Analysis of gene expression profiles reveals the regulatory network of cold‐inducible RNA‐binding protein mediating the growth of BHK‐21 cells

Tang, Cheng; Wang, Yuanwei; Lan, Daoliang; Feng, Xiaohui; Zhu, Xin; Nie, Pin; Yue, Hua

doi:10.1002/cbin.10438

Cited by 16 publications

(10 citation statements)

References 45 publications

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“…This was also suggested by experiments in ref. 60, which found that a specifically cold-sensitive RNA-binding protein influences circadian transcription in mice, as well as prior work examining circadian responses to cold temperatures (61,62).…”

Section: Resultsmentioning

confidence: 88%

Temperature compensation and temperature sensation in the circadian clock

Kidd

Young

Siggia

2015

Proc. Natl. Acad. Sci. U.S.A.

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All known circadian clocks have an endogenous period that is remarkably insensitive to temperature, a property known as temperature compensation, while at the same time being readily entrained by a diurnal temperature oscillation. Although temperature compensation and entrainment are defining features of circadian clocks, their mechanisms remain poorly understood. Most models presume that multiple steps in the circadian cycle are temperature-dependent, thus facilitating temperature entrainment, but then insist that the effect of changes around the cycle sums to zero to enforce temperature compensation. An alternative theory proposes that the circadian oscillator evolved from an adaptive temperature sensor: a gene circuit that responds only to temperature changes. This theory implies that temperature changes should linearly rescale the amplitudes of clock component oscillations but leave phase relationships and shapes unchanged. We show using timeless luciferase reporter measurements and Western blots against TIMELESS protein that this prediction is satisfied by the Drosophila circadian clock. We also review evidence for pathways that couple temperature to the circadian clock, and show previously unidentified evidence for coupling between the Drosophila clock and the heat-shock pathway.circadian clock | temperature compensation | mathematical models C ircadian rhythms are daily oscillations in gene expression and protein concentration that regulate sleep (1, 2), metabolism (3,4), and a host of other biological processes (5-8). Circadian oscillations are known to be present in nearly all animals and plants, as well as some fungi and bacteria (9). In all organisms in which circadian oscillations have been observed, circadian oscillations satisfy three defining properties (10). First, circadian oscillations are self-sustained and spontaneously maintain a period of about 24 h. Second, the circadian rhythm is sensitive to light and temperature and can be synchronized to external oscillations in the quantity of either. Third, the period of the circadian oscillation is "temperature-compensated"; that is, the endogenous period of the oscillation is relatively insensitive to temperature.The genetic basis of circadian clocks has been elucidated in considerable detail over the past two decades, particularly in the fruitfly Drosophila melanogaster, the mouse Mus musculus, and the bread mold Neurospora crassa (11). In Drosophila, a self-sustained circadian oscillation in neurons is generated when a pair of proteins, PERIOD (PER) and TIMELESS (TIM), dimerize and, after some delay, translocate into the nucleus, where the proteins repress their own transcription by inactivating a transcription factor dimer composed of the proteins CLOCK and CYCLE. Light sensitivity is mediated by the blue light photoreceptor CRYPTOCHROME (CRY), which upon activation binds TIMELESS and promotes TIMELESS degradation. A remarkably similar mechanism underlies circadian clocks in mouse and Neurospora. The circadian clock of cyanobacteria has also bee...

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Section: Resultsmentioning

confidence: 88%

Temperature compensation and temperature sensation in the circadian clock

Kidd

Young

Siggia

2015

Proc. Natl. Acad. Sci. U.S.A.

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“…CIRBP, which is the first cold-shock protein identified in mammals, was recently identified as a proinflammatory cytokine (22). As a sensor protein, which expression increases in response to stress, CIRBP plays important roles in tumor recurrence (23,24). A study by Zhang et al (25) has shown that CIRBP plays key roles in hypoxia-induced cell cycle arrest and may be utilized for preventing hypoxia-induced neonatal brain injury.…”

Section: Discussionmentioning

confidence: 99%

CIRBP protects H9C2 cells against myocardial ischemia through inhibition of NF-κB pathway

Long

Jiang

Feng

et al. 2017

Braz J Med Biol Res

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Myocardial ischemia is a major cause of death and remains a disease with extremely deficient clinical therapies and a major problem worldwide. Cold inducible RNA-binding protein (CIRBP) is reported to be involved in multiple pathological processes, including myocardial ischemia. However, the molecular mechanisms of myocardial ischemia remain elusive. Here, we first overexpressed CIRBP by transfection of pc-CIRBP (pcDNA3.1 containing coding sequenced for CIRBP) and silenced CIRBP by transfection of small interfering RNA targeting CIRBP (siCIRBP). pcDNA3.1 and the negative control of siCIRBP (siNC) were transfected into H9C2 cells to act as controls. We then constructed a cell model of myocardial ischemia through culturing cells in serum-free medium with hypoxia in H9C2 cells. Subsequently, AlamarBlue assay, flow cytometry and western blot analysis were used, respectively, to assess cell viability, reactive oxygen species (ROS) level and apoptosis, and expression levels of IκBα, p65 and Bcl-3. We demonstrated that CIRBP overexpression promoted cell proliferation (P<0.001), inhibited cell apoptosis (P<0.05), reduced ROS level (P<0.001), down-regulated phosphorylated levels of IκBα and p65 (P<0.01 or P<0.001), and up-regulated expression of Bcl-3 (P<0.001) in H9C2 cells with myocardial ischemia. The influence of CIRBP knockdown yielded opposite results. Our study revealed that CIRBP could protect H9C2 cells against myocardial ischemia through inhibition of NF-κB pathway.

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“…Previous work has demonstrated that post‐transcriptional biological activities contribute up to 33.15% of the total variation of RNA‐protein correlations (Wu et al, ). Recent in vitro and in vivo RNA binding protein identification studies have enabled us to start in‐depth explorations of the principles governing post‐transcriptional control in regulating important pluripotency factors through identifying their RBPs (Henics et al, ; Tang et al, ).…”

Section: Introductionmentioning

confidence: 99%

Nanog RNA‐binding proteins YBX1 and ILF3 affect pluripotency of embryonic stem cells

Guo

Xue

Yang

et al. 2016

Cell Biology International

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Nanog is a well-known transcription factor that plays a fundamental role in stem cell self-renewal and the maintenance of their pluripotent cell identity. There remains a large data gap with respect to the spectrum of the key pluripotency transcription factors' interaction partners. Limited information is available concerning Nanog-associated RNA-binding proteins (RBPs), and the intrinsic protein-RNA interactions characteristic of the regulatory activities of Nanog. Herein, we used an improved affinity protocol to purify Nanog-interacting RBPs from mouse embryonic stem cells (ESCs), and 49 RBPs of Nanog were identified. Among them, the interaction of YBX1 and ILF3 with Nanog mRNA was further confirmed by in vitro assays, such as Western blot, RNA immunoprecipitation (RIP), and ex vivo methods, such as immunofluorescence staining and fluorescent in situ hybridization (FISH), MS2 in vivo biotin-tagged RNA affinity purification (MS2-BioTRAP). Interestingly, RNAi studies revealed that YBX1 and ILF3 positively affected the expression of Nanog and other pluripotency-related genes. Particularly, downregulation of YBX1 or ILF3 resulted in high expression of mesoderm markers. Thus, a reduction in the expression of YBX1 and ILF3 controls the expression of pluripotency-related genes in ESCs, suggesting their roles in further regulation of the pluripotent state of ESCs.

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Analysis of gene expression profiles reveals the regulatory network of cold‐inducible RNA‐binding protein mediating the growth of BHK‐21 cells

Cited by 16 publications

References 45 publications

Temperature compensation and temperature sensation in the circadian clock

Temperature compensation and temperature sensation in the circadian clock

CIRBP protects H9C2 cells against myocardial ischemia through inhibition of NF-κB pathway

Nanog RNA‐binding proteins YBX1 and ILF3 affect pluripotency of embryonic stem cells

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