Up-Regulation of Galectin-3 in Acute Renal Failure of the Rat

Nishiyama, Junichiro; Kobayashi, Shuzo; Ishida, Aki; Nakabayashi, Iwao; Tajima, O.; Miura, Soichiro; Katayama, Masatoki; Nogami, Hisashi

doi:10.1016/s0002-9440(10)64595-6

Cited by 94 publications

(99 citation statements)

References 46 publications

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“…Their upregulation was detected as early as within a few hours and returned to baseline within 1 d. These are considered the early response genes to renal injury. The increase in gene expression of Pax-2 (8,11), activin-A (10), platelet-derived growth factor (PDGF) (32), ciliary neurotrophic factor (CNTF) (33), hepatocyte growth factor receptor (c-Met) (34), galectin-3 (35), and transforming growth factor-␤1 (TGF-␤1) (36) persisted for several days, and these genes are thought to be responsible for tubular regeneration. The upregulation of LIF was observed on 1 d after the ischemic insult and persisted for 7 d. Its time course suggests that LIF participates in the regeneration process.…”

Section: Discussionmentioning

confidence: 99%

“…The expression pattern of galectin-3 is similar to that of LIF. Galectin-3 is expressed in ureteric bud-derived structures in fetal and adult kidney and re-expressed in injured proximal tubule cells (35,38). One hypothesis to explain the re-expression in cells of different origin in disease is that the regenerating proximal tubule cells are dedifferentiated and have different characteristics.…”

Section: Discussionmentioning

confidence: 99%

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Leukemia Inhibitory Factor Is Involved in Tubular Regeneration after Experimental Acute Renal Failure

Yoshino

Monkawa

Tsuji

et al. 2003

Journal of the American Society of Nephrology

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Abstract. Leukemia inhibitory factor (LIF) is known to play a crucial role in the conversion of mesenchyme into epithelium during nephrogenesis. This study was carried out to test the hypothesis that LIF and LIF receptor (LIFR) are involved in the renal epithelial regeneration after acute renal failure. First, the authors investigated the spatiotemporal expression of LIF and LIFR in fetal and adult rat kidney. In developing kidney, LIF was expressed in the ureteric buds and LIFR was located in nephrogenic mesenchyme and the ureteric buds; in adult kidney, LIF and LIFR expression was confined to the collecting ducts. Next, the authors examined the expression of LIF and LIFR during the recovery phase after ischemia-reperfusion injury. Real-time PCR analysis revealed that LIF mRNA expression was significantly increased from day 1 to day 7 after reperfusion and that LIFR mRNA was upregulated from day 4 to day 14. Histologic analysis demonstrated that the increased expression of LIF mRNA and protein was most marked in the outer medulla, especially in the S3 segment of the proximal tubules. To elucidate the mitogenic role of LIF in the regeneration process, cultured rat renal epithelial (NRK 52E) cells were subjected to ATP depletion (an in vitro model of acute renal failure), and LIF expression was found to be enhanced during recovery after ATP depletion. Blockade of endogenous LIF with a neutralizing antibody significantly reduced the cell number and DNA synthesis during the recovery period. These results suggest that LIF participates in the regeneration process after tubular injury.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Leukemia Inhibitory Factor Is Involved in Tubular Regeneration after Experimental Acute Renal Failure

Yoshino

Monkawa

Tsuji

et al. 2003

Journal of the American Society of Nephrology

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“…Galectin-3 mRNA expression in renal tubules was shown to be upregulated early after IRI and toxin-induced AKI and persisted for 7 days following injury [9]. Importantly, galectin-3 has been implicated in the development of myocardial fibrosis and heart failure in an experimental model of AKI [10].…”

Section: Pathophysiologic Mechanisms Of Aki-induced Cardiac Injurymentioning

confidence: 99%

“…The strongest evidence of a cardiorenal link between AKI and the development of cardiac fibrosis is the β-galactoside-binding lectin galectin-3 [9,10]. Galectin-3 mRNA expression in renal tubules was shown to be upregulated early after IRI and toxin-induced AKI and persisted for 7 days following injury [9].…”

Section: Pathophysiologic Mechanisms Of Aki-induced Cardiac Injurymentioning

confidence: 99%

Cardiorenal Syndrome Type 3: Pathophysiologic and Epidemiologic Considerations

Bagshaw

Hoste

Braam

et al. 2013

Contributions to Nephrology

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Cardiorenal syndrome (CRS) type 3 is a subclassification of the CRS whereby an episode of acute kidney injury (AKI) precipitates and contributes to the development of acute cardiac injury. There is limited understanding of the pathophysiologic mechanisms of how AKI contributes to acute cardiac injury and/or dysfunction. An episode of AKI may have effects that depend on the severity and duration of AKI and that both directly and indirectly predispose to an acute cardiac event. Moreover, baseline susceptibility will modify the subsequent risk for cardiac events associated with AKI. Experimental data suggest cardiac injury may be directly induced by inflammatory mediators, oxidative stress, apoptosis and activation of neuroendocrine systems early after AKI. Likewise, AKI may be associated with physiologic derangements (i.e. volume overload; metabolic acidosis, retention of uremic toxins, hyperkalemia; hypocalcemia), alterations to coronary vasoreactivity, and ventricular remodeling and fibrosis that indirectly exert negative effects on cardiac function. AKI may also adversely impact cardiac function by contributing to alternations in drug pharmacokinetics and pharmacodynamics. Additional experimental and transla-

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“…One group studied two models of AKI in the rat (ischemic and nephrotoxic) and found that galectin-3 was intensely upregulated and prevented chronic tubular injury by limiting apoptosis, enhancing matrix remodeling and attenuating fibrosis [66]. However, another group using an ischemiareperfusion model in wild-type versus knockout mice demonstrated that in early AKI the knockout mice seemed protected, with lower levels of interleukin-6, fewer ROS, less macrophage infiltration and lower peak concentrations of urea [67].…”

Section: Galectin-3mentioning

confidence: 99%