolism ; Mitochondrial Membranes/metabolism ; Myocytes, Cardiac/metabolism ; Rats
Chemical Substances	Adenine Nucleotide Translocator 2 ; Mitochondrial Membrane Transport Proteins ; Adenosine Triphosphate (8L70Q75FXE) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2020-11-25
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells9122542
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Delayed low pressure at reperfusion: A new approach for cardioprotection.

Ferrera, René / Benhabbouche, Souhila / Da Silva, Claire Crola / Alam, Muhammad Rizwan / Ovize, Michel

The Journal of thoracic and cardiovascular surgery

2015 Volume 150, Issue 6, Page(s) 1641–8.e2

Abstract: Objectives: The aims of this study were to evaluate whether the delayed application of low-pressure reperfusion could reduce lethal reperfusion injury and whether the inhibition of the opening of the mitochondrial permeability transition pore is ... ...

Abstract	Objectives: The aims of this study were to evaluate whether the delayed application of low-pressure reperfusion could reduce lethal reperfusion injury and whether the inhibition of the opening of the mitochondrial permeability transition pore is involved in this protection. Methods: Isolated rat hearts (n = 120) underwent 40 minutes of global ischemia followed by 60 minutes of reperfusion. Hearts were randomly assigned to the following groups: control, postconditioning (comprising 2 episodes of 30 seconds of ischemia and 30 seconds of reperfusion), and low-pressure reperfusion (using a reduction of perfusion pressure at 70 cm H2O for 10 minutes). In additional groups, postconditioning and low-pressure reperfusion were applied after a delay of 3, 10, and 20 minutes after the initial 40-minute ischemic insult. Results: As expected, infarct size (triphenyltetrazolium chloride staining) and lactate dehydrogenase release were significantly reduced in low-pressure reperfusion and postconditioning versus controls (P < .01), whereas functional parameters (coronary flow, rate pressure product) were improved (P < .01). Although delaying postconditioning by more than 3 minutes resulted in a loss of protection, low-pressure reperfusion still significantly reduced infarct size when applied as late as 20 minutes after reperfusion. This delayed low-pressure reperfusion protection was associated with an improved mitochondrial respiration, lower reactive oxygen species production, and enhanced calcium retention capacity, related to inhibition of permeability transition pore opening. Conclusions: We demonstrated for the first time that low-pressure reperfusion can reduce lethal myocardial reperfusion injury even when performed 10 to 20 minutes after the initiation of reperfusion.
MeSH term(s)	Animals ; Blood Pressure/physiology ; Disease Models, Animal ; Ischemic Preconditioning, Myocardial ; Male ; Mitochondrial Membrane Transport Proteins ; Myocardial Reperfusion Injury/prevention & control ; Random Allocation ; Rats ; Rats, Wistar
Chemical Substances	Mitochondrial Membrane Transport Proteins ; mitochondrial permeability transition pore
Language	English
Publishing date	2015-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3104-5
ISSN	1097-685X ; 0022-5223
ISSN (online)	1097-685X
ISSN	0022-5223
DOI	10.1016/j.jtcvs.2015.08.053
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uk I Zs.104: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito