Abstract
Circadian oscillations are regulated at both central and peripheral levels to maintain physiological homeostasis. The central circadian clock consists of a central pacemaker in the suprachiasmatic nucleus that is entrained by light dark cycles and this, in turn, synchronizes the peripheral clock inherent in other organs. Circadian dysregulation has been attributed to dysregulation of peripheral clock and also associated with several diseases. Components of the molecular clock are disrupted in lung diseases like chronic obstructive pulmonary disease (COPD), asthma and IPF. Airway epithelial cells play an important role in temporally organizing magnitude of immune response, DNA damage response and acute airway inflammation. Non-coding RNAs play an important role in regulation of molecular clock and in turn are also regulated by clock components. Dysregulation of these non-coding RNAs have been shown to impact the expression of core clock genes as well as clock output genes in many organs. However, no studies have currently looked at the potential impact of these non-coding RNAs on lung molecular clock. This review focuses on the ways how these non-coding RNAs regulate and in turn are regulated by the lung molecular clock and its potential impact on lung diseases.
Highlights
The physiology and behavior of mammals are subject to daily oscillations driven by an endogenous circadian clock that consists of a central pacemaker in the brain’s suprachiasmatic nucleus (SCN)
Our results have shown that TGF-β1 a cytokine upregulated in smokers and chronic obstructive pulmonary disease (COPD) patients alters the bronchial epithelial microRNAome [7]
Peripheral clocks play an important role in maintaining organ homeostasis; disruption of the peripheral clock can lead to disease states
Summary
The physiology and behavior of mammals are subject to daily oscillations driven by an endogenous circadian clock that consists of a central pacemaker in the brain’s suprachiasmatic nucleus (SCN). While most physiological processes were ‘driven’ by neural and hormonal output signals from the ‘central’ clock’, the discovery of ‘peripheral’ clocks within every tissue and organ of the body has provided a focus towards understanding the link between circadian disruption and diseases [5]. Other prominent ncRNAs involved in gene health and disease include long ncRNAs and small nucleolar RNAs (snoRNAs). NcRNAs play distinct roles in clock physiology They are involved in regulation of core clock genes and clock output genes. Our results have shown that TGF-β1 a cytokine upregulated in smokers and COPD patients alters the bronchial epithelial microRNAome [7] Some of these miRNAs are directly involved in regulating clock genes. This review discusses the reports of ncRNA mediated clock gene dysfunction observed in other tissues and its implications in lung diseases
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