Jing Pan1, Gil Mor2, Weina Ju3, Julia Zhong4, Xiucui Luo1, Paulomi Bole Aldo2, Mei Zhong5, Yanhong Yu5, Edmund C Jenkins3, William T Brown3, Nanbert Zhong1,3. 1. Center of Translational Medicine for Maternal and Children's Health, Lianyungang Maternal and Children's Hospital, Lianyungang, Jiangsu, China. 2. Department of Obstetrics Gynecology and Reproductive Sciences, Reproductive Immunology Unit, School of Medicine, Yale University, New Haven, CT, USA. 3. Department of Human Genetics, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY, USA. 4. Hunter College High School, New York, NY, USA. 5. Department of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Abstract
PROBLEM: We have previously determined that long non-coding RNAs (lncRNAs) are differentially expressed in preterm premature rupture of membranes (PPROM) and hypothesized that the collagenolysis ubiquitin-proteasome system may be activated by infection and inflammation. However, direct evidence of the involvement of lncRNAs in transcriptional and posttranscriptional regulation of the infection-triggered alteration of collagen is lacking. METHOD OF STUDY: A previously developed mouse model with MHV68 viral infection was assessed to determine whether viral infection may induce differential expression of lncRNAs in mouse placentas and amniotic sacs. RESULTS: Differential expression of lncRNAs that are associated with collagen was found in HMV68 viral-infected, compared to non-infected, mouse placentas and amniotic sacs. Differential expression of messenger RNAs (mRNAs) of collagen was also documented. CONCLUSIONS: Our data demonstrate, for the first time, that viral infection may induce the differential expression of lncRNAs that are associated with collagen. Based on this finding, we propose that lncRNA may have involved in regulating of infection-induced collagen transcription.
PROBLEM: We have previously determined that long non-coding RNAs (lncRNAs) are differentially expressed in preterm premature rupture of membranes (PPROM) and hypothesized that the collagenolysis ubiquitin-proteasome system may be activated by infection and inflammation. However, direct evidence of the involvement of lncRNAs in transcriptional and posttranscriptional regulation of the infection-triggered alteration of collagen is lacking. METHOD OF STUDY: A previously developed mouse model with MHV68viral infection was assessed to determine whether viral infection may induce differential expression of lncRNAs in mouse placentas and amniotic sacs. RESULTS: Differential expression of lncRNAs that are associated with collagen was found in HMV68 viral-infected, compared to non-infected, mouse placentas and amniotic sacs. Differential expression of messenger RNAs (mRNAs) of collagen was also documented. CONCLUSIONS: Our data demonstrate, for the first time, that viral infection may induce the differential expression of lncRNAs that are associated with collagen. Based on this finding, we propose that lncRNA may have involved in regulating of infection-induced collagen transcription.