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40
6
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Text
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URL Address
<a href="http://doi.org/" target="_blank" rel="noreferrer noopener">http://doi.org/</a>
Pages
E274-E275
Issue
12
Volume
127
ISSN
0009-7330
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January 2021 List
NEOMED College
NEOMED College of Medicine
NEOMED College of Graduate Studies
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Department of Integrative Medical Sciences
NEOMED Student Publications
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Title
A name given to the resource
Endothelial Trpv4 contributes to pressure overload-induced pathological hypertrophy via modulation of coronary angiogenesis
Publisher
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Circulation Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-12-04
Subject
The topic of the resource
Angiogenesis; Fibrosis; Ion channels; Cardiac hypertrophy;
Creator
An entity primarily responsible for making the resource
Adapala RK; Kanugula AK; Ohanyan VA; Paruchuri SM; Chilian WM; Thodeti CK
Identifier
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<a href="http://doi.org/" target="_blank" rel="noreferrer noopener"></a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
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journalArticle
2020
Adapala RK
angiogenesis
Cardiac hypertrophy
Chilian WM
Circulation research
Department of Integrative Medical Sciences
Fibrosis
Ion Channels
January 2021 List
journalArticle
Kanugula AK
NEOMED College of Graduate Studies
NEOMED College of Medicine
NEOMED Student Publications
Ohanyan VA
Paruchuri SM
Thodeti CK
-
Text
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URL Address
<a href="http://doi.org/10.1016/j.yjmcc.2021.07.008" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.yjmcc.2021.07.008</a>
ISSN
1095-8584
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<a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1016/j.yjmcc.2021.07.008" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1016/j.yjmcc.2021.07.008</a>
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August 2021 List
NEOMED College
NEOMED College of Medicine
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Department of Integrative Medical Sciences
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Title
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Reperfusion mediates heme impairment with increased protein cysteine sulfonation of mitochondrial complex III in the post-ischemic heart.
Publisher
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Journal of Molecular and Cellular Cardiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2021
2021-07-28
Subject
The topic of the resource
Complex III; Cysteine sulfonation; Heme damage; Myocardial ischemia and reperfusion; Oxidative stress; Protein structure
Creator
An entity primarily responsible for making the resource
Chen C; Kang PT; Zhang L; Xiao K; Zweier JL; Chilian WM; Chen Y-R
Description
An account of the resource
A serious consequence of myocardial ischemia-reperfusion injury (I/R) is oxidative damage, which causes mitochondrial dysfunction. The cascading ROS can propagate and potentially induce heme bleaching and protein cysteine sulfonation (PrSO 3 H) of the mitochondrial electron transport chain. Herein we studied the mechanism of I/R-mediated irreversible oxidative injury of complex III in mitochondria from rat hearts subjected to 30-min of ischemia and 24-h of reperfusion in vivo. In the I/R region, the catalytic activity of complex III was significantly impaired. Spectroscopic analysis indicated that I/R mediated the destruction of hemes b and c + c 1 in the mitochondria, supporting I/R-mediated complex III impairment. However, no significant impairment of complex III activity and heme damage were observed in mitochondria from the risk region of rat hearts subjected only to 30-min ischemia, despite a decreased state 3 respiration. In the I/R mitochondria, carbamidomethylated C 122 /C 125 of cytochrome c 1 via alkylating complex III with a down regulation of HCCS was exclusively detected, supporting I/R-mediated thioether defect of heme c 1 . LC-MS/MS analysis showed that I/R mitochondria had intensely increased complex III PrSO 3 H levels at the C 236 ligand of the [2Fe2S] cluster of the Rieske iron‑sulfur protein (uqcrfs1), thus impairing the electron transport activity. MS analysis also indicated increased PrSO 3 H of the hinge protein at C 65 and of cytochrome c 1 at C 140 and C 220 , which are confined in the intermembrane space. MS analysis also showed that I/R extensively enhanced the PrSO 3 H of the core 1 (uqcrc1) and core 2 (uqcrc2) subunits in the matrix compartment, thus supporting the conclusion that complex III releases ROS to both sides of the inner membrane during reperfusion. Analysis of ischemic mitochondria indicated a modest reduction from the basal level of complex III PrSO 3 H detected in the mitochondria of sham control hearts, suggesting that the physiologic hyperoxygenation and ROS overproduction during reperfusion mediated the enhancement of complex III PrSO 3 H. In conclusion, reperfusion-mediated heme damage with increased PrSO 3 H controls oxidative injury to complex III and aggravates mitochondrial dysfunction in the post-ischemic heart. (Copyright © 2018. Published by Elsevier Ltd.)
