Viral Infection‐Induced Differential Expression of Lnc<scp>RNA</scp>s Associated with Collagen in Mouse Placentas and Amniotic Sacs

Pan, Jing; Mor, Gil; Ju, Weina; Zhong, Julia Li; Luo, Xian; Aldo, Paulomi; Zhong, Ming; Yu, Yang; Jenkins, Edmund C.; Brown, W. Ted; Zhong, Nanbert

doi:10.1111/aji.12406

Cited by 6 publications

(9 citation statements)

References 65 publications

(93 reference statements)

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“…In our previous study, lncRNAs that are differentially expressed in human placentas delivered from PPROM and sPTL were found to be involved in more than 20 functional pathways (Luo et al, 2013). The patterns of differentially expressed lncRNAs and pathways identified from placentas of PPROM and sPTL were similar to those we observed in our study of human miscarriages (Wang et al, 2014) and of a viral-infected mouse model (Pan et al, 2015), suggesting that deregulation and dysfunction of the ubiquitin-proteasome-collagen (CUP) pathway may be one of the pathogenic mechanisms underlying the adverse outcomes of pregnancies, including PPROM.…”

Section: Introductionsupporting

confidence: 86%

“…The current study is a continuing investigation of the regulatory role of lncRNAs in the molecular pathogenesis of sPTB, based on our previous studies, in which we identified differential expression of lncRNAs in sPTL and PPROM (Luo et al, 2013; Pan et al, 2015). In the current study, we analyzed the DEPs of the lncRNAs and the mRNAs that are associated with the CUP pathway that may also associate with PPROM (Zhong et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

“…qRT-PCR was employed for validation, as reported earlier (Luo et al, 2013; Wang et al, 2014; Pan et al, 2015). In the discovery study, fold changes >2 and p < 0.05 were set as cut-offs and were considered significant.…”

Section: Methodsmentioning

confidence: 99%

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Ubiquitin-Proteasome-Collagen (CUP) Pathway in Preterm Premature Rupture of Fetal Membranes

et al. 2017

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Spontaneous preterm birth (sPTB) occurs before 37 gestational weeks, with preterm premature rupture of the membranes (PPROM) and spontaneous preterm labor (sPTL) as the predominant adverse outcomes. Previously, we identified altered expression of long non-coding RNAs (lncRNAs) and message RNAs (mRNAs) related to the ubiquitin proteasome system (UPS) in human placentas following pregnancy loss and PTB. We therefore hypothesized that similar mechanisms might underlie PPROM. In the current study, nine pairs of ubiquitin-proteasome-collagen (CUP) pathway–related mRNAs and associated lncRNAs were found to be differentially expressed in PPROM and sPTL. Pathway analysis showed that the functions of their protein products were inter-connected by ring finger protein. Twenty variants including five mutations were identified in CUP-related genes in sPTL samples. Copy number variations were found in COL19A1, COL28A1, COL5A1, and UBAP2 of sPTL samples. The results reinforced our previous findings and indicated the association of the CUP pathway with the development of sPTL and PPROM. This association was due not only to the genetic variation, but also to the epigenetic regulatory function of lncRNAs. Furthermore, the findings suggested that the loss of collagen content in PPROM could result from degradation and/or suppressed expression of collagens.

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Section: Introductionsupporting

confidence: 86%

Section: Discussionmentioning

confidence: 99%

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Ubiquitin-Proteasome-Collagen (CUP) Pathway in Preterm Premature Rupture of Fetal Membranes

et al. 2017

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“…On the other hand, novel mechanisms in the pathogenesis of PPROM suggest the initiation of additional new research. Furthermore, our data has shown that lncRNAs associated with collagen, MMP, proteasome 26S, and ubiquitin specific peptidase were differentially expressed in placentas and amniochorionic membranes of HMV68 viral infected mice, compared to non-infected, which further indicated that there is a closed link to infection, UPS, collagen and membrane rupture [141]. Therefore, combined with the reviewed data above, a novel molecular pathogenesis of PPROM may be concluded that UPS-related lncRNAs are triggered by infection and inflammation in PPROM, which regulate intracellular and/or extracellular UPS systems to control the content of collagens in ECM, and finally result in occurrence of PPROM for the ECM degradation in fetal membrane.…”

