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Advancements in Genetic Engineering
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Research Article

Long Non-Coding RNAs, Ubiquitin Proteasome System, Collagen Degradation and Preterm Premature Rupture of Membrane

Nanbert Zhong1,2*, Leilei Wang2, Xiucui Luo2 and Jing Pan2
1New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY, USA
2Center of Translational Medicine for Maternal and Children’s Health, Lianyungang Maternal and Children’s Hospital, Lianyungang, Jiangsu, China
Corresponding Author : Nanbert Zhong
Department of Human Genetics
New York State Institute for Basic Research in Developmental Disabilities
1050 Forest Hill Road, Staten Island, NY 10314, USA
Tel: 7184945242/4882
E-mail: [email protected]
Received November 07, 2014; Accepted February 11, 2015; Published February 13, 2015
Citation: Zhong N, Wang L, Luo X, Pan J (2015) Long Non-Coding RNAs, Ubiquitin Proteasome System, Collagen Degradation and Preterm Premature Rupture of Membrane. Adv Genet Eng 3:117. doi:10.4172/2169-0111.1000117
Copyright: © 2015 Zhong N, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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

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