Abstract
Preterm Premature Rupture of the Fetal Membranes (PPROM) is a reproductive system disorder and a major cause of prematurity. Several major etiologic factors have been linked to PPROM, one of which is the weakness of the amniochorion Extra Cellular Matrix (ECM) caused by collagen degradation. With increasingly deeper research studies on the human genome, rapidly growing evidence has suggested that abnormally expressed non-coding RNAs (ncRNAs) are involved with multiple diseases. Among various ncRNAs, the long non-coding RNAs (lncRNAs) have attracted more attention and were found to correlate with various inflammation-related conditions or diseases. Recent studies demonstrated that lncRNAs might be involved in regulation of the ubiquitin proteasome system (UPS) in PPROM. The UPS is an ATP-dependent enzyme process that targets substrate proteins, tagged with an isopeptide chain composed of covalently linked molecules of ubiquitin, for degradation by the 26S proteasome, and deeply involved in the regulation of most basic cellular processes. Here, we reviewed the UPS system, the collagen in extracellular matrix (ECM), the PPROM as well as lncRNAs. We hypothesize that a novel pathogenic pathway of “infection/inflammation lncRNA, UPS, collagen, membrane rupture” for exploring the molecular pathogenesis of PPROM
Highlights
Preterm Premature Rupture of the fetal Membranes (PPROM) is a reproductive system disorder, which is the major cause of prematurity [1]
Several major etiologic factors have been linked to PPROM, one of which is the weakness of the amniochorion Extra Cellular Matrix (ECM) caused by collagen degradation
The host inflammatory response initiated by bacteria or bacterial components (LPS) activates ECM collagen-specific matrix metalloproteinases (MMPs) that lead to ECM degradation through degrading collagens in ECM, predisposing the fetal membrane to rupture [56]
Summary
Preterm Premature Rupture of the fetal Membranes (PPROM) is a reproductive system disorder, which is the major cause of prematurity [1]. Through the degradation mechanism above, UPS could be involved in various cellular processes, such as regulation of gene expression [24], protein cell cycle control [25], regulation of signal transduction [26,27], and mitochondrial intermembrane function [28].
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