Abstract
Accumulating evidence suggests that long non-coding RNA H19 correlates with several aging processes. However, the role of H19 in aging remains unclear. Many studies have elucidated a close connection between H19 and inflammatory genes. Chronic systemic inflammation is an established factor associated with various diseases during aging. Thus, H19 might participate in the development of age-related diseases by interplay with inflammation and therefore provide a protective function against age-related diseases. We investigated the inflammatory gene network of H19 to understand its regulatory mechanisms. H19 usually controls gene expression by acting as a microRNA sponge, or through mir-675, or by leading various protein complexes to genes at the chromosome level. The regulatory gene network has been intensively studied, whereas the biogenesis of H19 remains largely unknown. This literature review found that the epithelial-mesenchymal transition (EMT) and an imprinting gene network (IGN) might link H19 with inflammation. Evidence indicates that EMT and IGN are also tightly controlled by environmental stress. We propose that H19 is a stress-induced long non-coding RNA. Because environmental stress is a recognized age-related factor, inflammation and H19 might serve as a therapeutic axis to fight against age-related diseases.
Highlights
Aging is characterized by multiple organ malfunctions, and is an inevitable biological process
Oxidative stress-induced loss of imprinting (LOI) of insulin-like growth factor 2 (IGF2) is mediated through nuclear factor kappa B (NFkB) activation, and the binding of NFkB with CCCTC-binding factor (CTCF) indicates that NFkB helps to block CTCF from the H19 DMR [79]
We investigate the inflammatory gene network of H19 to understand its regulatory mechanisms
Summary
Aging is characterized by multiple organ malfunctions, and is an inevitable biological process. Inflammation is associated with age-dependent tumor pathogenesis. Continuous inflammatory responses lead to tumors by inducing cell overgrowth; cancer has been regarded as a wound that never heals. Emerging evidence suggests that inflammation plays critical roles in tissue regeneration by activating cell migration and proliferation or clearing undesired cells. The effect of inflammatory reactions on tissue regeneration can vary depending on pathological stage [5, 6]. Inflammation is immediately initiated by recruiting essential cells and activating aging-related inflammatory factors such as tissue necrosis factor (TNF-a), soluble TNF receptor II (TNFRII), C-reactive protein, interleukin (IL)-6, IL-18, IL-15, and adiponectin [7]. Long non-coding RNA (lncRNA) participates in regulating diverse biological processes, and their roles in aging have recently been focused. This review summarizes the network of H19 that is involved in regulating inflammation and aging
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