Section: The Possible Connection Between Ups and Pprommentioning

confidence: 63%

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

Wang¹

2015

Adv Genet Eng

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“…25 Our earlier studies have demonstrated that transcripts including coding and long non-coding RNAs involved in the pathogenic pathway of cytokine and chemokine receptor interactions were differentially expressed and associated with early miscarriages and late preterm birth. [26][27][28][29][30] As a result, we proposed that the epigenetic regulation of the chemokine-cytokine pathway could present a common epi-pathogenic mechanism associated with variant adverse outcomes of pregnancy. 31…”

Section: Pathogenic Mechanismmentioning

confidence: 99%

Transcriptomics‐determined chemokine‐cytokine pathway presents a common pathogenic mechanism in pregnancy loss and spontaneous preterm birth

Wang

Pan

Tian

et al. 2021

American J Rep Immunol

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Problem: Various etiological factors, such as infection and inflammation, may induce the adverse outcomes of pregnancy of miscarriage, stillbirth, or preterm birth. The pathogenic mechanisms associated with these adverse pregnancies are yet unclear.We hypothesized that a common pathogenic mechanism may underlie variant adverse outcomes of pregnancy, which are induced by genetic-environmental factors. The specific objective of the current study is to uncover the common molecular mechanism(s) by identifying the specific transcripts that are present in variant subtypes of pregnancy loss and preterm birth. Method of Study:Transcriptomic profiling was performed with RNA expression microarray or RNA sequencing of placentas derived from pregnancy loss (which includes spontaneous miscarriage, recurrent miscarriage, and stillbirth) and spontaneous preterm birth, followed by bioinformatic analysis of multi-omic integration to identify pathogenic molecules and pathways involved in pathological pregnancies. Results:The enrichment of common differentially expressed genes between fullterm birth and preterm birth and pregnancy loss of miscarriage and stillbirth revealed different pathophysiological pathway(s), including cytokine signaling dysregulated in spontaneous preterm birth, defense response, graft-versus-host disease, antigen processing and presentation, and T help cell differentiation in spontaneous miscarriage. Thirty-three genes shared between spontaneous preterm birth and spontaneous miscarriage were engaged in pathways of interferon gamma-mediated signaling and of antigen processing and presentation. For spontaneous miscarriage, immune response was enriched in the fetal tissue of chorionic villi and in the maternal facet of the placental sac. The transcript of nerve growth factor receptor was identified as the common molecule that is differentially expressed in all adverse pregnancies: spontaneous preterm birth, stillbirth, spontaneous miscarriage, and recurrent miscarriage.Superoxide dismutase 2 was up-regulated in all adverse outcomes of pregnancy except for recurrent miscarriage. Cytokine-cytokine receptor interaction was the common pathway in spontaneous preterm birth and spontaneous miscarriage. Defense How to cite this article: Wang P, Pan J, Tian X, et al.Transcriptomics-determined chemokine-cytokine pathway presents a common pathogenic mechanism in pregnancy loss and spontaneous preterm birth. Am J Reprod Immunol.

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Viral Infection‐Induced Differential Expression of LncRNAs Associated with Collagen in Mouse Placentas and Amniotic Sacs

Abstract: 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.

Cited by 6 publications

References 65 publications

Ubiquitin-Proteasome-Collagen (CUP) Pathway in Preterm Premature Rupture of Fetal Membranes

Ubiquitin-Proteasome-Collagen (CUP) Pathway in Preterm Premature Rupture of Fetal Membranes

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

Transcriptomics‐determined chemokine‐cytokine pathway presents a common pathogenic mechanism in pregnancy loss and spontaneous preterm birth

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