Parathyroid hormone treatment after myocardial infarction promotes cardiac repair by enhanced neovascularization and cell survival

Zaruba, Marc-Michael; Hüber, Bruno; Brunner, Stefan; Deindl, Elisabeth; Dávid, Róbert; Fischer, R; Assmann, G.; Herbach, Nadja; Grundmann, Sebastian; Wanke, Rüdiger; Mueller-Hoecker, Josef; Franz, Wolfgang-Michael

doi:10.1093/cvr/cvm080

Cited by 69 publications

(69 citation statements)

References 40 publications

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“…The elevated expression of TGF-β may also contribute to the adversary effects of PTH treatment on LVH (Ruiz-Ortega et al, 2007). Our finding is seemingly in contrast with a previous report stating that PTH exerted beneficial effects in a mouse model of myocardial infarction (MI) by improving stem cell mobilization (Zaruba et al, 2008). Since a severe loss of cardiomyocytes occurs in MI, a replacement of the dead cells with viable cells is a valuable strategy for the treatment of MI.…”

Section: Discussioncontrasting

confidence: 61%

“…Sham/ saline and TAB/saline groups received daily subcutaneous injection of 0.1 ml of saline (0.9% NaCl) for 2 weeks. Sham/PTH and TAB/ PTH groups received daily subcutaneous injections of PTH 1-34 (80 μg/kg/d) for same period (Bachem), as previously described (Zaruba et al, 2008). Echocardiography was again performed 4 weeks after the completion of the PTH and saline treatments.…”

Section: Saline and Pth (1-34) Administrationmentioning

confidence: 99%

“…Recently, PTH was shown to exert beneficial effects in a mouse model of myocardial infarction (MI) by improving stem cell mobilization (Zaruba et al, 2008). This finding raised an interesting question as to whether or not PTH treatment would be beneficial for other types of cardiovascular abnormalities.…”

Section: Introductionmentioning

confidence: 99%

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Parathyroid hormone accelerates decompensation following left ventricular hypertrophy

et al. 2010

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Abbreviations: FS, fractional shortening; LVH, left ventricular hypertrophy; LVIDs, left ventricular internal dimension at systole; LVPWs, left ventricular posterior wall thickness at systole; PTH, parathyroid hormone; TAB, transverse aortic banding AbstractParathyroid hormone (PTH) treatment was previously shown to improve cardiac function after myocardial infarction by enhancing neovascularization and cell survival. In this study, pressure overload-induced left ventricular hypertrophy (LVH) was induced in mice by transverse aortic banding (TAB) for 2 weeks. We subsequently evaluated the effects of a 2-week treatment with PTH or saline on compensated LVH. After another 4 weeks, the hearts of the mice were analyzed by echocardiography, histology, and molecular biology. Echocardiography showed that hearts of the PTH-treated mice have more severe failing phenotypes than the saline-treated mice following TAB with a greater reduction in fractional shortening and left ventricular posterior wall thickness and with a greater increase in left ventricular internal dimension. Increases in the heart weight to body weight ratio and lung weight to body weight ratio following TAB were significantly exacerbated in PTH-treated mice compared to saline-treated mice. Molecular markers for heart failure, fibrosis, and angiogenesis were also altered in accordance with more severe heart failure in the PTH-treated mice compared to the saline-treated mice following TAB. In addition, the PTH-treated hearts were manifested with increased fibrosis accompanied by an enhanced SMAD2 phosphorylation. These data suggest that the PTH treatment may accelerate the process of decompensation of LV, leading to heart failure.

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Section: Discussioncontrasting

confidence: 61%

Section: Saline and Pth (1-34) Administrationmentioning

confidence: 99%

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Parathyroid hormone accelerates decompensation following left ventricular hypertrophy

et al. 2010

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“…Thus, comparing the obtained results with the data of our previous studies [18], as well as with the latest published findings [24][25][26], we can assume that the increase of PTH levels in blood of patients suffering from heart failure has a compensatory modulating significance for supporting heart activity.…”

Section: Resultssupporting

confidence: 81%

Dose-dependent effect of parathyroid hormone 1-34 fragment and its influence mechanism on the functional activity of isolated heart

Ter-Markosyan¹,

Harutunyan²,

Sargsyan³

et al. 2012

OJMIP

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The present investigation is the continuation of our prior clinical studies on the content of parathyroid hormone (PTH), its paracrine analog, parathyroid hormone-related protein (PTHrP) and electrolytes in blood of patients with heart failure. The results of these studies formed the basis for the nomination of the hypothesis on PTH and PTHrP compensatorymodulating effect on the contractile activity of heart. The objective of this study is to elucidate the mechanism of the compensatory-modulating effect of PTH on heart functional activity, which is realized by the study of effective doses of PTH by pharmacological analysis, using different inhibitors. The dose-dependent effect of PTH on the heart contraction rate and amplitude is studied on the frog isolated heart by the method of non-invasive registration of heart contractile activity. The method is based on the photoelectric principle of the reflected from the contractile object light ray transformation into an electric signaling. It is shown that the most effective dose that has positive chronotropic and inotropic effects on heart is 10 -10 M hormone. To clarify the mechanism of PTH physiological dose action on the contractile activity of heart PTH 1-34 is combined with Ca-channel as well as phosphodiesterase blockers. The mentioned substances are applied based on the fact that PTH effect on target cells is mediated by secondary messengers, particularly calcium ions and cAMP. Based on the data obtained by combination of hormone with Verapamil (10 -5 M) and Theophylline (10 -4 M), we concluded on the involvement of calcium ions in the realization of chronotropic and cAMP in the inotropic effects on the heart.

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“…10,61 In the context of cardiovascular disease, PTH augments the number of recruited progenitor cells in the heart and improves the recovery of function after acute myocardial infarction in mice. 62 Of note, PTH exhibits several other effects (eg, it acts as vasodilator); thus, it remains to be deciphered to what extent progenitor cell mobilization contributes to the beneficial effects seen.…”

Section: Modulators Of the Endosteal Nichementioning

confidence: 99%

Regulation of Bone Marrow-Derived Vascular Progenitor Cell Mobilization and Maintenance

Dimmeler

2010

ATVB

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Abstract-Cell therapy is a promising option for treating ischemic diseases and heart failure. Bone marrow-derived vasculogenic cells, including progenitor cells and proangiogenic cells, have been shown to augment the functional recovery after ischemia. However, cardiovascular diseases affect the functional activity of the endogenous progenitor cell pools. The local microenvironment, also termed the stem cell niche, provides essential cues that maintain stem and progenitor cell functions and direct cell fate decisions in the bone marrow. A disturbed niche might lead to cell dysfunction (eg, by exhaustion). In addition, the niche controls mobilization of the cells into the circulation. This review will discuss the impact of cardiovascular disease on stem cell niches and summarize strategies targeting the niche for mobilization of vasculogenic cells.

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Parathyroid hormone treatment after myocardial infarction promotes cardiac repair by enhanced neovascularization and cell survival

Cited by 69 publications

References 40 publications

Parathyroid hormone accelerates decompensation following left ventricular hypertrophy

Parathyroid hormone accelerates decompensation following left ventricular hypertrophy

Dose-dependent effect of parathyroid hormone 1-34 fragment and its influence mechanism on the functional activity of isolated heart

Regulation of Bone Marrow-Derived Vascular Progenitor Cell Mobilization and Maintenance

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