Identification of stathmin as a novel marker of cell proliferation in the recovery phase of acute ischemic renal failure

Zahedi, Kamyar; Wang, Zhaohui; Barone, Sharon; Tehrani, Kathy; Yokota, Naoko; Petrovic, Snezana; Rabb, Hamid; Soleimani, Manoocher

doi:10.1152/ajpcell.00432.2003

Cited by 22 publications

(28 citation statements)

References 54 publications

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“…31). Previous studies have demonstrated that the expression of stathmin increases in the proximal tubules of kidneys subjected to IRI (44). Stathmin was expressed by dedifferentiated and actively proliferating proximal tubule cells in the corticomedullary junction and in the S3 segment of the proximal tubule (39).…”

Section: Discussionmentioning

confidence: 92%

“…Stathmin is an important molecule that is known to play a critical role in the process of mitosis and the regulation of the microtubule cytoskeleton. In ATN, recent reports have shown that stathmin is a marker of dedifferentiated, mitotically active epithelial cells that may contribute to tubular regeneration after ATN (44). Interestingly, in stathmin-deficient mice subjected to IRI, aberrant regulation of cell cycle progression, which impaired or at least delayed the process of tubular repair and recovery after acute renal injury, has been described (45).…”

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confidence: 99%

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Comparison of protective effects of trimetazidine against experimental warm ischemia of different durations: early and long-term effects in a pig kidney model

Jayle¹,

Favreau²,

Zhang³

et al. 2007

American Journal of Physiology-Renal Physiology

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Acute renal failure (ARF) is often the consequence of an ischemia-reperfusion injury (IRI) and associated with high mortality. Warm ischemia (WI) is a crucial factor of tissue damage, and tissue destruction led by ischemia-reperfusion (I/R) can impact the early and long-term functional outcome. Trimetazidine (TMZ) is an anti-ischemic drug. Previously, we already verified its protective effect on a cold-ischemic pig kidney model by directly adding TMZ into the preservation solution (Faure JP, Baumert H, Han Z, Goujon JM, Favreau F, Dutheil D, Petit I, Barriere M, Tallineau C, Tillement JP, Carretier M, Mauco G, Papadopoulos V, Hauet T. Biochem Pharmacol 66: 2241–2250, 2003; Faure JP, Petit I, Zhang K, Dutheil D, Doucet C, Favreau F, Eugene M, Goujon JM, Tillement JP, Mauco G, Vandewalle A, Hauet T. Am J Transplant 4: 495–504, 2004). In this study, we aimed to study the potential effect of TMZ pretreatment (5 mg/kg iv 24 h before WI) on the injury caused by WI for 45, 60, and 90 min and reperfusion in a WI pig kidney model. Compared with sham-operated (control) and uninephrectomized animals (UNX), TMZ pretreatment significantly reduced deleterious effects after 45 min, and particularly 60 and 90 min, of WI by improving the recovery of renal function and minimizing the inflammatory response commonly prevalent in ischemic kidney injury. Compared with controls (control group and UNX group), it was observed that 1) hypoxia-inducible factor-1 (HIF-1α) expression occurred earlier and with a higher intensity in the TMZ-treated groups; 2) the reduction of IRI during the first week following reperfusion was correlated with an earlier and greater expression of stathmin, which is involved in the process of tubular repair; and 3) the tubulointerstitial fibrosis was reduced, particularly after 60 and 90 min of WI. In conclusion, TMZ made the warm-ischemic kidneys more resistant to the deleterious impact of a single episode of I/R and reduced early and long-term subsequent damage.

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Section: Discussionmentioning

confidence: 92%

mentioning

confidence: 99%

Comparison of protective effects of trimetazidine against experimental warm ischemia of different durations: early and long-term effects in a pig kidney model

Jayle¹,

Favreau²,

Zhang³

et al. 2007

American Journal of Physiology-Renal Physiology

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“…Kidneys were fixed in 4% paraformaldehyde, embedded in paraffin, and cut into sections of 4 m. Immunofluorescent staining of stathmin and proliferating-cell nuclear antigen (PCNA) were prepared, as previously described (33,36). Briefly, paraformaldehydefixed, paraffin-embedded sections were washed in PBS and blocked.…”

Section: Proliferation Assaysmentioning

confidence: 99%

Lipocalin-2-induced renal regeneration depends on cytokines

Vinuesa

Solà²,

Jung³

et al. 2008

American Journal of Physiology-Renal Physiology

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“…according to established models and as previously described in detail (28)(29)(30). In brief, male Sprague Dawley rats (200-300 g) or CF57 black mice were anesthetized by intraperitoneal injection with pentobarbital sodium.…”

Section: Kidney Ir Injury: Animal Model Kidney Ir Injury Was Inducedmentioning

confidence: 99%

“…Single- and double-immunofluorescence labeling with anti-TSP-1 antibodies was performed in our laboratories as described in ref. 28. The mouse monoclonal anti-TSP-1 antibody (Neomarkers; Lab Vision Corp.) detects the collagen type-V binding domain as the epitope, and its binding to TSP was unaffected by glucoseaminoglycans, hyluronic acid, or heparin.…”

Section: Kidney Ir Injury: Animal Model Kidney Ir Injury Was Inducedmentioning

confidence: 99%

Identification of thrombospondin 1 (TSP-1) as a novel mediator of cell injury in kidney ischemia

Thakar

Zahedi

Revelo

et al. 2005

Journal of Clinical Investigation

122

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Thrombospondin 1 (TSP-1) is a matricellular protein that inhibits angiogenesis and causes apoptosis in vivo and in vitro in several cancerous cells and tissues. Here we identify TSP-1 as the molecule with the highest induction level at 3 hours of IR injury in rat and mouse kidneys subjected to ischemia/reperfusion (IR) injury using the DNA microarray approach. Northern hybridizations demonstrated that TSP-1 expression was undetectable at baseline, induced at 3 and 12 hours, and returned to baseline levels at 48 hours of reperfusion. Immunocytochemical staining identified the injured proximal tubules as the predominant sites of expression of TSP-1 in IR injury and showed colocalization of TSP-1 with activated caspase-3. Addition of purified TSP-1 to normal kidney proximal tubule cells or cells subjected to ATP depletion in vitro induced injury as demonstrated by cytochrome c immunocytochemical staining and caspase-3 activity. The deleterious role of TSP-1 in ischemic kidney injury was demonstrated directly in TSP-1 null mice, which showed significant protection against IR injury-induced renal failure and tubular damage. We propose that TSP-1 is a novel regulator of ischemic damage in the kidney and may play an important role in the pathophysiology of ischemic kidney failure.

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Identification of stathmin as a novel marker of cell proliferation in the recovery phase of acute ischemic renal failure

Abstract: . Identification of stathmin as a novel marker of cell proliferation in the recovery phase of acute ischemic renal failure.

Cited by 22 publications

References 54 publications

Comparison of protective effects of trimetazidine against experimental warm ischemia of different durations: early and long-term effects in a pig kidney model

Comparison of protective effects of trimetazidine against experimental warm ischemia of different durations: early and long-term effects in a pig kidney model

Lipocalin-2-induced renal regeneration depends on cytokines

Identification of thrombospondin 1 (TSP-1) as a novel mediator of cell injury in kidney ischemia

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