Pathogenesis and Protection of Ischemia and Reperfusion Injury in Myocardium

Asano, Gorō; Takashi, En; Ishiwata, Toshiyuki; Onda, Munehiko; Yokoyama, Munehiro; Naito, Zenya; Ashraf, Muhammad; Sugisaki, Yuuichi

doi:10.1272/jnms.70.384

Cited by 42 publications

(33 citation statements)

References 20 publications

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“…Recently, some studies have provided evidence that adult bone marrow cells can give rise to or fuse with cells outside their tissue of origin, including heart, brain, and liver (29)(30)(31). Several reports also indicate that cells of bone marrow origin can become functioning endothelial cells and that this population is important in revascularization following injury (32)(33)(34)(35)(36)(37). Our findings are consistent with such observations on the endothelium and focus attention on the renal vasculature as an important site for repair.…”

Section: Discussionsupporting

confidence: 90%

Restoration of tubular epithelial cells during repair of the postischemic kidney occurs independently of bone marrow-derived stem cells

Duffield¹,

Park²,

Hsiao³

et al. 2005

J. Clin. Invest.

532

469

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Ischemia causes kidney tubular cell damage and abnormal renal function. The kidney is capable of morphological restoration of tubules and recovery of function. Recently, it has been suggested that cells repopulating the ischemically injured tubule derive from bone marrow stem cells. We studied kidney repair in chimeric mice expressing GFP or bacterial β-gal or harboring the male Y chromosome exclusively in bone marrow-derived cells. In GFP chimeras, some interstitial cells but not tubular cells expressed GFP after ischemic injury. More than 99% of those GFP interstitial cells were leukocytes. In female mice with male bone marrow, occasional tubular cells (0.06%) appeared to be positive for the Y chromosome, but deconvolution microscopy revealed these to be artifactual. In β-gal chimeras, some tubular cells also appeared to express β-gal as assessed by X-gal staining, but following suppression of endogenous (mammalian) β-gal, no tubular cells could be found that stained with X-gal after ischemic injury. Whereas there was an absence of bone marrow-derived tubular cells, many tubular cells expressed proliferating cell nuclear antigen, which is reflective of a high proliferative rate of endogenous surviving tubular cells. Upon i.v. injection of bone marrow mesenchymal stromal cells, postischemic functional renal impairment was reduced, but there was no evidence of differentiation of these cells into tubular cells of the kidney. Thus, our data indicate that bone marrow-derived cells do not make a significant contribution to the restoration of epithelial integrity after an ischemic insult. It is likely that intrinsic tubular cell proliferation accounts for functionally significant replenishment of the tubular epithelium after ischemia.

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Section: Discussionsupporting

confidence: 90%

Restoration of tubular epithelial cells during repair of the postischemic kidney occurs independently of bone marrow-derived stem cells

Duffield¹,

Park²,

Hsiao³

et al. 2005

J. Clin. Invest.

532

469

View full text Add to dashboard Cite

show abstract

“…These challenges are primarily related to the smaller circulatory volume, the immaturity of most organ systems, and the increased capillary membrane permeability of neonates and infants [32,33]. Moreover, cardiomyocytes can be affected by hypoxic conditions, and the ischemic effects can induce rapid or gradual changes in the membrane systems that cause reversible or irreversible injury [34]. Experimental studies of myocardial ischemia and reperfusion have established that reperfusion also has negative consequences during circulatory interruption [35,36].…”

Section: Cardiopulmonary Bypass and Myocardial Protectionmentioning

confidence: 99%

Myocardial Ischemia in Congenital Heart Disease: A Review

Carmona¹,

Mata²,

Oliveira³

et al. 2013

Ischemic Heart Disease

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“…24 Glibenclamide, an inhibitor of cardiac mitoK ATP channels, has been reported to prevent ischemic pre-conditioning suggesting that PC-mediated cardioprotection is at least partly due to opening of K ATP channels. 5,[25][26][27] The opening of mito K ATP channels causes the depolarization of mitochondria and reduces Ca þþ overload during I/R. 5,26,27 It has also been shown that the signaling pathway between atrial muscarinic cholinergic receptors, heterotrimeric G-proteins and single muscarinic K þ channels can be interrupted by Ras p21 or one of its guanosine triphosphatase activating proteins.…”

Section: -27mentioning

confidence: 99%

“…5,[25][26][27] The opening of mito K ATP channels causes the depolarization of mitochondria and reduces Ca þþ overload during I/R. 5,26,27 It has also been shown that the signaling pathway between atrial muscarinic cholinergic receptors, heterotrimeric G-proteins and single muscarinic K þ channels can be interrupted by Ras p21 or one of its guanosine triphosphatase activating proteins. [28][29][30] Results from the present study show that removal of Ras-GTPasemediated inhibition of mitoK ATP channels is partially responsible for cardioprotection due to FPT III.…”

Section: -27mentioning

confidence: 99%

Cardioprotection from ischemia‐reperfusion injury due to Ras‐GTPase inhibition is attenuated by glibenclamide in the globally ischemic heart

Al-Rashdan

Canatan

Al‐Maghrebi

et al. 2006

Cell Biochemistry & Function

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The present study was designed to see if acute local inhibition of Ras-GTPase before or after ischemia (during perfusion) would produce protection against ischemia and reperfusion (I/R)-induced cardiac dysfunction. The effect of glibenclamide, an inhibitor of cardiac mitochondrial ATP-sensitive potassium (mitoK(ATP)) channels, on Ras-GTPase-mediated cardioprotection was also studied. A 40 min episode of global ischemia followed by a 30 min reperfusion in perfused rat hearts produced significantly impaired cardiac function, measured as left ventricular developed pressure (P(max)) and left ventricular end-diastolic pressure (LVEDP). Perfusion with Ras-GTPase inhibitor FPT III before I/R [FPT(pre)], significantly enhanced cardiac recovery in terms of left ventricular contractility. P(max) was significantly higher at the end of 30 min reperfusion in FPT(pre)-treated hearts compared to pre-conditioned hearts. However, the degree of improvement in left ventricular contractility was significantly less when FPT III was given only after ischemia during reperfusion [FPT(post)]. Combination treatment with FPT III and glibenclamide before I/R resulted in significant reduction of FPT III-mediated cardioprotection. These data suggest that activation of Ras-GTPase signaling pathways during ischemia are critical in the development of left ventricular dysfunction and that opening of mitoK(ATP) channels, at least in part, contributes to cardioprotection produced by Ras-GTPase inhibition.

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Pathogenesis and Protection of Ischemia and Reperfusion Injury in Myocardium

Cited by 42 publications

References 20 publications

Restoration of tubular epithelial cells during repair of the postischemic kidney occurs independently of bone marrow-derived stem cells

Restoration of tubular epithelial cells during repair of the postischemic kidney occurs independently of bone marrow-derived stem cells

Myocardial Ischemia in Congenital Heart Disease: A Review

Cardioprotection from ischemia‐reperfusion injury due to Ras‐GTPase inhibition is attenuated by glibenclamide in the globally ischemic heart

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