Rabbit Anti-Human BMAL1 (Acetyl Lys538) (a.a. 501-550) Polyclonal antibody

Recent research has shown expression of clock genes in peripheral tissue explants, targeting multiple pathways leading to the entrainment of circadian rhythms. Temporal variations are not solely regulated by photoperiod, but factors such as maternal feed availability can entrain fetal circadian clock. Currently, a paucity of information exists for clock gene expression and short-term temporal transcript abundance in the bovine placenta, which is essential for proper offspring development. Therefore, the objective of this study was to determine the effect of early to mid-gestational nutrient restriction on clock genes, angiogenic factors, and nutrient sensing genes mRNA transcript abundance in placental explants during a 24 h period. Placentomes from adequately fed and nutrient restricted heifers were collected via Cesarean section at day 180 of gestation; separated into caruncular and cotyledonary tissue and placed in culture media for a 24 h period. The mRNA transcript abundance of clock genes (ARNTL, CRY1, and PER2), angiogenic factors (HIF1A and VEGFA), and nutrient sensing genes (NAMPT and NR3C1) was determined every 4 h. Clock genes were expressed in caruncular and cotyledonary explant tissue. The caruncular explant transcript abundance of the clock genes was not influenced by time (P > 0.05); while ARNTL abundance decreased over time in the cotyledon explant (P < 0.05). A main effect of time was observed for HIF1A, VEGFA, and NR3C1 in the caruncular tissue (P < 0.05). Although, angiogenic factors and nutrient sensing genes in cotyledonary tissue displayed evident temporal variation in transcript abundance (P < 0.05). Nutrient restriction did not alter (P > 0.15) mRNA transcript abundance of clock genes, angiogenic factors, or nutrient sensing genes in either caruncular or cotyledonary tissue. Interestingly, these data may indicate limited transmission and synchronization of maternal and fetal temporal variations in transcript abundance. These findings demonstrate that multiple timepoint collections are needed in future studies due to the innate existence of temporal oscillations observed in the bovine placenta. (C) 2020 Elsevier Inc. All rights reserved.

Objectives Treatment with angiotensin converting enzyme (ACE)-inhibitors favorably affects glucose metabolism and the development of diabetes mellitus by largely elusive mechanisms. To identify these mechanisms, we studied the effect of ACE-inhibition on gene expression in skeletal muscle, a primary target tissue for insulin in glucose homeostasis. Methods A subject-blinded and analyst-blinded, placebo-controlled study was conducted in nine healthy men. Two consecutive muscle biopsies were conducted before and 9 h after a single dose of either 10-mg ramipril (n = 6) or placebo (n = 3), (randomly allocated). Muscle ribonucleic acid was subjected to transcriptome profiling. Results In both ramipril-treated or placebo-treated individuals, the majority of genes with differential expression between the two time points belonged to the family of diurnally regulated genes, such as the NR1D1 and NR1D2 genes (nuclear receptor subfamily 1, group D, members 1 and 2) or members of the period homolog family (PER1-3). Ramipril significantly modulated the expression of other diurnally regulated genes, such as aryl hydrocarbon receptor nuclear translocator-like (ARNTL), encoding aryl hydrocarbon receptor nuclear translocator-like, a core component of the circadian clock (P = 0.02). Concomitant attenuation of NR1D1 downregulation (- 2.4-fold compared with - 4.1-fold in placebo; P = 0.04), a transcriptional repressor of ARNTL, supported the view that ramipril might modulate glucose homeostasis pathways involving the NR1D1 ARNTL axis. Conclusion As circadian rhythms are deranged in patients who are diabetic, modulated expression of circadian clock genes by ramipril could explain the favorable metabolic effects of therapeutic ACE-inhibition. Pharmacogenetics and Genomics 21:751-759 (C) 2011 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.