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Göteborgs universitets publikationer

Role of JNK activation in pancreatic β-cell death by streptozotocin

Författare och institution:
Hwanju Cheon (-); Jae Min Cho (-); Sunshin Kim (-); Seung-Hoon Baek (-); Moon-Kyu Lee (-); Kwang-Won Kim (-); Seong-Woon Yu (-); Giovanni Solinas (Institutionen för medicin, avdelningen för molekylär och klinisk medicin); Soung Soo Kim (-); Myung-Shik Lee (-)
Publicerad i:
Molecular and Cellular Endocrinology, 321 ( 2 ) s. 131–137
ISSN:
0303-7207
Publikationstyp:
Artikel, refereegranskad vetenskaplig
Publiceringsår:
2010
Språk:
engelska
Fulltextlänk:
Sammanfattning (abstract):
c-Jun N-terminal kinase (JNK) is activated by cellular stress and plays critical roles in diverse types of cell death. However, role of JNK in β-cell injury is obscure. We investigated the role for JNK in streptozotocin (STZ)-induced β-cell death. STZ induced JNK activation in insulinoma or islet cells. JNK inhibitors attenuated insulinoma or islet cell death by STZ. STZ-induced JNK activation was decreased by PARP inhibitors, suggesting that JNK activation is downstream of PARP-1. Phosphatase inhibitors induced activation of JNK and abrogated the suppression of STZ-induced JNK activation by PARP inhibitors, suggesting that the inhibition of phosphatases is involved in the activation of JNK by STZ. STZ induced production of reactive oxygen species (ROS) as potential inhibitors of phosphatases, which was suppressed by PARP inhibitors. PARP-1 siRNA attenuated insulinoma cell death and JNK activation after STZ treatment, which was reversed by MKP (MAP kinase phosphatase)-1 siRNA. These results suggest that JNK is activated by STZ downstream of PARP-1 through inactivation of phosphatases such as MKP, which plays important roles in STZ-induced β-cell death.
Ämne (baseras på Högskoleverkets indelning av forskningsämnen):
MEDICIN OCH HÄLSOVETENSKAP ->
Medicinska grundvetenskaper
Nyckelord:
JNK, beta-cells, Insulin, Diabetes
Postens nummer:
241725
Posten skapad:
2016-09-13 16:13

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