Cited 20 times in
Role of tissue transglutaminase in age-associated ventricular stiffness
DC Field | Value | Language |
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dc.contributor.author | 오영준 | - |
dc.date.accessioned | 2017-11-02T08:17:38Z | - |
dc.date.available | 2017-11-02T08:17:38Z | - |
dc.date.issued | 2017 | - |
dc.identifier.issn | 0939-4451 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/154304 | - |
dc.description.abstract | Aging is associated with increased cardiomyocyte loss, left-ventricular hypertrophy, and the accumulation of extracellular matrix, which results in declining cardiac function. The role of the matrix crosslinking enzyme, tissue transglutaminase (TG2), in age-related myocardial stiffness, and contractile function remains incompletely understood. In this study, we examined the role of TG2 in cardiac function, and determined whether TG2 inhibition can prevent age-associated changes in cardiac function. Male Fisher rats (18-month-old) were administered the transglutaminase inhibitor cystamine (study group) or saline (age-matched controls) for 12 weeks via osmotic mini-pumps. Cardiac function was determined by echocardiography and invasive pressure-volume loops. Rat hearts were dissected out, and TG2 expression, activity, and S-nitrosation were determined. Young (6-month-old) males were used as controls. TG2 activity significantly increased in the saline-treated but not in the cystamine-treated aging rat hearts. TG2 expression also increased with age and was unaltered by cystamine treatment. Aged rats showed increased left ventricular (LV) end-systolic dimension and a decrease in fractional shortening compared with young, which was not affected by cystamine. However, cystamine treatment preserved the preload-independent index of LV filling pressure and restored end-diastolic pressure, end-diastolic pressure-volume relationships, and arterial elastance toward young. An increase in TG2 activity contributes to age-associated increase in diastolic stiffness, thereby contributing to age-associated diastolic dysfunction. TG2 may thus represent a novel target for age-associated diastolic heart failure. | - |
dc.description.statementOfResponsibility | restriction | - |
dc.publisher | Springer-Verlag | - |
dc.relation.isPartOf | AMINO ACIDS | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Aging/metabolism* | - |
dc.subject.MESH | Aging/pathology | - |
dc.subject.MESH | Animals | - |
dc.subject.MESH | Blood Pressure | - |
dc.subject.MESH | Cystamine/pharmacology | - |
dc.subject.MESH | Echocardiography | - |
dc.subject.MESH | Elasticity | - |
dc.subject.MESH | Enzyme Inhibitors/pharmacology | - |
dc.subject.MESH | Extracellular Matrix/drug effects | - |
dc.subject.MESH | Extracellular Matrix/enzymology | - |
dc.subject.MESH | Extracellular Matrix/pathology | - |
dc.subject.MESH | GTP-Binding Proteins/antagonists & inhibitors | - |
dc.subject.MESH | GTP-Binding Proteins/genetics | - |
dc.subject.MESH | GTP-Binding Proteins/metabolism* | - |
dc.subject.MESH | Gene Expression | - |
dc.subject.MESH | Heart Ventricles/enzymology* | - |
dc.subject.MESH | Heart Ventricles/physiopathology | - |
dc.subject.MESH | Hypertrophy, Left Ventricular/enzymology* | - |
dc.subject.MESH | Hypertrophy, Left Ventricular/genetics | - |
dc.subject.MESH | Hypertrophy, Left Ventricular/physiopathology | - |
dc.subject.MESH | Hypertrophy, Left Ventricular/prevention & control | - |
dc.subject.MESH | Infusion Pumps, Implantable | - |
dc.subject.MESH | Male | - |
dc.subject.MESH | Myocardium/enzymology | - |
dc.subject.MESH | Myocardium/pathology | - |
dc.subject.MESH | Myocytes, Cardiac/drug effects | - |
dc.subject.MESH | Myocytes, Cardiac/enzymology* | - |
dc.subject.MESH | Myocytes, Cardiac/pathology | - |
dc.subject.MESH | Rats | - |
dc.subject.MESH | Rats, Inbred F344 | - |
dc.subject.MESH | Transglutaminases/antagonists & inhibitors | - |
dc.subject.MESH | Transglutaminases/genetics | - |
dc.subject.MESH | Transglutaminases/metabolism* | - |
dc.title | Role of tissue transglutaminase in age-associated ventricular stiffness | - |
dc.type | Article | - |
dc.publisher.location | Austria | - |
dc.contributor.college | College of Medicine | - |
dc.contributor.department | Dept. of Anesthesiology and Pain Medicine | - |
dc.contributor.googleauthor | Young Jun Oh | - |
dc.contributor.googleauthor | Vanessa C. Pau | - |
dc.contributor.googleauthor | Jochen Steppan | - |
dc.contributor.googleauthor | Gautam Sikka | - |
dc.contributor.googleauthor | Valeriani R. Bead | - |
dc.contributor.googleauthor | Daniel Nyhan | - |
dc.contributor.googleauthor | Benjamin D. Levine | - |
dc.contributor.googleauthor | Dan E. Berkowitz | - |
dc.contributor.googleauthor | Lakshmi Santhanam | - |
dc.identifier.doi | 10.1007/s00726-016-2295-z | - |
dc.contributor.localId | A02389 | - |
dc.relation.journalcode | J00124 | - |
dc.identifier.eissn | 1438-2199 | - |
dc.identifier.pmid | 27438265 | - |
dc.identifier.url | https://link.springer.com/article/10.1007%2Fs00726-016-2295-z | - |
dc.subject.keyword | Cardiac aging | - |
dc.subject.keyword | Hypertrophy | - |
dc.subject.keyword | Tissue transglutaminase | - |
dc.contributor.alternativeName | Oh, Young Jun | - |
dc.contributor.affiliatedAuthor | Oh, Young Jun | - |
dc.citation.title | Amino Acids | - |
dc.citation.volume | 49 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | 695 | - |
dc.citation.endPage | 704 | - |
dc.identifier.bibliographicCitation | AMINO ACIDS, Vol.49(3) : 695-704, 2017 | - |
dc.date.modified | 2017-11-01 | - |
dc.identifier.rimsid | 42273 | - |
dc.type.rims | ART | - |
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