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<a href="http://doi.org/10.1016/j.yjmcc.2021.07.008" target="_blank" rel="noreferrer noopener">10.1016/j.yjmcc.2021.07.008</a>
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journalArticle
2021
August 2021 List
Chen C
Chen Y-R
Chilian WM
Complex III
Cysteine sulfonation
Department of Integrative Medical Sciences
Heme damage
Journal of molecular and cellular cardiology
journalArticle
Kang PT
Myocardial ischemia and reperfusion
NEOMED College of Medicine
Oxidative Stress
Protein Structure
Xiao K
Zhang L
Zweier JL
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1139/cjpp-2020-0581" target="_blank" rel="noreferrer noopener">http://doi.org/10.1139/cjpp-2020-0581</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
ISSN
1205-7541 0008-4212
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February 2021 List
NEOMED College
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Department of Integrative Medical Sciences
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Title
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Micro-RNA Regulation of Vascular Smooth Muscle Cells and Its Significance in Cardiovascular Diseases.
Date
A point or period of time associated with an event in the lifecycle of the resource
2021
2021-02-02
Subject
The topic of the resource
Cardiovascular Diseases; vascular; micro-RNA
Creator
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Nguyen DND;Chilian WM;Zain SM;Daud MF;Pung YF
Description
An account of the resource
Cardiovascular disease (CVD) is among the leading causes of death worldwide. Micro-RNAs (miRNAs), regulatory molecules that repress protein expression, have attracted considerable attention in CVD research. The vasculature plays a big role in CVD development and progression and dysregulation of vascular cells underlies the root of many vascular diseases. This review provides a brief introduction of the biogenesis of miRNAs and exosomes, followed by overview of the regulatory mechanisms of miRNAs in vascular smooth muscle cells (VSMCs) intracellular signaling during phenotypic switching, senescence, calcification and neointimal hyperplasia. Evidence of extracellular signaling of VSMCs and other cells via exosomal and circulating miRNAs was also presented. Lastly, current drawbacks and limitations of miRNA studies in CVD research and potential ways to overcome these disadvantages were discussed in detail. In-depth understanding of VSMC regulation via miRNAs will add substantial knowledge and advance research in diagnosis, disease progression and/or miRNA-derived therapeutic approaches in CVD research.
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<a href="http://doi.org/10.1139/cjpp-2020-0581" target="_blank" rel="noreferrer noopener">10.1139/cjpp-2020-0581</a>
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journalArticle
Publisher
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Canadian Journal Of Physiology And Pharmacology
2021
Canadian journal of physiology and pharmacology
CARDIOVASCULAR diseases
Chilian WM
Daud MF
Department of Integrative Medical Sciences
February 2021 List
journalArticle
micro-RNA
NEOMED College of Medicine
Nguyen DND
Pung YF
Vascular
Zain SM
-
Text
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<a href="http://doi.org/10.1161/CIRCRESAHA.120.317715" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/CIRCRESAHA.120.317715</a>
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ISSN
1524-4571 0009-7330
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February 2021 List
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Department of Integrative Medical Sciences
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Title
A name given to the resource
Myocardial Blood Flow Control by Oxygen Sensing Vascular Kvβ Proteins.
