Transforming growth factor ? and epidermal growth factor expression in experimental murine polycystic kidney disease

1996 ◽  
Vol 10 (2) ◽  
pp. 181-184
Author(s):  
Malcolm R. Ogborn ◽  
Sanjay Sareen
1998 ◽  
Vol 275 (3) ◽  
pp. F387-F394 ◽  
Author(s):  
William E. Sweeney ◽  
Ellis D. Avner

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.


2021 ◽  
Vol 8 (2) ◽  
pp. 65-73
Author(s):  
Kamila Orzechowska ◽  
SN Muhammad ◽  
H Mokamil

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.


1990 ◽  
Vol 138 (1) ◽  
pp. 225-230 ◽  
Author(s):  
Vincent H. Gattone ◽  
Glen K. Andrews ◽  
Niu Fu-wen ◽  
Laurie J. Chadwick ◽  
Robert M. Klein ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document