Publication: Involvement of endogenous prostaglandin E2 in tubular epithelial regeneration through inhibition
of apoptosis and epithelial-mesenchymal transition in
cisplatin-induced rat renal lesions
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Date
2010
Authors
Yamamoto Emi ; Izawa, Takeshi ; Juniantito, Vetnizah ; Kuwamura, Mitsuru ; Sugiura, Kikuya ; Takeuchi, Tadayoshi
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
In the kidney, prostaglandin (PG) E2 is the
main PG, playing important roles in maintaining
homeostasis or development of pathological settings.
Roles of PGE2 in renal lesions remain to be clarified.
The expression patterns of PGE2 synthesis enzymes such
as cyclooxygenase (COX)-1, COX-2 and microsomal
PGE synthase (mPGES)-1, and PGE2 receptors (EP2 and
EP4) were examined in cisplatin-induced rat renal
failure. The immunoexpressions for COX-1, mPGES-1
and EP4 receptor were increased exclusively in the
affected renal tubules, but those of COX-2 and EP2
receptor were not detected; increased expression of
COX-1 was confirmed at mRNA level. Using rat renal
epithelial cell line (NRK-52E), the effects of PGE2 on
cell proliferation were investigated. The addition of
PGE2 or 11-deoxy-PGE1 (EP4 receptor agonist) to
NRK-52E increased the cell number, indicating the
effects of PGE2 via EP4 receptor. Furthermore, 11-
deoxy-PGE1-treated NRK-52E cells underwent the
G0/G1 arrest and decreased apoptosis. NRK-52E treated
with transforming growth factor (TGF)-ß1, an inducer of
epithelial-mesenchymal transition (EMT), in the
presence of 11-deoxy-PGE1 decreased the mRNA
expression of α-smooth muscle actin (a marker of
myofibroblasts). Collectively, the present study shows
that COX-1 plays more important roles than dose COX-
2 in cisplatin-induced rat renal failure; the product,
PGE2, may regulate renal epithelial regeneration via EP4
receptor through inhibition of apoptosis and EMT.
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