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Article ; Online: Isolation and Characterization of Cardiac Progenitor Cells.

Dixit, Parul / Katare, Rajesh G

Methods in molecular biology (Clifton, N.J.)

2019 Volume 2029, Page(s) 161–173

Abstract: Cardiac progenitor cells (CPCs) are gaining interest as a therapeutic option for the treatment of the heart. Due to the limited pool of CPCs residing in the heart, it is essential to isolate and expand the CPCs in vitro. Here we describe the protocol for ...

Abstract	Cardiac progenitor cells (CPCs) are gaining interest as a therapeutic option for the treatment of the heart. Due to the limited pool of CPCs residing in the heart, it is essential to isolate and expand the CPCs in vitro. Here we describe the protocol for isolation and culture of the heterogeneous population of CPCs from right atrial appendage and left ventricular tissue collected from patients undergoing on-pump coronary artery bypass graft surgery for the treatment of ischemic heart disease. Our protocol is developed to simultaneously isolate, culture, and characterize the CPCs from both atrial and ventricular tissues. We also describe the protocol for flow cytometry and immunohistochemical characterization of the isolated CPCs.
MeSH term(s)	Cells, Cultured ; Coronary Artery Bypass/methods ; Coronary Vessels/cytology ; Flow Cytometry/methods ; Heart Ventricles/cytology ; Humans ; Myocardium/cytology ; Myocytes, Cardiac/cytology
Language	English
Publishing date	2019-07-04
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-9631-5_13
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Article ; Online: Concise Review: Challenges in Regenerating the Diabetic Heart: A Comprehensive Review.

Satthenapalli, Venkata R / Lamberts, Regis R / Katare, Rajesh G

Stem cells (Dayton, Ohio)

2017 Volume 35, Issue 9, Page(s) 2009–2026

Abstract: Stem cell therapy is one of the promising regenerative strategies developed to improve cardiac function in patients with ischemic heart diseases (IHD). However, this approach is limited in IHD patients with diabetes due to a progressive decline in the ... ...

Abstract	Stem cell therapy is one of the promising regenerative strategies developed to improve cardiac function in patients with ischemic heart diseases (IHD). However, this approach is limited in IHD patients with diabetes due to a progressive decline in the regenerative capacity of stem cells. This decline is mainly attributed to the metabolic memory incurred by diabetes on stem cell niche and their systemic cues. Understanding the molecular pathways involved in the diabetes-induced deterioration of stem cell function will be critical for developing new cardiac regeneration therapies. In this review, we first discuss the most common molecular alterations occurring in the diabetic stem cells/progenitor cells. Next, we highlight the key signaling pathways that can be dysregulated in a diabetic environment and impair the mobilization of stem/progenitor cells, which is essential for the transplanted/endogenous stem cells to reach the site of injury. We further discuss the possible methods of preconditioning the diabetic cardiac progenitor cell (CPC) with an aim to enrich the availability of efficient stem cells to regenerate the diseased diabetic heart. Finally, we propose new modalities for enriching the diabetic CPC through genetic or tissue engineering that would aid in developing autologous therapeutic strategies, improving the proliferative, angiogenic, and cardiogenic properties of diabetic stem/progenitor cells. Stem Cells 2017;35:2009-2026.
MeSH term(s)	Animals ; Diabetes Mellitus/pathology ; Diabetes Mellitus/physiopathology ; Epigenesis, Genetic ; Exosomes/metabolism ; Heart/physiopathology ; Humans ; Regeneration ; Stem Cells/metabolism
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1143556-2
ISSN	1549-4918 ; 1066-5099
ISSN (online)	1549-4918
ISSN	1066-5099
DOI	10.1002/stem.2661
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Zs.A 1894: Show issues

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Article ; Online: Pericytes from human veins for treatment of myocardial ischemia.

Katare, Rajesh G / Madeddu, Paolo

Trends in cardiovascular medicine

2013 Volume 23, Issue 3, Page(s) 66–70

Abstract: Stem cell therapies promise to regenerate the infarcted heart through the replacement of dead cardiac cells and stimulation of neovascularization. New research from our laboratory shows the transplantation of stem cells from human veins helps heart ... ...

