Heart transplantation changes the expression of distinct gene families

Ngimbous, Bedel; Bourgeois, Francine; Mas, Christophe; Simonneau, Michel; Moalic, Jean‐Marie

doi:10.1152/physiolgenomics.00013.2001

Cited by 5 publications

(3 citation statements)

References 53 publications

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“…Thus, it might be hypothesised that oxidative stress may contribute to deterioration of the allograft by activating molecular mechanisms similar to those found in ageing. This hypothesis is supported by the recent finding, in a rat heart transplant model, of a downregulation of genes involved in energy metabolism and protein synthesis regulation, similar to that reported for senescent mouse skeletal muscle (Ngimbous et al 2001).…”

Section: Left Ventricular Dysfunctionsupporting

confidence: 81%

Exercise after heart transplantation

Marconi¹,

Marzorati²

2003

European Journal of Applied Physiology

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Exercise intolerance in heart transplant recipients (HTR) has a multifactorial origin, involving complex interactions among cardiac, neurohormonal, vascular, skeletal muscle and pulmonary abnormalities. However, the role of these abnormalities may differ as a function of time after transplantation and of many other variables. The present review is aimed at evaluating the role of cardiac, pulmonary and muscular factors in limiting maximal aerobic performance of HTR, and the benefits of chronic exercise. Whereas pulmonary function does not seem to affect gas exchange until a critical value of diffusing lung capacity is attained, cardiac and skeletal muscle function deterioration may represent relevant factors limiting maximal and submaximal aerobic performance. Cardiac function is mainly limited by chronotropic incompetence and diastolic dysfunction, whereas muscle activity seems to be limited by impaired oxygen supply as a consequence of the reduced capillary network. The latter may be due to either immunosuppressive regimen or deconditioning. Endurance and strength training may greatly improve muscle function and maximal aerobic performance of HTR, and may also reduce side effects of immunosuppressive therapy and control risk factors for cardiac allograft vasculopathy. For the above reasons exercise should be considered an important therapeutic tool in the long-term treatment of heart transplant recipients.

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Section: Left Ventricular Dysfunctionsupporting

confidence: 81%

Exercise after heart transplantation

Marconi¹,

Marzorati²

2003

European Journal of Applied Physiology

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“…Cerebella were collected, immediately frozen in liquid nitrogen, and total RNA was isolated using TRI-Reagent (Applied Biosystems). Subsequently, cDNA was synthesized with the Quantitect Reverse Transcription kit (Qiagen), and real-time PCR reactions were performed using the SYBR® Green method (Invitrogen) with previously described primers for MMP-3 and 18S rRNA [8,9]. Relative gene expression was calculated using the gene expression CT difference (GED) formula [10] and represented as fold difference towards levels at P6.…”

Section: Real-time Pcrmentioning

confidence: 99%

An Aberrant Cerebellar Development in Mice Lacking Matrix Metalloproteinase-3

et al. 2011

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Cell-cell and cell-matrix interactions are necessary for neuronal patterning and brain wiring during development. Matrix metalloproteinases (MMPs) are proteolytic enzymes capable of remodelling the pericellular environment and regulating signaling pathways through cleavage of a large degradome. MMPs have been suggested to affect cerebellar development, but the specific role of different MMPs in cerebellar morphogenesis remains unclear. Here, we report a role for MMP-3 in the histogenesis of the mouse cerebellar cortex. MMP-3 expression peaks during the second week of postnatal cerebellar development and is most prominently observed in Purkinje cells (PCs). In MMP-3 deficient (MMP-3(-/-)) mice, a protracted granule cell (GC) tangential migration and a delayed GC radial migration results in a thicker and persistent external granular layer, a retarded arrival of GCs in the inner granular layer, and a delayed GABAergic interneuron migration. Importantly, these neuronal migration anomalies, as well as the consequent disturbed synaptogenesis on PCs, seem to be caused by an abnormal PC dendritogenesis, which results in reduced PC dendritic trees in the adult cerebellum. Of note, these developmental and adult cerebellar defects might contribute to the aberrant motor phenotype observed in MMP-3(-/-) mice and suggest an involvement of MMP-3 in mouse cerebellar development.

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“…Not all the changes seen in unloading have been interpreted as beneficial -the issue of atrophy with decreased contractile reserve has been raised (180,183,193), together with controversy regarding cellular calcium regulation and increased myocardial collagen and fibrosis (178,194). However, progression to full fibrosis does not occur, and the changes in protein metabolism reported (increased protein synthesis and simultaneously increased protein degradation, based on mammalian target of rapamycin (mTOR) and ubiquitin proteosome proteolysis (UPP) levels) (195,196) suggest an active remodelling process, dissimilar in nature to the true atrophy seen in skeletal muscle denervation (decreased mTOR and increased UPP) (196).…”

Section: Unloadingmentioning

confidence: 99%

Myocardial substrate metabolism in heart disease

Rhys¹

2012

Front Biosci

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Heart transplantation changes the expression of distinct gene families

Cited by 5 publications

References 53 publications

Exercise after heart transplantation

Exercise after heart transplantation

An Aberrant Cerebellar Development in Mice Lacking Matrix Metalloproteinase-3

Myocardial substrate metabolism in heart disease

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