Troponin T switching in the developing rat heart

Saggin, Leopoldo; Ausoni, Simonetta; Gorza, Luisa; Sartore, Saverio; Schiaffino, Stefano

doi:10.1016/s0022-2828(87)80686-7

Cited by 98 publications

(133 citation statements)

References 13 publications

Supporting

Mentioning

123

Contrasting

Unclassified

Order By: Relevance

“…They identified two distinct isoforms of troponin I in rat cardiac muscle, one predominant in embryonic, fetal and early neonatal hearts, and one predominant in adults. The adult isoform is specifically recognized by monoclonal antibody that is nonreactive with the embryonic variant (Saggin et al, 1989). No such study has been applied to human hearts, but it could be the reason why the kit used in this study could not detect early infantile cardiac troponin I.…”

Section: Discussionmentioning

confidence: 97%

See 1 more Smart Citation

Structural and functional affection of the heart in protein energy malnutrition patients on admission and after nutritional recovery

et al. 2005

View full text Add to dashboard Cite

Background and objectives: The pathogenesis of different malnutrition diseases was suggested to affect the heart. This study was designed to detect cardiac affection in protein energy malnutrition (PEM) patients, whether clinically or by electrocardiogram (ECG) and echocardiogram, and to assess the value of the cardiac marker troponin I in patients at risk of myocardial injury with special emphasis on the effect of nutritional rehabilitation. Patients and methods: The present study was carried out on 30 PEM infants (16 nonedematous -14 edematous) and 10 apparently healthy age and sex-matched infants acting as the control group. All studied infants were subjected to full history taking laying stress on dietetic history, thorough clinical and anthropometric measurements. Echocardiography and ECG were also performed. Laboratory investigations were performed including complete blood count, CRP, total proteins, albumin, liver and kidney functions as well as estimation of troponin-I in blood by immulite. Following initial evaluation, all malnourished infants were subjected to nutritional rehabilitation program for approximately 8 weeks, after which the patients were reevaluated using the same preinterventional parameters. Results: The results of the present study demonstrated that electrical properties of myocardium assessed by ECG showed significant decrease of R wave and QTc interval in patients compared to controls with significant improvement after nutritional rehabilitation. Echocardigraphic changes showed that cardiac mass index was significantly lower in both groups of malnourished cases compared to the controls with significant increase after nutritional rehabilitation. The study showed that the parameters of left ventricular (LV) systolic function which are the ejection fraction, fractional shortening and velocity of circumferential fiber shortening were not significantly reduced in patients compared to the controls. The diastolic function also showed no significant difference in the E wave/A wave (e/a) ratio between patients and controls. However, the systolic time interval showed significantly higher LV pre-ejection index in patients in comparison to controls. Edematous and nonedematous cases did not show any significant differences in ECG and echocardigraphic data before or after nutritional rehabilitation. The hearts of two severely affected patients uniquely demonstrated marked decrease of LV end diastolic diameter (LEVDd) together with the detection of troponin-I in their sera. Conclusion: We can conclude that malnutrition, regardless of its type, has a definite effect on cardiac volume, muscle mass, as well as the electrical properties of the myocardium. The systolic functions of the heart are affected more than the diastolic functions and this affection becomes manifest only in severe cases and may constitute a bad prognostic parameter thus necessitating more intense management and strict follow-up of such cases.

show abstract

Section: Discussionmentioning

confidence: 97%

“…Another explanation for why troponin I was only detected in two patients in spite of the cardiac affection detected in many studied cases was offered by, Saggin et al (1989). They identified two distinct isoforms of troponin I in rat cardiac muscle, one predominant in embryonic, fetal and early neonatal hearts, and one predominant in adults.…”

Section: Discussionmentioning

confidence: 99%

Structural and functional affection of the heart in protein energy malnutrition patients on admission and after nutritional recovery

et al. 2005

View full text Add to dashboard Cite

show abstract

“…cardiac β to α myosin heavy chain, slow skeletal troponin I to cardiac troponin I, etc), troponin T is a notable exception since there is a single cardiac gene and different alternatively spliced isoforms. The cardiac troponin T is expressed as a longer protein form at the embryonic stage but is subsequently replaced by a shorter isoform resulting from transcripts with fewer exons [34][35]. If the mutation affecting titin alternative splicing affects global splicing, we would expect that the troponin T might show persistence of the embryonic form into adulthood.…”

