Redox activation of JNK2α2 mediates thyroid hormone-stimulated proliferation of neonatal murine cardiomyocytes.

ABSTRACT: Mitochondria-generated reactive oxygen species (mROS) are frequently associated with DNA damage and cell cycle arrest, but physiological increases in mROS serve to regulate specific cell functions. T3 is a major regulator of mROS, including hydrogen peroxide (H₂O₂). Here we show that exogenous thyroid hormone (T3) administration increases cardiomyocyte numbers in neonatal murine hearts. The mechanism involves signaling by mitochondria-generated H₂O₂ (mH₂O₂) acting via the redox sensor, peroxiredoxin-1, a thiol peroxidase with high reactivity towards H₂O₂ that activates c-Jun N-terminal kinase-2α2 (JNK2α2). JNK2α2, a relatively rare member of the JNK family of mitogen-activated protein kinases (MAPK), ph

SUBMITTER: Tan L 

PROVIDER: S-EPMC6881338 | biostudies-literature | 2019 Nov

REPOSITORIES: biostudies-literature