Hypomorphic expression of parathyroid Bmal1 disrupts the internal parathyroid circadian clock and increases parathyroid cell proliferation in response to uremia
Søren Egstrand, Maria L. Mace, Marya Morevati, Anders Nordholm, Lars H. Engelholm, Jesper Skovhus Thomsen, Annemarie Brüel, Tally Naveh‐Many, Yuliu Guo, Klaus Ølgaard, Ewa Lewin
Abstract
ircadian rhythms in activity, metabolism, hormone secretion, and cell cycle are maintained by a molecular circadian clock (CC) to anticipate the daily recurrent changes of conditions such as light-dark cycle and food availability. In mammals, the primary circadian pacemaker is the CC in the suprachiasmatic nucleus of the hypothalamus from where circadian regulation is conveyed via neural, endocrine, and metabolic pathways. In addition to this central pacemaker, a CC has been demonstrated in some peripheral tissues, and we have for the first time recently shown that a CC operates in parathyroid glands (PTGs). 2 Both central and peripheral CCs consist of the same set of circadian regulator genes and proteins, which are working in conjunction,