Section: Discussionmentioning

confidence: 99%

“…Cardiac troponin T has been shown previously to both undergo developmental transitions and be alternatively spliced [34][35], so wild type and homozygous mutant rats were examined at ages between 1 and 31 days (Figure 4). Western blots from wild type animals at one day of age showed a major upper embryonic-neonatal band and a lower band with less staining intensity.…”

Section: Does the Mutation Affect Another Muscle Alternatively Splicementioning

confidence: 99%

Mutation that dramatically alters rat titin isoform expression and cardiomyocyte passive tension

Greaser

Warren

Esbona

et al. 2008

Journal of Molecular and Cellular Cardiology

102

View full text Add to dashboard Cite

Titin is a very large alternatively spliced protein that performs multiple functions in heart and skeletal muscle. A rat strain is described with an autosomal dominant mutation that alters the isoform expression of titin. While wild type animals go through a developmental program where the 3.0 MDalton N2B becomes the major isoform expressed by two to three weeks after birth (~85%), the appearance of the N2B is markedly delayed in heterozygotes and never reaches more than 50% of the titin in the adult. Homozygote mutants express a giant titin of the N2BA isoform type (3.9 MDalton) that persists as the primary titin species through ages of more than one and half years. The mutation does not affect the isoform switching of troponin T, a protein that also is alternatively spliced with developmental changes. The basis for the apparently greater size of the giant titin in homozygous mutants was not determined, but additional length was not due to inclusion of sequence from larger numbers of PEVK exons or the Novex III exon. Passive tension measurements using isolated cardiomyocytes from homozygous mutants showed that cells could be stretched to sarcomere lengths greater than 4 µm without breakage. This novel rat model should be useful for exploring the potential role of titin in the Frank-Starling relationship and mechano-sensing/signaling mechanisms.

show abstract

“…Troponin I (TnI), the inhibitory component of the troponin complex, exhibits a developmentally regulated pattern of gene expression within the hearts of mammals (Sabry and Dhoot, 1989;Saggin et al, 1989;Murphy et al, 1991;Gorza et al, 1993) and birds (Hastings et al, 1991). In these organisms, TnIs, the TnI isoform characteristic of slow-twitch muscle fibers, is the predominant TnI isoform within their hearts during embryogenesis and, later in development, is completely replaced by the slightly larger cardiac-specific TnI isoform (TnIc).…”

Section: Introductionmentioning

confidence: 99%

Amphibian cardiac troponin I gene's organization, developmental expression, and regulatory properties are different from its mammalian homologue

Warkman

Atkinson

2003

Developmental Dynamics

View full text Add to dashboard Cite

In mammals, the expression of the troponin I-slow (TnIs) isoform is predominant in the heart during embryogenesis and, shortly after birth, is replaced by the cardiac-specific isoform, TnIc; a developmental switch thought to be mediated by thyroid hormone. Whereas, in Xenopus, TnIc is expressed at the onset of heart formation and is the only TnI isoform expressed in the heart. Herein, we demonstrate that the expression patterns of these genes appear to be common within the anuran lineage and, unlike their mammalian counterparts, are not affected by thyroid hormone. To elucidate the regulatory mechanism(s) governing the expression of the amphibian TnIc gene, we characterized the TnIc gene from Rana catesbeiana and used its 5 -flanking region to drive expression of green fluorescent protein in the Xenopus transgenic system. Our results demonstrate that a 300-bp minimal promoter containing intact GATA and CArG-box elements is sufficient to drive expression of this reporter gene in a pattern that mimics, both spatially and temporally, the expression of the endogenous Xenopus TnIc gene. Developmental Dynamics 229:275-288, 2004.

show abstract

Troponin T switching in the developing rat heart

Cited by 98 publications

References 13 publications

Structural and functional affection of the heart in protein energy malnutrition patients on admission and after nutritional recovery

Structural and functional affection of the heart in protein energy malnutrition patients on admission and after nutritional recovery

Mutation that dramatically alters rat titin isoform expression and cardiomyocyte passive tension

Amphibian cardiac troponin I gene's organization, developmental expression, and regulatory properties are different from its mammalian homologue

Contact Info

Product

Resources

About