scholarly journals Epidermal growth factor receptor activity mediates renal cyst formation in polycystic kidney disease.

1998 ◽  
Vol 101 (5) ◽  
pp. 935-939 ◽  
Author(s):  
W G Richards ◽  
W E Sweeney ◽  
B K Yoder ◽  
J E Wilkinson ◽  
R P Woychik ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Kidney Disease ◽  
Epidermal Growth Factor ◽  
Polycystic Kidney Disease ◽  
Renal Cyst ◽  
Growth Factor Receptor ◽  
Cyst Formation ◽  
Polycystic Kidney ◽  
Epidermal Growth

scholarly journals Role of epidermal growth factor receptor and microbial infections in polycystic kidney disease

2021 ◽  
Vol 8 (2) ◽  
pp. 65-73
Author(s):  
Kamila Orzechowska ◽  
SN Muhammad ◽  
H Mokamil
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Kidney Disease ◽  
Epidermal Growth Factor ◽  
Polycystic Kidney Disease ◽  
Kinase Inhibitor ◽  
Growth Factor Receptor ◽  
Polycystic Kidney ◽  
Epidermal Growth

Background: Autosomal Dominant Polycystic Kidney Disease (ADPKD) is a frequently inherited diseases associated with the presence of fluid-filled cysts. Epidermal Growth Factor Receptor (EGFR) plays role in cysts development Material and methods: The following tools (PubMed, PubMed Central, Medline Search Engine, Locate and Google Scholar) were used in literature search. Key words used to search for relevant literature are: Polycystic Kidney Disease, Epidermal Growth Factor Receptor, Tyrosine Kinase Inhibitor, Renal Cyst Formation and Renal Cyst Infection. The studies beyond 10 years were not included in present study. Analysis: The cross-examination of research papers allowed to analyse literature around role of EGFR in ADPKD pathophysiology, EGFR TKI as treatment of ADPKD and role of microbial cyst infections in disease progression. Results: There is a small body of literature that look at EGFR, Tyrosine Kinase Inhibitor (TKI) and cyst infection in ADPKD over the last decade. The ‘crosstalk’ between Src and EGFR was observed to have an impact on cyst development and progression. Therefore, the combined treatment with different compounds can be a desirable approach in the treatment of ADPKD. There has been observed relationship between cyst infections, decrease in kidney function and PKD gene mutation. Endotoxins of Gram-negative bacteria could be involved in disease development. Conclusion: The understanding of mechanisms of ADPKD and several cancers has led to the identification of molecular targets, and one of these is EGFR. The further study could establish the role of endotoxin in ADPKD development and its interaction with EGFR.

scholarly journals Functional activity of epidermal growth factor receptors in autosomal recessive polycystic kidney disease

1998 ◽  
Vol 275 (3) ◽  
pp. F387-F394 ◽  
Author(s):  
William E. Sweeney ◽  
Ellis D. Avner
Keyword(s):  
Growth Factor ◽  
Kidney Disease ◽  
Epidermal Growth Factor ◽  
Polycystic Kidney Disease ◽  
Autosomal Recessive ◽  
Apical Surface ◽  
Polycystic Kidney ◽  
High Affinity ◽  
Epidermal Growth

Evidence from a number of laboratories suggests a potential role for the epidermal growth factor (EGF)-transforming growth factor-α-epidermal growth factor receptor (EGF-R) axis in promoting epithelial hyperplasia and cyst formation in autosomal recessive polycystic kidney disease (ARPKD). As previously reported, in the C57BL-6Jcpk/cpk (CPK), BALB/c-bpk/bpk (BPK), and C3H-orpk/orpk (ORPK) murine models of ARPKD, as well as in human ARPKD and human ADPKD, the EGF-R is mislocated to the apical surface of cystic collecting tubule (CT) epithelial cells. The present studies demonstrate that cells from cystic and control CTs can be isolated and that these cells maintain their in vivo EGF-R phenotype in vitro. Domain-specific high-affinity ligand binding was assessed by standard Scatchard analysis, and selective ligand stimulation of apical vs. basolateral EGF-R in these cells was followed by measurement of receptor autophosphorylation and determination of cell proliferation. These studies demonstrate that in vitro apically expressed EGF-Rs exhibit high-affinity binding for EGF, autophosphorylate in response to EGF, and transmit a mitogenic signal when stimulated by the appropriate ligand.

scholarly journals cAMP Regulates Cell Proliferation and Cyst Formation in Autosomal Polycystic Kidney Disease Cells

2000 ◽  
Vol 11 (7) ◽  
pp. 1179-1187 ◽  
Author(s):  
KAZUSHIGE HANAOKA ◽  
WILLIAM B. GUGGINO
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Kidney Disease ◽  
Epidermal Growth Factor ◽  
Fluid Secretion ◽  
Cyst Formation ◽  
Polycystic Kidney ◽  
Epidermal Growth ◽  
Cyst Growth

Abstract. Both epithelial cell proliferation and fluid accumulation are responsible for cyst growth in autosomal dominant polycystic kidney disease (ADPKD). It was previously reported that the cystic fibrosis transmembrane conductance regulator (CFTR) is expressed in cysts from ADPKD patients and suggested that cAMP-stimulated Cl-and fluid secretion occurs through CFTR. The purpose of this study was to investigate the role of cell proliferation in cyst formation in ADPKD and to explore further the role of fluid secretion in cyst growth. Primary cultures both of ADPKD epithelial cells and a mixed population of normal renal epithelial cells isolated from the cortex (HRCE cells) were used. This study tested whether cAMP was involved both in stimulating cell proliferation and formation of cystsin vitro.3H-Thymidine incorporation assays showed that epidermal growth factor stimulated proliferation both in ADPKD cells and HRCE cells. In addition, cAMP stimulated DNA synthesis and cell proliferation in ADPKD, but not HRCE, cells. The effects of cAMP and epidermal growth factor on cell growth in ADPKD cells were additive. cAMP also stimulated cyst enlargement and fluid secretion in ADPKD cells. By contrast, cyst formation and enlargement from HRCE cells occurred without cAMP. Fluid secretion into the cyst lumen was blocked by diphenylamine carboxylic acid (DPC) and glibenclamide in ADPKD cells but blocked only by DPC in HRCE cells. This study showed that ADPKD cells have unique characteristics ; cAMP stimulates fluid secretion and cell proliferation, indicating cAMP plays a very important role in cyst growth during the course of ADPKD.

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