In vivo gene transfection with heat shock protein 70 enhances myocardial tolerance to ischemia-reperfusion injury in rat.

Suzuki, Ken; Sawa, Yoshiki; Kaneda, Yasufumi; Ichikawa, Hajime; Shirakura, R; Matsuda, Hikaru

doi:10.1172/jci119327

Cited by 163 publications

(82 citation statements)

References 34 publications

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“…[1][2][3] Successful gene expression has followed direct intramyocardial injection, [4][5][6][7][8][9][10][11] the introduction into the myocardium of cells transfected ex vivo, [12][13][14] pericardial gene transfer, 15 intracoronary dwell in the arrested heart, [16][17][18][19] and percutaneous transarterial coronary infusion (PTCI). 8,[20][21][22][23] Most investigators have concentrated on the feasibility and characterisation of in vivo myocardial gene transfer and therefore used biologically inert reporter genes.…”

Section: Introductionmentioning

confidence: 99%

β-Galactosidase staining following intracoronary infusion of cationic liposomes in the in vivo rabbit heart is produced by microinfarction rather than effective gene transfer: a cautionary tale

et al. 1998

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The myocardium is a potential target for the expression of conversion at day 3 with associated myocardial damage. exogenous genes to treat inherited and acquired diseases.We hypothesised that the damage was associated with Although adenovirus-mediated gene transfer has resulted macro-aggregates of cationic liposomes-DNA occluding in high-level gene transfer in vivo via direct intramyocardial the microcirculation. When such aggregates were excluded injection and via a percutaneous intra-arterial route, the no X-gal conversion was seen in vivo. In order to show time-course of gene expression is limited by host immune that X-gal conversion occurs in areas of infarction in the responses. It was the aim of this study to test whether catmyocardium we caused closed chest infarction by ionic liposome-mediated gene transfer, which does not sufdeploying a platinum micro-embolisation coil in the circumfer from the aforementioned problems, was feasible in the flex coronary artery. At day 3 X-gal conversion was adult rabbit myocardium via a percutaneous transluminal observed in the territory supplied by the occluded artery. approach. Doses of plasmid DNA encoding lacZ from 200-Thus, microinfarction causes the false positive appearance 800 g complexed to cationic liposomes resulted in X-gal of gene transfer when using a lacZ reporter gene.

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Section: Introductionmentioning

confidence: 99%

β-Galactosidase staining following intracoronary infusion of cationic liposomes in the in vivo rabbit heart is produced by microinfarction rather than effective gene transfer: a cautionary tale

et al. 1998

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“…Moreover, the level of HSP 72 has been directly correlated to the degree of heat stress-induced cardioprotection in the rat (Hutter et al, 1994) and in the rabbit (Marber et al, 1994). Furthermore, improved functional recovery or reduced infarct size has been observed in transgenic mouse and rat hearts overexpressing HSP 72 and subjected to an ischaemia-reperfusion sequence (Marber et al, 1995;Plumier et al, 1995;Hutter et al, 1996;Suzuki et al, 1997). By the same manner, it has been shown that the overexpression of HSP 27 or 72 protects rat cardiomyocytes against ischaemia insult (Martin et al, 1997;Mestril et al, 1996).…”

Section: Discussionmentioning

confidence: 90%

Role of nitric oxide synthases in the infarct size‐reducing effect conferred by heat stress in isolated rat hearts

Arnaud¹,

Laubriet²,

Joyeux³

et al. 2001

British J Pharmacology

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1 Nitric oxide (NO) donors are known to induce both delayed cardioprotection and myocardial heat stress protein (HSP) expression. Moreover, heat stress (HS), which also protects myocardium against ischaemic damages, is associated with a NO release. Therefore, we have investigated the implication of NO in HS-induced resistance to myocardial infarction, in the isolated rat heart model. 2 Rats were divided in six groups (n=10 in each group), subjected or not to heat stress (428C internal temperature, 15 min) and treated or not with nitro-L-arginine-methylester (L-NAME) a nonselective inhibitor of NO synthase isoforms, or L-N 6 -(1-imino-ethyl)lysine (L-NIL), a selective inhibitor of the inducible NO synthase. Twenty-four hours after heat stress, their hearts were isolated, retrogradely perfused, and subjected to a 30-min occlusion of the left coronary artery followed by 120 min of reperfusion. 3 Infarct-to-risk ratio was signi®cantly reduced in HS (18.7+1.6%) compared to Sham (33.0+1.7%) hearts. This e ect was abolished in L-NAME-treated (41.7+3.1% in HS+L-NAME vs 35.2+3.0% in Sham+L-NAME ) and L-NIL-treated (36.1+3.4% in HS+L-NIL vs 42.1+4.6% in Sham+L-NIL) groups. Immunohistochemical analysis of myocardial HSP 27 and 72 showed an HS-induced increase of these proteins, which was not modi®ed by L-NAME pretreatment. 4 We conclude that NO synthases, and in particular the inducible isoform, appear to play a role in the heat stress-induced cardioprotection, independently of HSP 27 and 72 levels. Further investigations are required to elucidate the precise role of HSPs in this adaptive response.