Abstract	Stem cell therapies promise to regenerate the infarcted heart through the replacement of dead cardiac cells and stimulation of neovascularization. New research from our laboratory shows the transplantation of stem cells from human veins helps heart healing after an acute ischemic insult. Using a mouse model, we demonstrated that pericytes expanded from redundant human leg veins relocate around the vessels of the peri-infarct zone and release factors that promote reparative angiogenesis and cardiomyocyte survival and inhibit interstitial fibrosis. We plan to perform a first-in-man clinical trial with human pericytes in patients with refractory myocardial ischemia in the next 5 years.
MeSH term(s)	Animals ; Cell Survival ; Disease Models, Animal ; Fibrosis ; Humans ; Lower Extremity/blood supply ; Mice ; Myocardial Ischemia/pathology ; Myocardial Ischemia/physiopathology ; Myocardial Ischemia/therapy ; Myocardium/pathology ; Neovascularization, Physiologic ; Pericytes/transplantation ; Regeneration ; Veins/cytology
Language	English
Publishing date	2013-01-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1097434-9
ISSN	1873-2615 ; 1050-1738
ISSN (online)	1873-2615
ISSN	1050-1738
DOI	10.1016/j.tcm.2012.09.002
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Zs.A 3419: Show issues

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Article ; Online: Engineered heart tissue: a novel tool to study the ischemic changes of the heart in vitro.

Katare, Rajesh G / Ando, Motonori / Kakinuma, Yoshihiko / Sato, Takayuki

PloS one

2010 Volume 5, Issue 2, Page(s) e9275

Abstract: Background: Understanding the basic mechanisms and prevention of any disease pattern lies mainly on development of a successful experimental model. Recently, engineered heart tissue (EHT) has been demonstrated to be a useful tool in experimental ... ...

Abstract	Background: Understanding the basic mechanisms and prevention of any disease pattern lies mainly on development of a successful experimental model. Recently, engineered heart tissue (EHT) has been demonstrated to be a useful tool in experimental transplantation. Here, we demonstrate a novel function for the spontaneously contracting EHT as an experimental model in studying the acute ischemia-induced changes in vitro. Methodology/principal findings: EHT was constructed by mixing cardiomyocytes isolated from the neonatal rats and cultured in a ring-shaped scaffold for five days. This was followed by mechanical stretching of the EHT for another one week under incubation. Fully developed EHT was subjected to hypoxia with 1% O(2) for 6 hours after treating them with cell protective agents such as cyclosporine A (CsA) and acetylcholine (ACh). During culture, EHT started to show spontaneous contractions that became more synchronous following mechanical stretching. This was confirmed by the increased expression of gap junctional protein connexin 43 and improved action potential recordings using an optical mapping system after mechanical stretching. When subjected to hypoxia, EHT demonstrated conduction defects, dephosphorylation of connexin-43, and down-regulation of cell survival proteins identical to the adult heart. These effects were inhibited by treating the EHT with cell protective agents. Conclusions/significance: Under hypoxic conditions, the EHT responds similarly to the adult myocardium, thus making EHT a promising material for the study of cardiac functions in vitro.
MeSH term(s)	Animals ; Animals, Newborn ; Cell Culture Techniques ; Cell Hypoxia ; Cell Survival ; Cells, Cultured ; Connexin 43/metabolism ; Female ; Heart/physiology ; Heart/physiopathology ; Humans ; Immunoblotting ; Microscopy, Electron ; Myocardial Contraction ; Myocardial Ischemia/metabolism ; Myocardial Ischemia/pathology ; Myocardial Ischemia/physiopathology ; Myocardium/cytology ; Myocardium/metabolism ; Myocardium/ultrastructure ; Myocytes, Cardiac/cytology ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/ultrastructure ; Proto-Oncogene Proteins c-akt/metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Rats ; Rats, Wistar ; Tissue Engineering/methods
Chemical Substances	Connexin 43 ; Proto-Oncogene Proteins c-bcl-2 ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2010-02-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0009275
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Article ; Online: Acetylcholine Suppresses Ventricular Arrhythmias and Improves Conduction and Connexin-43 Properties During Myocardial Ischemia in Isolated Rabbit Hearts.

