Publication: Gene expression and cell turnover in human renal dysplasia
Authors
Woolf, A.S. ; Winyard, A.J.D.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Kidney malformations are common causes of
chronic renal failure in children. Dysplastic kidneys
represent a unique model of perturbed epithelialmesenchymal
interaction which leads to the formation of
malformed branching tubules surrounded by undifferentiated
and metaplastic mesenchymal cells. We
have found that human dysplastic epithelia express
PAX2 (a transcription factor), BCL2 (a survival factor)
and galectin-3 (a cell adhesionlsignaling molecule).
These genes are implicated in oncogenesis and their
persistent expression may drive proliferation of
dysplastic cysts, hence explaining the massive growth of
some multicystic dysplastic kidneys. We have also
detected prominent apoptosis in undifferentiated tissues
around dysplastic epithelia, and this may provide a
potential mechanism for the well-documented regression
of dysplastic kidneys. Hence, although these kidneys
may not have any excretory function, it is incorrect to
consider them as 'end stage organs' because they are
highly active in terms of cell turnover and gene
expression; furthermore, these processes can be
correlated with patterns of tissue growth and involution.
Further elucidation of 'molecular lesions' in renal
malformations may lead to novel therapies to enhance
the differentiation of progenitor cells.
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