Study of endoplasmatic reticulum stress-related proteins in the maternal pancreatic islets remodeling during the peripartum / Estudo da expressão das proteínas envolvidas no estresse de retículo endoplasmático durante o remodelamento das ilhotas pancreáticas maternas no período perinatal

AUTOR(ES)
DATA DE PUBLICAÇÃO

2009

RESUMO

During gestation occurs increase on the proliferation and apoptosis reduction of pancreatic b cells. Prolactin (PRL) promotes these changes which are reverted after delivery. Dexametasone (DEX) in vitro opposed to PRL. We evaluate whether endoplasmatic reticulum stress (ERS) was involved on post-delivery apoptosis and glycocorticoids (GC) participate on this mechanism. DNA fragmentation increased on the 3rd day post-delivery (L3), in parallel with pAKT diminution and inductor of apoptosis-TRB3 augment by ERS. BiP, ATF4, CHOP along with binding of CHOP and CHOP-ATF4 to the TRB3 promoter increased in L3. ERS inhibitor-PBA restored pAKT, CHOP levels and inhibited apoptosis. RINm5F cells with DEX (24h) showed increase in BiP, ATF4, p-eIF2 and in active XBP-1. DEX induced TRB3, but inhibited the binding of CHOP to TRB3. The 72h treatment did not alter p-eIF2a, diminished active XBP-1 and promoted apoptosis; the unique event reverted by PRL. We concluded that apoptosis of islets in L3 is generated by ERS; nevertheless this mechanism is not induced by GC.

ASSUNTO(S)

glicocorticóides pregnancy apoptose pancreatic islets endoplasmic reticulum stress estresse do retículo endoplasmático apoptosis lactation lactação ilhotas pancreáticas gravidez glucocorticoids

ACESSO AO ARTIGO

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