Aiba, Takeshi / Noda, Takashi / Hidaka, Ichiro / Inagaki, Masashi / Katare, Rajesh G / Ando, Motonori / Sunagawa, Kenji / Sato, Takayuki / Sugimachi, Masaru

Journal of cardiovascular electrophysiology

2015 Volume 26, Issue 6, Page(s) 678–685

Abstract: Introduction: Acetylcholine (ACh), a vagal efferent neurotransmitter, markedly improves survival in rats with myocardial ischemia (MI) by preventing ischemic loss of gap junction (Gj) and by inducing anti-apoptotic cascades. However, ... ...

Abstract	Introduction: Acetylcholine (ACh), a vagal efferent neurotransmitter, markedly improves survival in rats with myocardial ischemia (MI) by preventing ischemic loss of gap junction (Gj) and by inducing anti-apoptotic cascades. However, electrophysiological mechanisms of the antiarrhythmic effect of ACh after acute MI are still unclear. Methods: Acute MI was induced by ligation of the left anterior descending (LAD) coronary artery in Langendorff-perfused rabbit hearts with (ACh(+):n = 11) or without (ACh(-):n = 12) 10 μmol/L ACh delivered continuously starting at 5 minutes before LAD ligation. Action potentials on the left ventricular (LV) anterior surface (≈2×2 cm) were recorded by optical mapping during pacing from the LV epicardium (BCL = 500 milliseconds). Conduction velocities (CVs) at 256 sites were calculated and the ventricular tachycardia/ventricular fibrillation (VT/VF) susceptibility was also assessed by programmed electrical stimulation before and 30 minutes after MI. The amount and distribution of Gj protein connexin-43 was analyzed by immunoblotting and immunohistochemistry. Results: Averaged CV in the ischemic border zone (IBZ) was significantly slower in ACh(-) than in ACh(+) (21 ± 7 vs. 34 ± 6 cm/s; P < 0.01). Short-coupled extra stimulus further decreased CV of IBZ in ACh(-) (13 ± 4 cm/s) but did not change that in ACh(+) (34 ± 5 cm/s), leading to a high incidence of conduction block in IBZ in ACh(-) but not in ACh(+) (83% vs. 0%). VT/VF after MI were induced in ACh(-) but suppressed in ACh(+) (10/12 vs. 3/11; P < 0.01). Connexin-43 in the LV anterior wall was significantly reduced after MI in ACh(-) but not in ACh(+). Conclusion: ACh may suppress VT/VF by preventing loss of Gj and improving CV in IBZ during acute MI.
MeSH term(s)	Acetylcholine/pharmacology ; Action Potentials ; Animals ; Cholinergic Agonists/pharmacology ; Connexin 43/metabolism ; Heart Conduction System/drug effects ; Immunoblotting ; Male ; Myocardial Ischemia/drug therapy ; Myocardial Ischemia/metabolism ; Perfusion/methods ; Rabbits ; Tachycardia, Ventricular/metabolism ; Tachycardia, Ventricular/prevention & control ; Ventricular Fibrillation/metabolism ; Ventricular Fibrillation/prevention & control ; Voltage-Sensitive Dye Imaging
Chemical Substances	Cholinergic Agonists ; Connexin 43 ; Acetylcholine (N9YNS0M02X)
Language	English
Publishing date	2015-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1025989-2
ISSN	1540-8167 ; 1045-3873
ISSN (online)	1540-8167
ISSN	1045-3873
DOI	10.1111/jce.12663
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Zs.A 2863: Show issues

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Article ; Online: Preliminary experience for the evaluation of the intraoperative graft patency with real color charge-coupled device camera system: an advanced device for simultaneous capturing of color and near-infrared images during coronary artery bypass graft.

Handa, Takemi / Katare, Rajesh G / Sasaguri, Shiro / Sato, Takayuki

Interactive cardiovascular and thoracic surgery

2009 Volume 9, Issue 2, Page(s) 150–154

Abstract: We developed a new color charge-coupled device (CCD) camera for the intraoperative indocyanine green (ICG) angiography. This device consists of a combination of custom-made optical filters and an ultra-high sensitive CCD image sensor, which can detect ... ...