Date
A point or period of time associated with an event in the lifecycle of the resource
2021
2021-01-27
Subject
The topic of the resource
coronary arteris; microcirculation; myogenic tone; nicotinamide adenine dinucleotide; voltage-gated potassium channels
Creator
An entity primarily responsible for making the resource
Ohanyan V;Raph SM;Dwenger MM;Hu X;Pucci T;Mack GD;Moore IJB;Chilian WM;Bhatnagar A;Nystoriak MA
Description
An account of the resource
Rationale: Voltage-gated potassium (Kv) channels in vascular smooth muscle are essential for coupling myocardial blood flow (MBF) with the metabolic demand of the heart. These channels consist of a transmembrane pore domain that associates with auxiliary Kvβ1 and Kvβ2 proteins, which differentially regulate Kv function in excitable cells. Nonetheless, the physiological role of Kvβ proteins in regulating vascular tone and metabolic hyperemia in the heart remains unknown. Objective: To test the hypothesis that Kvβ proteins confer oxygen sensitivity to vascular tone and are required for regulating blood flow in the heart. Methods and Results: Mice lacking Kvβ2 subunits exhibited suppressed MBF, impaired cardiac contractile performance, and failed to maintain elevated arterial blood pressure in response to catecholamine-induced stress. In contrast, ablation of Kvβ1.1 reduced cardiac workload, modestly elevated MBF, and preserved cardiac function during stress compared with wild type mice. Coronary arteries isolated from Kvβ2-/-, but not Kvβ1.1-/-, mice, had severely blunted vasodilation to hypoxia when compared with arteries from wild type mice. Moreover, vasodilation of small diameter coronary and mesenteric arteries due to L-lactate, a biochemical marker of reduced tissue oxygenation and anaerobic metabolism, was significantly attenuated in vessels isolated from Kvβ2-/- mice. Inducible enhancement of the Kvβ1:Kvβ2 ratio in Kv1 channels of arterial smooth muscle abolished L-lactate-induced vasodilation and suppressed the relationship between MBF and cardiac workload.Conclusions: The Kvβ proteins differentially regulate vascular tone and myocardial blood flow, whereby Kvβ2 promotes and Kvβ1.1 inhibits oxygen-dependent vasodilation and augments blood flow upon heightened metabolic demand.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/CIRCRESAHA.120.317715" target="_blank" rel="noreferrer noopener">10.1161/CIRCRESAHA.120.317715</a>
Format
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journalArticle
Publisher
An entity responsible for making the resource available
Circulation Research
2021
Bhatnagar A
Chilian WM
Circulation research
coronary arteris
Department of Integrative Medical Sciences
Dwenger MM
February 2021 List
Hu X
journalArticle
Mack GD
Microcirculation
Moore IJB
myogenic tone
NEOMED College of Medicine
nicotinamide adenine dinucleotide
Nystoriak MA
Ohanyan V
Pucci T
Raph SM
voltage-gated potassium channels
-
Text
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URL Address
<a href="http://doi.org/10.3390/ijms21218118" target="_blank" rel="noreferrer noopener">http://doi.org/10.3390/ijms21218118</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Issue
21
Volume
21
ISSN
1422-0067 1422-0067
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Update Year & Number
October 2020 List
NEOMED College
NEOMED College of Medicine
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Department of Integrative Medical Sciences
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Title
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Ischemic heart disease pathophysiology paradigms overview: From plaque activation to microvascular dysfunction.
