Early response as shown by enhancement of transglutaminase 1 expression after cisplatin-induced acute kidney injury

Furukawa, Kentaro; Yamane, Minoru; Tatsukawa, Hideki; Hitomi, Kiyotaka

doi:10.1016/j.abb.2015.09.021

Cited by 4 publications

(4 citation statements)

References 17 publications

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“…Most previous in vivo studies on kidney diseases have limited their attention to analyzing only TG2 5 , 9 , 15 – 17 , 24 , 25 . However, our previous study demonstrated that the expression and activity of TG1 significantly increased in renal tubular epithelium in the early phase of acute kidney injury 18 . Moreover, the present study also showed a marked enhancement of TG1 activity from the early stage of renal fibrosis.…”

Section: Discussionmentioning

confidence: 84%

“…Even for the same substrate protein, TG isozymes differ with regard to their reactivity and specificity 39 . Among their family, a number of articles reported that TG2 predominantly appears to have substantial role in renal disease 5 , 9 , 15 – 18 . Indeed, TG inhibitor NUT281 almost completely suppressed the induction of renal fibrosis in rat subjected to 5/6-nephrectomy 15 , whereas TG2KO mice showed a partial reduction in the progress of renal fibrosis in UUO-treated mice 16 .…”

Section: Discussionmentioning

confidence: 99%

“…Several previous studies have investigated the involvement of TGs in renal disease 5 , 9 , 15 – 18 and showed that TG2 appears to play an important predominant role in the disease. Indeed, a TG2 knockout mouse (TG2KO) model was used to demonstrate a 50% suppression of increased fibrillary collagen, macrophage infiltration, and active TGF-β1 after unilateral ureteral obstruction (UUO) 16 .…”

Section: Introductionmentioning

confidence: 99%

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Isozyme-specific comprehensive characterization of transglutaminase-crosslinked substrates in kidney fibrosis

Tatsukawa

Otsu

Tani

et al. 2018

Sci Rep

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Chronic kidney disease is characterized by prolonged decline in renal function, excessive accumulation of ECM, and progressive tissue fibrosis. Transglutaminase (TG) is a crosslinking enzyme that catalyzes the formation of covalent bonds between glutamine and lysine residues, and is involved in the induction of renal fibrosis via the stabilization of ECM and the activation of TGF-β1. Despite the accumulating evidences indicating that TG2 is a key enzyme in fibrosis, genetic knockout of TG2 reduced by only 50% the elevated protein crosslinking and fibrous protein in renal fibrosis model, whereas treatment with TG inhibitor almost completely reduced these levels. Here, we also clarified the distributions of TG isozymes and their in situ activities and identified the isozyme-specific crosslinked substrates for both TG1 and TG2 in fibrotic kidney. We found that TG1 activity was markedly enhanced in renal tubular epithelium and interstitial areas, whereas TG2 activity increased only in the extracellular space. In total, 47 and 67 possible candidates were identified as TG1 and TG2 substrates, respectively, only in fibrotic kidney. Among them, several possible substrates related to renal disease and fibrosis were identified. These findings provide novel insights into the mechanisms of renal fibrosis through the targeting of isozyme-specific TG substrates.

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Section: Discussionmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Isozyme-specific comprehensive characterization of transglutaminase-crosslinked substrates in kidney fibrosis

Tatsukawa

Otsu

Tani

et al. 2018

Sci Rep

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“…Furukawa et al evaluated the utility of renal TG1 as an early biomarker of kidney injury in ICR mice treated with cisplatin 20 mg/kg/day. 22 The authors reported an increase in expression and activity of TG1 in the proximal tubule within 24 h, with no increases in SCr, suggesting the use of this protein as an early indicator of kidney damage. A recent publication has profiled potential kidney injury proteins in the urine up to 10 days after cancer patients received a single cisplatin dose.…”

Section: Platinum Compoundsmentioning

confidence: 94%

<p>Identification of Novel Biomarkers for Predicting Kidney Injury Due to Drugs Using “Omic” Strategies</p>

Awdishu¹,

Atilano-Roque²,

Tuey³

et al. 2020

PGPM

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Drug-induced kidney injury accounts for 20% of community-and hospitalacquired cases of acute kidney injury (AKI). The incidence is higher among older individuals, who often have co-existing morbidities and are exposed to more diagnostic procedures and therapies. While demographic and clinical components have been identified as risk factors, the proposed cellular mechanisms of drug-induced kidney injury are numerous and complicated. There are also limitations recognized in the use of traditional biomarkers, such as serum creatinine and blood urea nitrogen, to provide high sensitivity, specificity, and timeliness to identification of drug-induced kidney injury. Therefore, novel biomarkers are currently being investigated, identified, developed, and validated for their performance over the traditional biomarkers. This review will provide an overview of drug-induced kidney injury and will discuss what is known regarding "omic" (proteomic, genomic, transcriptomic, and metabolomic) biomarker strategies for drugs known to induce nephrotoxicity.

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Detection and identification of potential transglutaminase 2 substrates in the mouse renal glomeruli

Ito

Tatsukawa

Yamaguchi

et al. 2018

Archives of Biochemistry and Biophysics

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Early response as shown by enhancement of transglutaminase 1 expression after cisplatin-induced acute kidney injury

Cited by 4 publications

References 17 publications

Isozyme-specific comprehensive characterization of transglutaminase-crosslinked substrates in kidney fibrosis

Isozyme-specific comprehensive characterization of transglutaminase-crosslinked substrates in kidney fibrosis

<p>Identification of Novel Biomarkers for Predicting Kidney Injury Due to Drugs Using “Omic” Strategies</p>

Detection and identification of potential transglutaminase 2 substrates in the mouse renal glomeruli

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