Abstract	We developed a new color charge-coupled device (CCD) camera for the intraoperative indocyanine green (ICG) angiography. This device consists of a combination of custom-made optical filters and an ultra-high sensitive CCD image sensor, which can detect simultaneously color and near-infrared (NIR) rays from 380 to 1200 nm. We showed a comparison between our system and other devices for the preliminary experience. We routinely performed both transit-time flowmetry (TFM) and color images for intraoperative assessment, thallium-scintigraphy for the early postoperative assessment, and then angiography after 1-year surgery. We also obtained intraoperative graft flows and images in 116 grafts. Although TFM indicated a graft patency, the CCD camera suspected perfusion failures in four grafts. Also the analysis of the ICG fluorescence intensity showed the significant hypoperfusion at the perfusion territory distal to the anastomosis (graft vs. perfusion territory; 230+/-26 vs. 156+/-13 a.u, P=0.02). When the CCD camera suspected a graft failure, CCD camera and angiography showed a comparable graft failure. The unique device that visualized ICG-enhanced structures against a background of natural myocardial color improved the visibility of abnormality in flow and perfusion. Our findings show that this device may become a standard intraoperative graft and perfusion assessment tool in coronary artery bypass graft (CABG).
MeSH term(s)	Aged ; Blood Flow Velocity ; Coronary Angiography ; Coronary Artery Bypass, Off-Pump ; Coronary Artery Disease/diagnosis ; Coronary Artery Disease/physiopathology ; Coronary Artery Disease/surgery ; Coronary Circulation ; Equipment Design ; Fluorescein Angiography/instrumentation ; Fluorescent Dyes ; Graft Occlusion, Vascular/diagnosis ; Graft Occlusion, Vascular/etiology ; Graft Occlusion, Vascular/physiopathology ; Humans ; Image Interpretation, Computer-Assisted ; Indocyanine Green ; Middle Aged ; Myocardial Perfusion Imaging ; Pilot Projects ; Predictive Value of Tests ; Spectroscopy, Near-Infrared/instrumentation ; Treatment Outcome ; Vascular Patency
Chemical Substances	Fluorescent Dyes ; Indocyanine Green (IX6J1063HV)
Language	English
Publishing date	2009-08
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2095298-3
ISSN	1569-9285 ; 1569-9293
ISSN (online)	1569-9285
ISSN	1569-9293
DOI	10.1510/icvts.2008.201418
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Zs.A 5730: Show issues

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Article ; Online: Vitamin B1 analog benfotiamine prevents diabetes-induced diastolic dysfunction and heart failure through Akt/Pim-1-mediated survival pathway.

Katare, Rajesh G / Caporali, Andrea / Oikawa, Atsuhiko / Meloni, Marco / Emanueli, Costanza / Madeddu, Paolo

Circulation. Heart failure

2010 Volume 3, Issue 2, Page(s) 294–305

Abstract: Background: The increasing incidence of diabetes mellitus will result in a new epidemic of heart failure unless novel treatments able to halt diabetic cardiomyopathy early in its course are introduced. This study aimed to determine whether the activity ... ...