Publisher
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International Journal of Molecular Sciences
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-10-30
Subject
The topic of the resource
atherosclerosis; ion channels; microcirculation; myocardial infarction; coronary blood flow; ischemic heart disease
Creator
An entity primarily responsible for making the resource
Severino P;D'Amato A;Pucci M;Infusino F;Adamo F;Birtolo LI;Netti L;Montefusco G;Chimenti C;Lavalle C;Maestrini V;Mancone M;Chilian WM;Fedele F
Description
An account of the resource
Ischemic heart disease still represents a large burden on individuals and health care resources worldwide. By conventions, it is equated with atherosclerotic plaque due to flow-limiting obstruction in large-medium sized coronary arteries. However, clinical, angiographic and autoptic findings suggest a multifaceted pathophysiology for ischemic heart disease and just some cases are caused by severe or complicated atherosclerotic plaques. Currently there is no well-defined assessment of ischemic heart disease pathophysiology that satisfies all the observations and sometimes the underlying mechanism to everyday ischemic heart disease ward cases is misleading. In order to better examine this complicated disease and to provide future perspectives, it is important to know and analyze the pathophysiological mechanisms that underline it, because ischemic heart disease is not always determined by atherosclerotic plaque complication. Therefore, in order to have a more complete comprehension of ischemic heart disease we propose an overview of the available pathophysiological paradigms, from plaque activation to microvascular dysfunction.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.3390/ijms21218118" target="_blank" rel="noreferrer noopener">10.3390/ijms21218118</a>
Format
The file format, physical medium, or dimensions of the resource
journalArticle
2020
Adamo F
Atherosclerosis
Birtolo LI
Chilian WM
Chimenti C
Coronary blood flow
D'Amato A
Department of Integrative Medical Sciences
Fedele F
Infusino F
International journal of molecular sciences
Ion Channels
Ischemic heart disease
journalArticle
Lavalle C
Maestrini V
Mancone M
Microcirculation
Montefusco G
myocardial infarction
NEOMED College of Medicine
Netti L
October 2020 List
Pucci M
Severino P
-
Text
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URL Address
<a href="http://doi.org/10.1152/ajpheart.00888.2020" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00888.2020</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
ISSN
1522-1539 0363-6135
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Update Year & Number
March 2021 List
NEOMED College
NEOMED College of Medicine
NEOMED Department
Department of Integrative Medical Sciences
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The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Exosomal microRNAs in the development of essential hypertension and its potential as biomarkers.
Publisher
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American Journal Of Physiology. Heart And Circulatory Physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2021
2021-02-12
Subject
The topic of the resource
extracellular vesicles; small non-coding RNA; clinical biomarker; high blood pressure; microvesicles
Creator
An entity primarily responsible for making the resource
Tan PPS; Hall D; Chilian WM; Chia YC; Mohd ZS; Lim HM; Kumar DN; Ching SM; Low TY; Noh MFM; Pung Y-F
Description
An account of the resource
MicroRNAs (miRNAs) are small regulatory molecules that are involved in post-transcriptional modifications. These non-coding RNAs are usually ferried by extracellular carriers such as exosomes or other protein and lipid carriers inside a range of body fluids including plasma and urine. Due to their ability to withstand harsh external conditions, exosomal miRNAs possess enormous potentials as non-invasive disease biomarkers for, notably hypertension, whereby exosomal miRNAs have been implicated in its pathophysiological processes. More importantly, alterations in the microenvironment as a result of disease progression can induce active and selective loading of miRNAs into exosomes. In this paper, we first review the mechanisms of miRNA loading into exosomes, followed by the roles of exosomal miRNAs in the development of hypertension; and the potentials of exosomal miRNAs as biomarkers in comparison to other free circulating miRNAs. Finally challenges and future research surrounding exosomal miRNAs will also be discussed. The information synthesized in this review summarizes current knowledge of non-invasive biomarkers for early hypertension diagnosis and for probing therapeutic efficacy.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00888.2020" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00888.2020</a>
Format
The file format, physical medium, or dimensions of the resource
journalArticle
2021
American journal of physiology. Heart and circulatory physiology
Chia YC
Chilian WM
Ching SM
clinical biomarker
Department of Integrative Medical Sciences
extracellular vesicles
Hall D
high blood pressure
journalArticle
Kumar DN
Lim HM
Low TY
March 2021 List
microvesicles
Mohd ZS
NEOMED College of Medicine
Noh MFM
Pung Y-F
small non-coding RNA
Tan PPS