Thioredoxins (Trxs) are a class of small molecular redox proteins that play an important role in
scavenging abnormally accumulated reactive oxygen species (ROS). Thioredoxin 2 (Trx2) is one member of
this family located in mitochondria. Trx2 protects cells from increased oxidative stress and has anti-apoptosis
function. Knockout of Trx2 in mice led to early embryonic lethality. However, the essential role of Trx2 during
embryogenesis remains unclear. To further investigate the role of Trx2 during embryonic development, we
performed Trx2 knockdown in zebrafish and investigated the regulation role of Trx2 during embryonic
development. Our results indicate that Trx2 had a high expression in early zebrafish embryos and its
knockdown in zebrafish led to defective liver development mainly due to increased hepatic cell death. The
increased ROS and the imbalance of members of the Bcl-2 family were involved in cell death induced by Trx2
suppression in zebrafish. The dysregulation of Bax, puma and Bcl-xl promoted the reduction of mitochondrial
trans-membrane potential and the mitochondria membrane permeabilization (MMP), which initiated the
mitochondrial apoptosis pathway. Additionally, we found that the increase of relocated GAPDH in mitochondria
may be another factor responsible for the mitochondrial catastrophe.
Keywords: Apoptosis, Bcl-2 family, liver morphogenesis, MPP, Trx2, zebrafish.
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