The mortality of MOP3 deficient mice with a systemic functional failure
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Published on: January 27, 2019
Yimin Sun1, Zhihui Yang, Zeqing Niu
1Department of Surgery, University of Nebrasaka Medical Center, Omaha, NE 68131-5805, USA.
Abstract:
MOP3 (also known as BMAL1), a master regulator of circadian rhythm, plays important roles in the regulation of cell differentiation and general physical functions. In the present studies, MOP3 deficient mice had significantly reduced body weight and showed remarkable mortality around six months of age. The levels of AST, ALT, BUN, or UREA in the blood of about four month-old MOP3(-/-) mice were significantly higher than MOP3(+/-) or MOP3(+/+) littermates. However, no apparent pathological changes in the livers, hearts, lungs or kidneys of about four month-old MOP3(-/-) mice were observed. In addition, altered levels of white blood cells, lymphocytes, and platelets in peripheral blood of MOP3(-/-)mice were detected. The results presented herein with MOP3-deficient mice offered the basic principle for the essential roles of MOP3 in keeping normal survival abilities in mice. This study may have significant clinical impacts on the consideration about the abnormality of circadian rhythms and sleeping disorders caused physical and metabolism dysfunctions as well as the mortality.
Insights
Mice lacking the circadian rhythm regulator MOP3 (BMAL1) experienced reduced body weight, increased mortality, and altered blood cell counts. This highlights MOP3
Area of Science:
- Chronobiology
- Molecular Biology
- Physiology
Background:
- The circadian rhythm master regulator MOP3 (BMAL1) is crucial for physiological functions.
- Its role in maintaining normal survival and metabolic homeostasis requires further elucidation.
Purpose of the Study:
- To investigate the physiological consequences of MOP3 deficiency in mice.
- To assess the impact of MOP3 on survival, body weight, and blood parameters.
Main Methods:
- Generation and analysis of MOP3-deficient (MOP3(-/-)) mice.
- Monitoring of body weight, mortality rates, and blood biochemical markers (AST, ALT, BUN, UREA).
- Hematological analysis of peripheral blood components (white blood cells, lymphocytes, platelets).
Main Results:
- MOP3(-/-) mice exhibited significantly reduced body weight and increased mortality around six months of age.
- Elevated levels of AST, ALT, BUN, and UREA were observed in MOP3(-/-) mice compared to controls.
- Alterations in white blood cell, lymphocyte, and platelet counts were detected in MOP3-deficient mice, despite no apparent organ pathology.
Conclusions:
- MOP3 is essential for maintaining normal survival and physiological functions in mice.
- MOP3 deficiency leads to metabolic and hematological dysfunctions.
- These findings underscore the clinical relevance of circadian rhythm abnormalities in metabolic disorders and mortality.
