scholarly journals Is There a Link between Orcadian Clock Protein PERIOD 3 (PER3) (rs57875989) Variant and the Severity of COVID-19 Infection?

2021 ◽  
Author(s):  
Gozde Yesil Sayin ◽  
Sacide Pehlivan ◽  
Istemi Serin ◽  
Alpay Medetalibeyoglu ◽  
Murat Kose ◽  
...  
Keyword(s):  
Clock Protein

scholarly journals Alteration of circadian machinery in monocytes underlies chronic kidney disease-associated cardiac inflammation and fibrosis

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yuya Yoshida ◽  
Naoya Matsunaga ◽  
Takaharu Nakao ◽  
Kengo Hamamura ◽  
Hideaki Kondo ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Clock Genes ◽  
Serum Levels ◽  
Serum Retinol ◽  
Cardiac Inflammation ◽  
Physiological Processes ◽  
G Protein Coupled ◽  
Clock Protein

AbstractDysfunction of the circadian clock has been implicated in the pathogenesis of cardiovascular disease. The CLOCK protein is a core molecular component of the circadian oscillator, so that mice with a mutated Clock gene (Clk/Clk) exhibit abnormal rhythms in numerous physiological processes. However, here we report that chronic kidney disease (CKD)-induced cardiac inflammation and fibrosis are attenuated in Clk/Clk mice even though they have high blood pressure and increased serum angiotensin II levels. A search for the underlying cause of the attenuation of heart disorder in Clk/Clk mice with 5/6 nephrectomy (5/6Nx) led to identification of the monocytic expression of G protein-coupled receptor 68 (GPR68) as a risk factor of CKD-induced inflammation and fibrosis of heart. 5/6Nx induces the expression of GPR68 in circulating monocytes via altered CLOCK activation by increasing serum levels of retinol and its binding protein (RBP4). The high-GPR68-expressing monocytes have increased potential for producing inflammatory cytokines, and their cardiac infiltration under CKD conditions exacerbates inflammation and fibrosis of heart. Serum retinol and RBP4 levels in CKD patients are also sufficient to induce the expression of GPR68 in human monocytes. Our present study reveals an uncovered role of monocytic clock genes in CKD-induced heart failure.

Rhythmic post-transcriptional regulation of the circadian clock protein mPER2 in mammalian cells: A real-time analysis

2006 ◽  
Vol 401 (1-2) ◽  
pp. 44-48 ◽  
Author(s):  
Keigo Nishii ◽  
Iori Yamanaka ◽  
Maya Yasuda ◽  
Yota B. Kiyohara ◽  
Yoko Kitayama ◽  
...  
Keyword(s):  
Transcriptional Regulation ◽  
Circadian Clock ◽  
Real Time ◽  
Mammalian Cells ◽  
Time Analysis ◽  
Real Time Analysis ◽  
Post Transcriptional Regulation ◽  
Clock Protein

scholarly journals The Circadian Clock Protein BMAL1 Is Necessary for Fertility and Proper Testosterone Production in Mice

2008 ◽  
Vol 23 (1) ◽  
pp. 26-36 ◽  
Author(s):  
J.D. Alvarez ◽  
Amanda Hansen ◽  
Teri Ord ◽  
Piotr Bebas ◽  
Patrick E. Chappell ◽  
...  
Keyword(s):  
Circadian Clock ◽  
Testosterone Production ◽  
Clock Protein

Changes of Blood Pressure Rhythm and Clock Protein Expression Levels in Spontaneously Hypertensive Rats After Ischemia-Reperfusion

2021 ◽  
Author(s):  
Jing Jin ◽  
Yumeng Liu ◽  
Jing Huang ◽  
Dong Zhang ◽  
Jian Ge ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Protein Expression ◽  
Circadian Clock ◽  
Spontaneously Hypertensive Rats ◽  
Ischemia Reperfusion ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Expression Levels ◽  
The Relationship ◽  
Clock Protein

Abstract Objective A variety of circadian patterns of blood pressure after ischemic stroke in patients with essential hypertension appear to be a potential risk of stroke recurrence, but the mechanism is still unclear. This study intends to reveal the changes in blood pressure rhythm and circadian clock protein expression levels in spontaneously hypertensive rats (SHR) after ischemia-reperfusion, and the relationship between the two. Methods Using the SHR middle cerebral artery occlusion experimental model, the systolic blood pressure was continuously monitored for 24 hours after the operation to observe the blood pressure rhythm. The rat tail vein blood was taken every 3h, and the serum CLOCK, BMAL1, PER1 and CRY1 protein expression levels were detected by Elisa. Pearson correlation analysis counted the relationship between SHR blood pressure rhythm and circadian clock protein fluctuation after ischemia-reperfusion. Results The proportion of abnormal blood pressure patterns in the SHR + tMCAO group was significantly higher than that in the SHR group, the serum CLOCK expression was relatively constant, and the circadian rhythm of BMAL1, PER1 and CRY1 protein expression changed significantly. Pearson analysis showed that PER1 protein level was negatively correlated with dipper (r = -0.565, P = 0.002) and extreme-dipper (r = -0.531, P = 0.001) blood pressure, and was significantly positively correlated with non-dipper blood pressure (r = 0.620, P < 0.001). Conclusion The rhythm pattern of blood pressure after ischemia-reperfusion in SHR is obviously disordered, and it is closely related to the regulation of Per1 gene.

scholarly journals Incidence of primary graft dysfunction after lung transplantation is altered by timing of allograft implantation

Thorax ◽  
2018 ◽  
Vol 74 (4) ◽  
pp. 413-416 ◽  
Author(s):  
Peter S Cunningham ◽  
Robert Maidstone ◽  
Hannah J Durrington ◽  
Rajamayier V Venkateswaran ◽  
Marcelo Cypel ◽  
...  
Keyword(s):  
Cohort Studies ◽  
Lung Transplantation ◽  
Organ Preservation ◽  
Retrospective Cohort ◽  
Circadian Regulation ◽  
Primary Graft Dysfunction ◽  
Graft Dysfunction ◽  
Donor Lung ◽  
Retrospective Cohort Studies ◽  
Clock Protein

The importance of circadian factors in managing patients is poorly understood. We present two retrospective cohort studies showing that lungs reperfused between 4 and 8 AM have a higher incidence (OR 1.12; 95% CI 1.03 to 1.21; p=0.01) of primary graft dysfunction (PGD) in the first 72 hours after transplantation. Cooling of the donor lung, occurring during organ preservation, shifts the donor circadian clock causing desynchrony with the recipient. The clock protein REV-ERBα directly regulates PGD biomarkers explaining this circadian regulation while also allowing them to be manipulated with synthetic REV-ERB ligands.

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