Expressions of receptor gene for hepatocyte growth factor in kidney after unilateral nephrectomy and renal injury

Ishibashi, Keiichiro; Sasaki, Sei; Sakamoto, Hisato; Hoshino, Yuji; Nakamura, Toshikazu; Marumo, Fumiaki

doi:10.1016/0006-291x(92)90465-w

Cited by 55 publications

(24 citation statements)

References 18 publications

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“…Mesangial cells and renal interstitial cells are able to express HGF mRNA, whereas tubular cells express the c-met HGF receptor [22, 23, 24]. The expression of these components is upregulated in the kidney following renal ischemia or toxic injury [9, 10, 25]. The activity of HGF in the renal parenchyma is increased in experimental ARF [8].…”

Section: Discussionmentioning

confidence: 99%

“…Growth factors (EGF, IGF-1, and HGF) are also involved in tubular regeneration after acute renal failure (ARF), and the renal expression of HGF [9], HGF receptor [10], and IGF-1 [11]is enhanced following acute renal injury. The administration of EGF, IGF-1, or HGF after ischemic [12, 13, 14]or toxic [15, 17]ARF attenuates the decrease in renal function, accelerates the functional and histological recovery, and reduces the mortality of the animals.…”

Section: Introductionmentioning

confidence: 99%

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Accelerated Recovery of Glycerol-Induced Acute Renal Failure in Rats with Previous Partial Hepatectomy

Homsi

Dias²,

Figueiredo³

et al. 1998

Nephron Exp Nephrol

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Several studies have reported a favorable effect following the administration of growth factors during the course of acute renal failure. To evaluate the effect of an increased endogenous production of growth factors, rats underwent 70% hepatectomy before glycerol-induced acute renal failure. The renal function was then monitored 12 and 48 h after glycerol injection in conscious rats. Twelve hours after the induction of acute renal failure, a reduction in creatinine clearance and sodium reabsorption was seen in both prehepatectomized and sham-hepatectomized rats. At 48 h, there was total recovery of glomerular filtration and tubular function in the prehepatectomized rats, whereas the sham-hepatectomized rats still had reduced glomerular filtration and sodium reabsorption. In rats treated with dexamethasone before hepatectomy and studied 48 h after the induction of acute renal failure, the protective action on renal function seen in prehepatectomized rats was totally blocked. A semiquantitative histological analysis done 48 h after the induction of acute renal failure demonstrated a fourfold increase in the number of necrotic tubules in both sham-hepatectomized and dexamethasone-treated rats as compared with hepatectomized rats. It is concluded that partial hepatectomy, a maneuver used to increase the endogenous synthesis of growth factors, accelerates recovery of renal function following glycerol-induced acute renal failure.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Accelerated Recovery of Glycerol-Induced Acute Renal Failure in Rats with Previous Partial Hepatectomy

Homsi

Dias²,

Figueiredo³

et al. 1998

Nephron Exp Nephrol

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“…[11][12][13][14] These same phenotypic responses are predicted to be important for tubule repair, and previous studies have demonstrated upregulation of message levels for both Hgf and the Met receptor in rodent models of ischemic and nephrotoxic injury. [15][16][17][18] Consistent with an important physiologic role for HGF-Met signaling in kidney repair, studies utilizing exogenously added Hgf, transgenically expressed Hgf, or neutralizing antibodies to Hgf in models of kidney injury all demonstrate a role for this pathway in the restoration of renal function. 8,17,[19][20][21][22][23] However, the cell type responsible and the mechanism by which Hgf promotes improved renal function remain unclear.…”