Abstract	Background: The increasing incidence of diabetes mellitus will result in a new epidemic of heart failure unless novel treatments able to halt diabetic cardiomyopathy early in its course are introduced. This study aimed to determine whether the activity of the Akt/Pim-1 signaling pathway is altered at critical stages of diabetic cardiomyopathy and whether supplementation with vitamin B1 analog benfotiamine (BFT) helps to sustain the above prosurvival mechanism, thereby preserving cardiomyocyte viability and function. Methods and results: Untreated streptozotocin-induced type 1 or leptin-receptor mutant type 2 diabetic mice showed diastolic dysfunction evolving to contractile impairment and cardiac dilatation and failure. BFT (70 mg/kg(-1)/d(-1)) improved diastolic and systolic function and prevented left ventricular end-diastolic pressure increase and chamber dilatation in both diabetic models. Moreover, BFT improved cardiac perfusion and reduced cardiomyocyte apoptosis and interstitial fibrosis. In hearts of untreated diabetic mice, the expression and activity of Akt/Pim-1 signaling declined along with O-N-acetylglucosamine modification of Akt, inhibition of pentose phosphate pathway, activation of oxidative stress, and accumulation of glycation end products. Furthermore, diabetes reduced pSTAT3 independently of Akt. BFT inhibited these effects of diabetes mellitus, thereby conferring cardiomyocytes with improved resistance to high glucose-induced damage. The phosphoinositide-3-kinase inhibitor LY294002 and dominant-negative Akt inhibited antiapoptotic action of BFT-induced and Pim-1 upregulation in high glucose-challenged cardiomyocytes. Conclusions: These results show that BFT protects from diabetes mellitus-induced cardiac dysfunction through pleiotropic mechanisms, culminating in the activation of prosurvival signaling pathway. Thus, BFT merits attention for application in clinical practice.
MeSH term(s)	Analysis of Variance ; Animals ; Apoptosis/drug effects ; Blood Flow Velocity ; Blotting, Western ; Carrier Proteins/metabolism ; Cells, Cultured ; Chromones/pharmacology ; Diabetes Mellitus, Experimental/complications ; Diastole ; Disease Models, Animal ; Enzyme-Linked Immunosorbent Assay ; Fibrosis/prevention & control ; Heart Failure/etiology ; Heart Failure/metabolism ; Heart Failure/prevention & control ; Immunohistochemistry ; Mice ; Microfilament Proteins ; Morpholines/pharmacology ; Oxidative Stress ; Proto-Oncogene Proteins c-pim-1/metabolism ; Random Allocation ; Reverse Transcriptase Polymerase Chain Reaction ; STAT3 Transcription Factor/metabolism ; Signal Transduction ; Thiamine/analogs & derivatives ; Thiamine/pharmacology ; Up-Regulation
Chemical Substances	Carrier Proteins ; Ccdc88a protein, mouse ; Chromones ; Microfilament Proteins ; Morpholines ; STAT3 Transcription Factor ; 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (31M2U1DVID) ; Proto-Oncogene Proteins c-pim-1 (EC 2.7.11.1) ; Thiamine (X66NSO3N35) ; benphothiamine (Y92OUS2H9B)
Language	English
Publishing date	2010-01-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2429459-7
ISSN	1941-3297 ; 1941-3289
ISSN (online)	1941-3297
ISSN	1941-3289
DOI	10.1161/CIRCHEARTFAILURE.109.903450
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Zs.A 6745: Show issues

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Article ; Online: Differential regulation of TNF receptors by vagal nerve stimulation protects heart against acute ischemic injury.

Katare, Rajesh G / Ando, Motonori / Kakinuma, Yoshihiko / Arikawa, Mikihiko / Yamasaki, Fumiyasu / Sato, Takayuki

Journal of molecular and cellular cardiology

2010 Volume 49, Issue 2, Page(s) 234–244

Abstract: Vagal nerve stimulation (VS) has been reported to improve the survival after both acute and chronic myocardial infarction through the release of neurotransmitter ACh. However, the precise mechanism behind its beneficial effect is still unknown. In this ... ...