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“…The degree of oxidative stress, and hence myocardial damage, depends on the severity of the ischemic period [41]. Reducing IR damage has been attempted via transfection with genes such as heat shock protein 70 [42][43][44], heme oxygenase [45,46] and nuclear factor κB (NFκB) [47]. Antioxidant gene therapy has been attempted with genes like superoxide dismutase (SOD) [48], which were observed to attenuate the damage due to IR injury.…”

Section: Pacemakingmentioning

confidence: 99%

Non‐viral gene therapy for myocardial engineering

Holladay

O’Brien

Pandit

2010

WIREs Nanomed Nanobiotechnol

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Despite significant advances in surgical and pharmacological techniques, myocardial infarction remains the main cause of morbidity in the developed world because no remedy has been found for the regeneration of infarcted myocardium. Once the blood supply to the area in question is interrupted, the inflammatory cascade, among other mechanisms, results in the damaged tissue becoming a scar. The goals of cardiac gene therapy are essentially to minimize damage, to promote regeneration or some combination thereof. While the vector is, in theory, less important than the gene being delivered, the choice of vector can have a significant impact. Viral therapies can have very high transfection efficiencies, but disadvantages include immunogenicity, retroviralmediated insertional mutagenesis and the expense and difficulty of manufacture. For these reasons, researchers have focused on non-viral gene therapy as an alternative. In this review, naked plasmid delivery, or the delivery of complexed plasmids, and cellmediated gene delivery to the myocardium will be reviewed. Pre-clinical and clinical trials in the cardiac tissue will form the core of the discussion. While unmodified stem cells are sometimes considered therapeutic vectors based on paracrine mechanisms of action basic understanding is limited. Thus, only genetically modified cells will be discussed as cell-mediated gene therapy.Ischemic heart disease, which includes acute damage due to myocardial infarction (MI) and chronic damage due to atherosclerotic narrowing of vessels, accounts for 35% of deaths reported in the United States every year [1]. MI, which is literally the death of cardiac tissue due to lack of 2 oxygen supply, is the result of the occlusion of a coronary artery. Within a few hours of interrupted blood supply, affected cardiomyocytes die. While the body has adaptive mechanisms, such as hypertrophy of the undamaged cardiac muscle and the development of collateral blood supply to minimize the damage, ischemic heart disease remains the most common cause of death in developed countries [2].The delivery of plasmid DNA to the myocardium is a complicated problem as the transfection efficiency of unmodified DNA is quite low, but complexation with agents designed to improve transfection can increase the cytotoxicity of the treatment [3]. Delivery of uncomplexed plasmid DNA is conceptually the simplest gene delivery technique, but these plasmids have extremely low transfection efficiencies in vitro and are not particularly effective in vivo. Compared to viral vectors, transgene expression is almost negligible and the expression time is also very limited [4]. However, there are significant advantages in using plasmids instead of viruses, such as ease of preparation (large and small scale), very low immunogenicity (as there are essentially no protein or membrane components in the plasmid), capacity for long term storage, ease of recombinant manipulation and much larger expression cassettes [4]. A variety of non-viral techniques are available to improve...

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In vivo gene transfection with heat shock protein 70 enhances myocardial tolerance to ischemia-reperfusion injury in rat.

Cited by 163 publications

References 34 publications

β-Galactosidase staining following intracoronary infusion of cationic liposomes in the in vivo rabbit heart is produced by microinfarction rather than effective gene transfer: a cautionary tale

β-Galactosidase staining following intracoronary infusion of cationic liposomes in the in vivo rabbit heart is produced by microinfarction rather than effective gene transfer: a cautionary tale

Role of nitric oxide synthases in the infarct size‐reducing effect conferred by heat stress in isolated rat hearts

Non‐viral gene therapy for myocardial engineering

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