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confidence: 99%

Met Activation Is Required for Early Cytoprotection after Ischemic Kidney Injury

Mason¹,

Hader

Marlier³

et al. 2014

Journal of the American Society of Nephrology

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Renal proximal tubule epithelial cells express high levels of the hepatocyte growth factor receptor Met, and both the receptor and ligand are upregulated after ischemic injury. Activation of the Met receptor after hepatocyte growth factor stimulation in vitro promotes activities involved in kidney repair, including cell survival, migration, and proliferation. However, characterizing the in vivo role of these signaling events in proximal tubule responses to kidney injury has been difficult because global Met knockout results in embryonic lethality due to placental and liver abnormalities. Here, we used gGT-Cre to knockout Met receptor expression selectively in the proximal tubules of mice (gGT-Cre;Met fl/fl ). The kidneys of these mice developed normally, but exhibited increased initial tubular injury, tubular cell apoptosis, and serum creatinine after ischemia/reperfusion compared with gGT-Cre;Met +/+ kidneys. These changes in gGT-Cre;Met fl/fl mice correlated with a selective reduction in PI3K/Akt activation in response to injury and subsequent decreases in inhibitory phosphorylation of the proapoptotic factor Bad and activating phosphorylation of the ribosomal regulatory protein p70-S6 kinase. Moreover, tubular cell proliferation after ischemia/reperfusion was delayed in gGT-Cre;Met fl/fl mice. In conclusion, this study identifies Met-dependent phosphoinositide 3-kinase activation in proximal tubules as a critical determinant of initial tubular cell survival and reparative proliferation after ischemic injury.

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“…Taken together, these findings indicate that the exogenous supply of HGF very likely enhances tyrosine phosphorylation of c-Met/HGF receptor in kidneys and ameliorates renal parameters of ARF mice. It has been reported that c-Met/HGF receptor is mainly expressed in the epithelial cells of kidneys [20, 21]. Therefore, these observations suggest that HGF acts immediately and directly on the kidney, possibly on the renal epithelial cells, and may protect the cells from HgCl 2 toxicity in early phase ARF.…”

Section: Discussionmentioning

confidence: 66%

Hepatocyte Growth Factor Protects Functional and Histological Disorders of HgCl<sub>2</sub>-Induced Acute Renal Failure Mice

Yamasaki

Nagano

Mori-Kudo

et al. 2002

Nephron

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Hepatocyte growth factor (HGF) enhances proliferation of renal epithelial cells as well as hepatocytes. HGF accelerates recovery from acute renal failure (ARF) in animal models. However, pharmacological profiles of HGF including its action mechanism has not been studied in detail. An HgCl₂-induced ARF mouse was used in this study to evaluate the efficacy of HGF. Single administrations of recombinant human HGF or vehicle were given to ARF mice 30 min after HgCl₂ injection. Renal function was monitored by measuring serum creatinine, blood urea nitrogen and creatinine clearance. In the ARF mice, there was a deterioration of renal function biochemical parameters and histological evidence of renal damage including acute tubular necrosis of proximal tubules. These were both significantly ameliorated by a single HGF administration. The effect of HGF was noticeable in the early phase of ARF (1 day after onset) when there was no histological evidence of increased labeling indexes in renal tubular epithelial cells. Western blot analysis of the c-Met/HGF receptor showed that tyrosine phosphorylation was enhanced immediately after HGF administration indicating direct activation of renal epithelial cells. HGF prevented increase of apoptotic nuclei with DNA fragmentation in renal epithelial cells which suggests cytoprotective activity of HGF on renal epithelial cells in the ARF mice.

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Expressions of receptor gene for hepatocyte growth factor in kidney after unilateral nephrectomy and renal injury

Cited by 55 publications

References 18 publications

Accelerated Recovery of Glycerol-Induced Acute Renal Failure in Rats with Previous Partial Hepatectomy

Accelerated Recovery of Glycerol-Induced Acute Renal Failure in Rats with Previous Partial Hepatectomy

Met Activation Is Required for Early Cytoprotection after Ischemic Kidney Injury

Hepatocyte Growth Factor Protects Functional and Histological Disorders of HgCl<sub>2</sub>-Induced Acute Renal Failure Mice

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