Involvement of microtubules in the tolerance of cardiomyocytes to cold ischemia-reperfusion

Devillard, L.; Vandroux, David; Tissier, Cindy; Dumont, Laure; Borgeot, Jessica; Rochette, Luc; Athias, Pierre

doi:10.1007/s11010-007-9594-3

Cited by 16 publications

(13 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Culture preparation (Devillard et al 2008) The primary cultures of neonatal rat cardiomyocytes were prepared from 2-to 4-day-old Wistar rat hearts, as previously described (Grynberg et al 1986). Briefly, cardiomyocytes were obtained from ventricular tissue by 10 dissociating steps of 10 min each at 37 C in 0.1% trypsin (Difco, Detroit, MI, USA).…”

Section: Nanoparticle and Nanohybrid Characterizationsmentioning

confidence: 99%

Titanate nanotubes: towards a novel and safer nanovector for cardiomyocytes*

et al. 2012

Self Cite

View full text Add to dashboard Cite

Actively contractile cardiomyocyte (CM) monolayer represents an interesting tool to study both cardiac diseases and injuries. However, this model is poorly transfectable with conventional agents. Consequently, there is a need to develop new carriers that could overcome this problem. Titanate nanotubes (TiONts) could be a potential candidate due to possibly higher cell uptake as a direct consequence of their shape. On the basis of this rationale, TiONts were assessed for their cytotoxicity and internalization pathways. Cytotoxicity was assessed for TiONts either functionalized with PEI or unfunctionalized and its spherical counterpart P25 TiO2. No cytotoxic effect was observed under TiONts, TiONts-PEI1800 and P25 TiO2 exposed conditions. The tubular morphology was found to be an important parameter promoting internalization while reversing the charge was assessed as non-additional. Internalization was found to occur by endocytosis and diffusion through the membrane. A preliminary transfection study indicated the potential of TiONts as a nanocarrier.

show abstract

Section: Nanoparticle and Nanohybrid Characterizationsmentioning

confidence: 99%

Titanate nanotubes: towards a novel and safer nanovector for cardiomyocytes*

et al. 2012

Self Cite

View full text Add to dashboard Cite

show abstract

“…This prevents damage or depolymerization during vitrification of the oocytes. Beside, previous studies reported that docetaxel was showed to repair the MT damage affected from freezing by induced the MTOC to reorganization of the MT network, which formed dense spindles of MT of cardiac cell within 4 and 8 h after warmed [12]. This may be a reason why docetaxel pretreatment improve the development of vitrified-warmed oocytes.…”

Section: Discussionmentioning

confidence: 94%

“…When cyclin, CDKs and MPF function abnormally, cell development cannot proceed to the next stage. Moreover, it has been reported that docetaxel at high concentrations induces the pro-apoptotic proteins Bax and Bak while it inhibits the anti-apoptotic proteins Bcl-2 and Bcl-x-long, thus leading to cell apoptosis [4,11,12,16]. It has been reported that the cryopreservation of oocytes at an ultra-low temperature (À196°C) induces the depolymerization of MT in the oocytes [29].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Pretreatment of in vitro matured bovine oocytes with docetaxel before vitrification: Effects on cytoskeleton integrity and developmental ability after warming

et al. 2015

View full text Add to dashboard Cite

“…Several lines of evidence seem to indicate that paclitaxel might be beneficial during myocardial ischaemia-reperfusion. Studies in isolated cell models demonstrated that treatment with the paclitaxel analogue, docetaxel, reduced LDH release and oxidative stress in monolayer cultures of newborn rat ventricles submitted to hypothermia and cold ischaemia-reperfusion (Devillard et al 2008). Regarding studies in whole cardiac preparations, pretreatment with 0.3-3 μM of paclitaxel was shown to improve heart rate, left ventricular developed pressure and work index in isolated rat and rabbit hearts subjected to regional ischaemia without reperfusion (Xiao et al 2010).…”

Section: Figure 1 Effects Of Paclitaxel On Microtubule Disruption Anmentioning

confidence: 99%

Microtubule stabilization with paclitaxel does not protect against infarction in isolated rat hearts

Rodríguez‐Sinovas

Abad

Sánchez

et al. 2014

Experimental Physiology

View full text Add to dashboard Cite

New Findings r What is the central question of this study?The microtubule network is disrupted during myocardial ischaemia-reperfusion injury. It was suggested that prevention of microtubule disruption with paclitaxel might reduce cardiac infarct size; however, the effects on infarction have not been studied. r What is the main finding and its importance?Paclitaxel caused a reduction in microtubule disruption and cardiomyocyte hypercontracture during ischaemia-reperfusion. However, it induced a greater increase in cytosolic calcium, which may explain the lack of effect against infarction that we have seen in isolated rat hearts. The large increase in perfusion pressure induced by paclitaxel in this model may have clinical implications, because detrimental effects of the drug were reported after its clinical application.Microtubules play a major role in the transmission of mechanical forces within the myocardium and in maintenance of organelle function. However, this intracellular network is disrupted during myocardial ischaemia-reperfusion. We assessed the effects of prevention of microtubule disruption with paclitaxel on ischaemia-reperfusion injury in isolated rat cardiomyocytes and hearts. Isolated rat cardiomyocytes were submitted to normoxia (1 h) or 45 min of simulated ischaemia (pH 6.4, 0% O 2 , 37°C) and reoxygenation, without or with treatment with the microtubule stabilizer, paclitaxel (10 −5 m), or the inhibitor of microtubule polymerization, colchicine (5 × 10 −6 m). Simulated ischaemia leads to microtubule disruption before the onset of ischaemic contracture. Paclitaxel attenuated both microtubule disruption and the incidence of hypercontracture, whereas treatment with colchicine mimicked the effects of simulated ischaemia and reoxygenation. In isolated normoxic rat hearts, treatment with paclitaxel induced concentration-dependent decreases in heart rate and left ventricular developed pressure and increases in perfusion pressure. Despite protection against hypercontracture, paclitaxel pretreatment did not modify infarct size (60.37 ± 2.27% in control hearts versus 58.75 ± 10.25, 55.44 ± 10.32 and 50.06 ± 10.14% after treatment with 10 −6 , 3 × 10 −6 and 10 −5 m of paclitaxel) after 60 min of global ischaemia and reperfusion in isolated rat hearts. Lack of protection was correlated with a higher increase in cytosolic calcium levels during simulated ischaemia in cardiomyocytes treated with paclitaxel (2.32 ± 0.15 versus 1.13 ± 0.16 a.u. in the presence or A. Rodríguez-Sinovas and E. Abad contributed equally to this work. A. Rodríguez-Sinovas and others absence of 10 −6 m paclitaxel, respectively, P < 0.05), but not with changes in aortic reactivity. In conclusion, microtubule stabilization with paclitaxel reduces hypercontracture in isolated rat cardiomyocytes but does not protect against infarction in isolated rat hearts.

show abstract

Involvement of microtubules in the tolerance of cardiomyocytes to cold ischemia-reperfusion

Cited by 16 publications

References 23 publications

Titanate nanotubes: towards a novel and safer nanovector for cardiomyocytes*

Titanate nanotubes: towards a novel and safer nanovector for cardiomyocytes*

Pretreatment of in vitro matured bovine oocytes with docetaxel before vitrification: Effects on cytoskeleton integrity and developmental ability after warming

Microtubule stabilization with paclitaxel does not protect against infarction in isolated rat hearts

Contact Info

Product

Resources

About