Role of membrane-bound heparin-binding epidermal growth factor-like growth factor (HB-EGF) in renal epithelial cell branching

Takemura, Tamiko; Hino, Shinjiro; Okada, Mituru; Murata, Yuka; Yanagida, Hidehiko; Ikeda, Miyoshi; Yoshioka, Kazuo; Harris, Raymond C.

doi:10.1046/j.1523-1755.2002.00358.x

Cited by 25 publications

(21 citation statements)

References 50 publications

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“…Our findings in rat NRK-52E and mouse S1 cells are reminiscent of branching morphogenesis observed in NRK-52E cells when exposed to unrelated heparin-binding epidermal growth factor-like growth factor (24). However, the earlier report on NRK-52E cells lacked evidence of specific tubular differentiation, and we cannot really equate the two observations.…”

Section: Discussioncontrasting

confidence: 47%

Acute-phase response protein serum amyloid A stimulates renal tubule formation: studies in vitro and in vivo

Kelly¹,

Kluve‐Beckerman²,

Dominguez³

2009

American Journal of Physiology-Renal Physiology

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Section: Discussioncontrasting

confidence: 47%

Acute-phase response protein serum amyloid A stimulates renal tubule formation: studies in vitro and in vivo

Kelly¹,

Kluve‐Beckerman²,

Dominguez³

2009

American Journal of Physiology-Renal Physiology

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“…Our findings have also identified additional problems downstream of IL-6 signaling after exposure to the high dose of DCVC, namely decreased expression of TGF-α, HB-EGF, and EGFr 24 and 36 hours after dosing ( Figures 3D, 4D, and 5D). Both TGF-α and HB-EGF are known to be critical to commit cells to enter the cell division by activating ERK1/2 and increasing DNA synthesis in response to renal injury (4,25,31). Furthermore, the high dose of DCVC significantly reduced IGF-1Rβ expression at early time points after dosing to almost undetectable levels 24 and 36 hours after dosing.…”

Section: Why Does a High Dose Of Dcvc Preventmentioning

confidence: 97%

“…HB-EGF localization following DCVC was similar to that seen in controls. TGF-α and HB-EGF have to bind to the epidermal growth factor receptor (EGFr) to elicit their mitogenic action (31). Therefore, the expression of EGFr was investigated ( Figure 5).…”

Section: Low Priming Dose Studies With 15 Mg Dcvc/kgmentioning

confidence: 99%

Molecular Mechanisms of Renal Tissue Repair in Survival from Acute Renal Tubule Necrosis: Role of ERK1/2 Pathway

et al. 2003

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Our earlier studies with S-(1,2-dichlorovinyl)-L -cysteine (DCVC) showed that prior administration of a low priming dose of 15 mg/kg, IP to mice, given 72 hours before administration of a normally lethal dose of DCVC (75 mg/kg, IP) led to renal tubule necrosis, however sustained renal tubule regeneration was observed and these mice recovered from renal failure and survived. The objective of the present study was to investigate the role of extracellular signal-regulated kinase (ERK) pathway in this autoprotection model. Following the priming dose of DCVC, IL-6 protein and mRNA increased markedly as early as 1 hour after dosing, peaking at 3 hours with a 1.5-fold increase in plasma. Immunocytochemistry on kidney sections using specific antibodies against TGF-α, HB-EGF, EGFr, IGF-1Rβ, Grb-2, and phospho-p44/42 MAP kinase (ERK1/2) revealed a significantly higher staining of these molecules 3 to 72 hours after dosing, indicating up regulation of the ERK pathway. Following a lethal dose of DCVC (75 mg/kg) the early increase in these signaling molecules was not sustained, being markedly reduced 24 and 36 hours after dosing, leading to inhibition of S-phase DNA synthesis, cell division and renal tubule repair. In contrast, prior treatment with a low dose of DCVC, followed by a high dose led to a sustained stimulation of the renal ERK pathway, renal tubule regeneration and recovery from acute renal failure. These results suggest that a sustained activation of the ERK1/2 pathway may be a key factor in enabling a continued renal tubule repair and hence protection from the progressive phase of DCVC-induced acute renal tubular necrosis in the mouse.

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“…Increased and/or altered expression of growth factors and receptors that regulate ureteric bud (UB) branching and collecting duct elongation in late stages of nephrogenesis (112)(113)(114)(115)(116)(117)(118) and promote tubular regeneration after renal injury (119-124) may play a role in PKD pathogenesis. These include members of the EGF family (EGF, TGF-α, heparin-binding EGF, and amphiregulin), HGF and IGF1, and their tyrosine kinase receptors, ErbB1 to ErbB4, MET, and IGF1R, respectively.…”

Section: Growth Factors/receptors As Targets For Pkd Treatmentmentioning

confidence: 99%

Genetic mechanisms and signaling pathways in autosomal dominant polycystic kidney disease

2014

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Recent advances in defining the genetic mechanisms of disease causation and modification in autosomal dominant polycystic kidney disease (ADPKD) have helped to explain some extreme disease manifestations and other phenotypic variability. Studies of the ADPKD proteins, polycystin-1 and -2, and the development and characterization of animal models that better mimic the human disease, have also helped us to understand pathogenesis and facilitated treatment evaluation. In addition, an improved understanding of aberrant downstream pathways in ADPKD, such as proliferation/secretion-related signaling, energy metabolism, and activated macrophages, in which cAMP and calcium changes may play a role, is leading to the identification of therapeutic targets. Finally, results from recent and ongoing preclinical and clinical trials are greatly improving the prospects for available, effective ADPKD treatments.

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Role of membrane-bound heparin-binding epidermal growth factor-like growth factor (HB-EGF) in renal epithelial cell branching

Cited by 25 publications

References 50 publications

Acute-phase response protein serum amyloid A stimulates renal tubule formation: studies in vitro and in vivo

Acute-phase response protein serum amyloid A stimulates renal tubule formation: studies in vitro and in vivo

Molecular Mechanisms of Renal Tissue Repair in Survival from Acute Renal Tubule Necrosis: Role of ERK1/2 Pathway

Genetic mechanisms and signaling pathways in autosomal dominant polycystic kidney disease

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