Thyroid hormone and cardioprotection: Study of p38 MAPK and JNKs during ischaemia and at reperfusion in isolated rat heart

Pantos, Constantinos; Malliopoulou, Vassiliki; Paizis, Ioannis; Moraitis, Panagiotis; Mourouzis, Iordanis; Tzeis, Stylianos; Karamanoli, Evangelia; Cokkinos, Demosthenes D.; Carageorgiou, Haris; Varonos, D.; Cokkinos, Dennis V.

doi:10.1007/978-1-4757-4712-6_22

Cited by 24 publications

(32 citation statements)

References 22 publications

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“…5 It is likely that reexpression of the fetal gene program in the overloaded ventricle, a common feature of cardiac disease, is enhanced by low tissue TH levels. Pantos and colleagues [51][52][53][54][55] have published numerous animal studies on the effects of THs on the heart, particularly during ischemia or MI. They have shown that short-and long-term T3ϩT4 treatment of rats with MI leads to improved LV function and remodeling.…”

Section: Th Metabolism During the Early Post-mi Phasementioning

confidence: 99%

Thyroid Replacement Therapy and Heart Failure

2010

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Section: Th Metabolism During the Early Post-mi Phasementioning

confidence: 99%

Thyroid Replacement Therapy and Heart Failure

2010

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“…Isolation of total protein content and Western blotting have been performed as previously described (Pantos et al 2001(Pantos et al , 2002a(Pantos et al , 2003a. Approximately 0·2 g frozen tissue was homogenized in ice-cold Tris-sucrose buffer (0·35 M sucrose, 10 mM Tris-HCl pH 7·5, 1 mM EDTA, 0·5 mM dithiothreitol, 0·1 mM phenylmethanesulfonyl fluoride) with a Polytron homogenizer and the resulting homogenate was centrifuged at 15 000 g for 20 min at 4 C. The supernatant, representing the total cell extract, was used for immunoblotting.…”

Section: Total Protein Preparationmentioning

confidence: 99%

“…In fact, thyroid hormone is shown to regulate the transcription of various myocyte-specific genes that encode important structural and regulatory proteins including myosin heavy chain isoforms and , sarcoplasmic reticulum calcium activated ATPase (SR Ca 2+ -ATPase), phospholamban, the -adrenergic receptor, adenylyl cyclase isoforms and various membrane ion channels . Furthermore, recent research has revealed that thyroid hormone can interfere with the regulation of important intracellular signalling transduction pathways (Fryer et al 1998, Pantos et al 2001, 2002a, 2003a that are thought to be involved in protection against ischaemia-reperfusion (I/R) (Speechly-Dick et al 1994, Kawamura et al 1998, Zhao et al 1998, Pantos et al 2000, Fryer et al 2001. In fact, chronic administration of T 4 results in changes in cardioprotective molecules such as protein kinase C (PKC) and mitogenactivated protein kinases (Fryer et al 1998, Pantos et al 2001, 2002a, 2003a and this was shown to be associated with increased post-ischaemic recovery of function (Buser et al 1990, Pantos et al 2002a, 2003a.…”

Section: Introductionmentioning

confidence: 99%

Propylthiouracil-induced hypothyroidism is associated with increased tolerance of the isolated rat heart to ischaemia-reperfusion

Pantos¹,

Malliopoulou²,

Mourouzis³

et al. 2003

Journal of Endocrinology

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The present study investigated the response of the hypothyroid heart to ischaemia-reperfusion. Hypothyroidism was induced in Wistar rats by oral administration of propylthiouracil (0·05%) for 3 weeks (HYPO rats), while normal animals (NORM) served as controls. Isolated hearts from NORM and HYPO animals were perfused in Langendorff mode and subjected to zero-flow global ischaemia followed by reperfusion (I/R). Post-ischaemic recovery of left ventricular developed pressure was expressed as % of the initial value (LVDP%). Basal expression of protein kinase C (PKC ) and PKC and phosphorylation of p46 and p54 c-jun NH 2 -terminal kinases (JNKs) in response to I/R were assessed by Western blotting. LVDP% was found to be significantly higher in HYPO hearts than in NORM. At baseline, PKC expression was 1·4-fold more in HYPO than in NORM hearts, P,0·05, while PKC was not changed. Furthermore, basal phospho-p54 and -p46 JNK levels were 2·2-and 2·6-fold more in HYPO than in NORM hearts, P,0·05. In response to I/R, in NORM hearts, phospho-p54 and -p46 JNK levels were 5·5-and 6·0-fold more as compared with the baseline values, P,0·05, while they were not significantly altered in HYPO hearts. HYPO hearts seem to display a phenotype of cardioprotection against ischaemia-reperfusion and this is associated with basal PKC overexpression and attenuated JNK activation after I/R.

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“…Evidence suggests that the p38 MAPK and JNK pathways have an important role in regulation of responses to cardiac I/R injury [23][24][25] . Inhibition of p38 activation results in improved myocardial function after I/R injury [26] . Our results suggested the possible role of JNK and p38 MAPK pathways in adaptive responses of myocardium to I/R injury.…”

Section: Discussionmentioning

confidence: 99%

Cardioprotection by polysaccharide sulfate against ischemia/reperfusion injury in isolated rat hearts

Chen

2008

Acta Pharmacol Sin

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Aim: Polysaccharide sulfate (PSS) is a new type of heparinoid synthesized with alginic acid as the basic material and then by chemical introduction of effective groups. Although PSS is successfully applied in ischemic cardio-cerebrovascular disease, its effect on cardiac function after ischemia/reperfusion (I/R) injury has previously not been investigated. The aim of the present study was to investigate whether PSS can protect the heart from I/R injury and the underlying mechanism of protection. Methods: Isolated rat hearts were perfused (Langendorff) and subjected to 20 min global ischemia followed by 60 min reperfusion with Kreb's Henseleit solution or PSS (0.3-100 mg/L). Myocardial contractile function was continuously recorded. Creatine kinase (CK) and lactate dehydrogenase (LDH) leakage were measured. Tumor necrosis factor-α (TNF-α) expression in cardiomyocytes was investigated. Western blot analysis for extracellular regulated kinases (ERKs), c-jun aminoterminal kinase (JNKs) and p38 mitogen-activated protein kinase (MAPK) activity was performed. Results: After I/R, cardiac contractility decreased, CK and LDH levels increased in the coronary effluent, and TNF-α expression increased in cardiomyocytes. PSS administration at concentrations of 1-30 mg/L improved cardiac contractility, reduced CK and LDH release and inhibited TNF-α production. Phosphorylated-p38MAPK (p-p38MAPK) and p-p54/p46-JNK increased in I/R rat hearts but diminished in PSS (1-30 mg/L) treated hearts. P-p44/p42-ERK levels were unchanged. In contrast, high concentrations of PSS (100 mg/L) had adverse effects that caused a worsening of heart function. Conclusion: PSS has dose-dependent cardioprotective effects on the rat heart after I/R injury. The beneficial effects may be mediated through normalization of the activity of p38 MAPK and JNK pathways as well as controlling the level of TNF-α expression.

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Thyroid hormone and cardioprotection: Study of p38 MAPK and JNKs during ischaemia and at reperfusion in isolated rat heart

Cited by 24 publications

References 22 publications

Thyroid Replacement Therapy and Heart Failure

Thyroid Replacement Therapy and Heart Failure

Propylthiouracil-induced hypothyroidism is associated with increased tolerance of the isolated rat heart to ischaemia-reperfusion

Cardioprotection by polysaccharide sulfate against ischemia/reperfusion injury in isolated rat hearts

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