Abstract	Vagal nerve stimulation (VS) has been reported to improve the survival after both acute and chronic myocardial infarction through the release of neurotransmitter ACh. However, the precise mechanism behind its beneficial effect is still unknown. In this study, we demonstrate the upregulation of tumor necrosis factor-alpha (TNF-alpha) and its cell survival TNF receptor-2 (TNFR2) as the mechanism behind VS induced myocardial protection. We investigated the effects of efferent VS on myocardial ischemic injury with in vivo and in vitro mouse models. In in vivo hearts VS significantly increased the expression of TNF-alpha both at the messenger and protein level after 3-hours of myocardial ischemia. In the in vitro studies ACh treatment before hypoxia, induced a significant upregulation of TNF-alpha compared to the untreated cardiomyocytes. Immunofluorescence analysis confirmed the synthesis of TNF-alpha by cardiomyocytes both in vivo and in vitro. VS also significantly reduced the myocardial infarct size (23.9+/-5.7% vs. 56+/-1.9%) and activated the cell survival Akt cascade system. Further, ACh upregulated the cell survival TNFR2 expression, while downregulating the cell destructive TNF receptor 1 (TNFR1) expression. These results were confirmed using the TNF receptors deficient mice, where the VS mediated protection was lost both in vivo and in vitro in TNFR2 (TNFR2(-/-)) and TNF receptors double knock out (TNFR1(-/-)2(-/-)) mice. VS and ACh protects the heart against acute ischemia or hypoxic injury by differentially regulating the TNF receptor subtypes.
MeSH term(s)	Acetylcholine/pharmacology ; Animals ; Apoptosis/drug effects ; Cell Survival/drug effects ; Gene Expression Regulation/drug effects ; Hypoxia/complications ; Hypoxia/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Myocardial Infarction/complications ; Myocardial Infarction/pathology ; Myocardial Ischemia/complications ; Myocardial Ischemia/genetics ; Myocardial Ischemia/pathology ; Myocardial Ischemia/prevention & control ; Myocardium/metabolism ; Myocardium/pathology ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; NF-kappa B/metabolism ; Receptors, Tumor Necrosis Factor, Type I/deficiency ; Receptors, Tumor Necrosis Factor, Type I/genetics ; Receptors, Tumor Necrosis Factor, Type I/metabolism ; Receptors, Tumor Necrosis Factor, Type II/deficiency ; Receptors, Tumor Necrosis Factor, Type II/genetics ; Receptors, Tumor Necrosis Factor, Type II/metabolism ; Signal Transduction/drug effects ; Tumor Necrosis Factor-alpha/genetics ; Tumor Necrosis Factor-alpha/metabolism ; Vagus Nerve Stimulation
Chemical Substances	NF-kappa B ; Receptors, Tumor Necrosis Factor, Type I ; Receptors, Tumor Necrosis Factor, Type II ; Tnfrsf1a protein, mouse ; Tumor Necrosis Factor-alpha ; Acetylcholine (N9YNS0M02X)
Language	English
Publishing date	2010-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80157-4
ISSN	1095-8584 ; 0022-2828
ISSN (online)	1095-8584
ISSN	0022-2828
DOI	10.1016/j.yjmcc.2010.03.007
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Zs.A 426: Show issues

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Article ; Online: Chronic intermittent fasting improves the survival following large myocardial ischemia by activation of BDNF/VEGF/PI3K signaling pathway.

Katare, Rajesh G / Kakinuma, Yoshihiko / Arikawa, Mikihiko / Yamasaki, Fumiyasu / Sato, Takayuki

Journal of molecular and cellular cardiology

2009 Volume 46, Issue 3, Page(s) 405–412

Abstract: Chronic heart failure (CHF) is the major cause of death in the developed countries. Calorie restriction is known to improve the recovery in these patients; however, the exact mechanism behind this protective effect is unknown. Here we demonstrate the ... ...

