Novel Mechanisms of Reproductive Hormone Action-Novel Mechanisms of Reproductive Hormone Action

Video Transcription

Video Summary

In this video, the speaker discusses the role of estrogen receptor alpha (ER-alpha) in osteoblast mitochondria and its effect on bone mass. Estrogen deficiency at menopause leads to loss of bone mass, or osteoporosis, and the speaker aims to understand how estrogens protect bones. They focus on osteoclasts, which are cells that remove bone matrix, and osteoblasts, which produce new bone. The speaker presents findings showing that estrogen inhibits osteoclast formation within the first 24 hours of culture. They also discuss the role of mitochondria in osteoclasts and how loss of mitochondrial ROS and SIRT3 can attenuate the loss of bone mass caused by estrogen deficiency. The speaker further explains that estrogens promote osteoclast apoptosis through mitochondrial death pathway genes. Estrogens also inhibit complex I activity and basal respiration in osteoclasts, as well as attenuating the interaction of TRAF6 and EXD, a protein involved in complex I assembly. Silencing of EXD impairs the stimulatory effects of RankL on mitochondria function. The speaker highlights the relevance of NAD levels and SIRT3 activity in estrogen's effects on cells, showing that nicotinamide riboside can rescue the decline in cell number caused by estrogen. Overall, the study suggests that estrogen's effects on osteoclasts and bone mass are mediated through ER-alpha and mitochondria function. The video concludes by acknowledging the researchers and funding sources, and the speaker answers questions about the role of reactive oxygen species, the direct effect of estrogen on osteoclast survival, and the effect of estrogen on multinucleation in osteoclasts.

Keywords

estrogen receptor alpha

ER-alpha

osteoblast mitochondria

bone mass

osteoporosis

osteoclasts

osteoblasts

mitochondrial ROS

SIRT3

osteoclast apoptosis

complex I activity

TRAF6

EXD


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