Abstract	Chronic heart failure (CHF) is the major cause of death in the developed countries. Calorie restriction is known to improve the recovery in these patients; however, the exact mechanism behind this protective effect is unknown. Here we demonstrate the activation of cell survival PI3kinase/Akt and VEGF pathway as the mechanism behind the protection induced by intermittent fasting in a rat model of established chronic myocardial ischemia (MI). Chronic MI was induced in rats by occlusion of the left coronary artery. Two weeks later, the rats were randomly assigned to a normal feeding group (MI-NF) and an alternate-day feeding group (MI-IF). After 6 weeks of observation, we evaluated the effect of intermittent fasting on cellular and ventricular remodeling and long-term survival after CHF. Compared with the normally fed group, intermittent fasting markedly improved the survival of rats with CHF (88.5% versus 23% survival, P<0.05). The heart weight body weight ratio was significantly less in the MI-IF group compared to the MI-NF group (3.4+/-0.17 versus 3.9+/-0.18, P<0.05). Isolated heart perfusion studies exhibited well preserved cardiac functions in the MI-IF group compared to the MI-NF group (P<0.05). Molecular studies revealed the upregulation of angiogenic factors such asHIF-1-alpha (3010+/-350% versus 650+/-151%), BDNF (523+/-32% versus 110+/-12%), and VEGF (450+/-21% versus 170+/-30%) in the fasted hearts. Immunohistochemical studies confirmed increased capillary density (P<0.001) in the border area of the ischemic myocardium and synthesis VEGF by cardiomyocytes. Moreover fasting also upregulated the expression of other anti-apoptotic factors such as Akt and Bcl-2 and reduced the TUNEL positive apoptotic nuclei in the border zone. Chronic intermittent fasting markedly improves the long-term survival after CHF by activation through its pro-angiogenic, anti-apoptotic and anti-remodeling effects.
MeSH term(s)	Animals ; Brain-Derived Neurotrophic Factor/biosynthesis ; Caloric Restriction ; Chronic Disease ; Enzyme Activation ; Fasting/metabolism ; Heart Failure/metabolism ; Heart Failure/mortality ; Humans ; Male ; Muscle Proteins/metabolism ; Myocardial Ischemia/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/biosynthesis ; Proto-Oncogene Proteins c-bcl-2/biosynthesis ; Rats ; Rats, Wistar ; Signal Transduction ; Up-Regulation ; Vascular Endothelial Growth Factor A/biosynthesis
Chemical Substances	Brain-Derived Neurotrophic Factor ; Muscle Proteins ; Proto-Oncogene Proteins c-bcl-2 ; Vascular Endothelial Growth Factor A ; vascular endothelial growth factor A, rat ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2009-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80157-4
ISSN	1095-8584 ; 0022-2828
ISSN (online)	1095-8584
ISSN	0022-2828
DOI	10.1016/j.yjmcc.2008.10.027
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Zs.A 426: Show issues

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Article: A HIF-1alpha-related gene involved in cell protection from hypoxia by suppression of mitochondrial function.

Kakinuma, Yoshihiko / Katare, Rajesh G / Arikawa, Mikihiko / Muramoto, Kazuyo / Yamasaki, Fumiyasu / Sato, Takayuki

FEBS letters

2008 Volume 582, Issue 2, Page(s) 332–340

Abstract: Recently, we reported that acetylcholine-induced hypoxia-inducible factor-1alpha protects cardiomyocytes from hypoxia; however, the downstream factors reducing hypoxic stress are unknown. We identified apoptosis inhibitor (AI) gene as being ... ...

Abstract	Recently, we reported that acetylcholine-induced hypoxia-inducible factor-1alpha protects cardiomyocytes from hypoxia; however, the downstream factors reducing hypoxic stress are unknown. We identified apoptosis inhibitor (AI) gene as being differentially expressed between von Hippel Lindau (VHL) protein-positive cells with high levels of GRP78 expression and VHL-negative cells with lower GRP levels, using cDNA subtraction. AI decreased GRP78 level, suppressed mitochondrial function, reduced oxygen consumption and, ultimately, suppressed hypoxia-induced apoptosis. By contrast, knockdown of the AI gene increased mitochondrial function. Hypoxic cardiomyocytes and ischemic myocardium showed increased AI mRNA expression. These findings suggest that AI is involved in suppressing mitochondrial function, thereby leading to cellular stress eradication and consequently to protection during hypoxia.
MeSH term(s)	Animals ; Base Sequence ; Cell Hypoxia/genetics ; Cell Line ; DNA Primers ; DNA, Complementary ; Heat-Shock Proteins/genetics ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Inhibitor of Apoptosis Proteins/genetics ; Mitochondria/physiology ; Molecular Chaperones/genetics ; RNA, Messenger/genetics ; Rats ; Von Hippel-Lindau Tumor Suppressor Protein/genetics
Chemical Substances	DNA Primers ; DNA, Complementary ; HIF1A protein, human ; Heat-Shock Proteins ; Hif1a protein, rat ; Hypoxia-Inducible Factor 1, alpha Subunit ; Inhibitor of Apoptosis Proteins ; Molecular Chaperones ; RNA, Messenger ; molecular chaperone GRP78 ; Von Hippel-Lindau Tumor Suppressor Protein (EC 2.3.2.27) ; VHL protein, human (EC 6.3.2.-)
Language	English
Publishing date	2008-01-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1016/j.febslet.2007.12.026
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