Project description:Background: Long non-coding RNAs (lncRNAs) are an important class of pervasive genes involved in a variety of biological functions. They are aberrantly expressed in many types of diseases. We want to study the lncRNAs profiles in preeclampsia. Preeclampsia has been observed in patients with molar pregnancy where a fetus is absent demonstrating that the placenta is sufficient to cause the condition. So we analyze the lncRNAs profiles in preeclampsia placentas. In this study, we described the lncRNAs profiles in 6 preeclampsia placentas (T) and 5 matched normal pregnancy placentas (N) tissues by microarray. Methodology/Principal Findings: With abundant and varied probes accounting 33,045 LncRNAs in our microarray, the number of lncRNAs that expressed at a certain level could be detected is 28,443. From the data we found there were 738 lncRNAs that differentially expressed (M-bM-^IM-%1.5 fold-change) among preeclampsia placentas compared with matched controls. Up to 18,063 coding transcripts could be detected in placenta samples through 30,215 coding transcripts probes. Coding-non-coding gene co-expression networks (CNC network) were constructed based on the correlation analysis between the differential expressed lncRNAs and mRNAs. According to the GO-Pathway analysis of differential expressed lncRNAs/mRNAs, we choose three lncRNAs to analyze the relationship between lncRNAs and preeclampsia. LOC391533, LOC284100, CEACAMP8 were evaluated by qPCR in 40 of preeclampsia placentas and 40 of controls. The results showed three lncRNAs were aberrantly expressed in preeclampsia placentas compared with controls. Conclusions/Significance: Our study is the first one to determine genome-wide lncRNAs expression patterns in preeclampsia placenta by microarray. The results displayed that clusters of lncRNAs were aberrantly expressed in preeclampsia placenta compared with controls, which revealed that lncRNAs differentially expressed in preeclampsia placenta may exert a partial or key role in preeclampsia development. Misregulation of LOC391533, LOC284100, CEACAMP8 might be associated with preeclampsia. Taken together, this study may provide potential targets for future treatment of preeclampsia and novel insights into preeclampsia biology. LncRNAs/mRNAs profiles in 6 preeclampsia placentas and 5 matched normal pregnancy placentas tissues by microarray using Arraystar v2.0.
Project description:Background: Long non-coding RNAs (lncRNAs) are an important class of pervasive genes involved in a variety of biological functions. They are aberrantly expressed in many types of diseases. We want to study the lncRNAs profiles in preeclampsia. Preeclampsia has been observed in patients with molar pregnancy where a fetus is absent demonstrating that the placenta is sufficient to cause the condition. So we analyze the lncRNAs profiles in preeclampsia placentas. In this study, we described the lncRNAs profiles in 6 preeclampsia placentas (T) and 5 matched normal pregnancy placentas (N) tissues by microarray. Methodology/Principal Findings: With abundant and varied probes accounting 33,045 LncRNAs in our microarray, the number of lncRNAs that expressed at a certain level could be detected is 28,443. From the data we found there were 738 lncRNAs that differentially expressed (≥1.5 fold-change) among preeclampsia placentas compared with matched controls. Up to 18,063 coding transcripts could be detected in placenta samples through 30,215 coding transcripts probes. Coding-non-coding gene co-expression networks (CNC network) were constructed based on the correlation analysis between the differential expressed lncRNAs and mRNAs. According to the GO-Pathway analysis of differential expressed lncRNAs/mRNAs, we choose three lncRNAs to analyze the relationship between lncRNAs and preeclampsia. LOC391533, LOC284100, CEACAMP8 were evaluated by qPCR in 40 of preeclampsia placentas and 40 of controls. The results showed three lncRNAs were aberrantly expressed in preeclampsia placentas compared with controls. Conclusions/Significance: Our study is the first one to determine genome-wide lncRNAs expression patterns in preeclampsia placenta by microarray. The results displayed that clusters of lncRNAs were aberrantly expressed in preeclampsia placenta compared with controls, which revealed that lncRNAs differentially expressed in preeclampsia placenta may exert a partial or key role in preeclampsia development. Misregulation of LOC391533, LOC284100, CEACAMP8 might be associated with preeclampsia. Taken together, this study may provide potential targets for future treatment of preeclampsia and novel insights into preeclampsia biology.
Project description:Preeclampsia is a severe placenta-related pregnancy disorder that is generally divided into two subtypes named early-onset preeclampsia (onset <34 weeks of gestation), and lateonset preeclampsia (onset ≥34 weeks of gestation), with distinct pathophysiological origins. Both forms of preeclampsia have been associated with maternal systemic inflammation. However, alterations in the placental immune system have been less well characterized. Here, we studied immunological alterations in early- and late-onset preeclampsia placentas using a targeted expression profile approach. RNA was extracted from snap-frozen placenta samples (healthy n=13, early-onset preeclampsia n=13, and late-onset preeclampsia n=6). The expression of 730 immune-related genes from the Pan Cancer Immune Profiling Panel was measured, and the data were analyzed Q10 in the advanced analysis module of nSolver software (NanoString Technology). The results showed that early-onset preeclampsia placentas displayed reduced expression of complement, and toll-like receptor (TLR) associated genes, specifically TLR1 and TLR4. Mast cells and M2 macrophages were also decreased in early-onset preeclampsia compared to healthy pl acentas. The findings were confirmed by an immunohistochemistry approach using 20 healthy, 19 early-onset preeclampsia, and 10 late-onset preeclampsia placentas. We conclude that the placental innate immune system is altered in early-onset preeclampsia compared to uncomplicated pregnancies. The absence of these alterations in late-onset preeclampsia placentas indicates dissimilar immunological profiles. The study revealed distinct pathophysiological processes in earlyonset and late-onset preeclampsia placentas and imply that a tailored treatment to each subtype is desirable.
Project description:Background: Early-onset preeclampsia (EOPE) and late-onset preeclampsia (LOPE) has been regarded as two different phenotypes with heterogeneous manifestation. The underlying mechanisms remain elusive. Aim to gain insight into the pathogenesis of the two traits, we analyzed the placental gene expression profiles in preeclampsia placentas. Methods: Whole genome-wide microarray was used to describe the gene expression profiles in the placenta tissues from patients with early-(n=7; <34 weeks), late-onset(n=8; >36 weeks) PE and their controls who delivered preterm (n=5;<34 weeks) or at term(n=5; >36 weeks) Genes were selected as differentially expressed upon a fold-changeâ?¥2 and q-value<0.05. qRT-PCR was undertaken to verify the results. Western blot was further performed to verify secreted genes at the protein level. Results: A total of 627 genes were differentially expressed in early-compared with late-onset PE. Of these, 177 genes were up-regulated and 450 genes down-regulated in early-onset PE. Go analysis showed significant alteration in several biological processes, in addition to the processes which have been found before, such as immune and inflammatory response, cell adhension, female pregnancy and blood vessel development. We also found alteration in G-protein coupled receptor protein signaling pathway, G protein-coupled receptor 124 (GPR124) (P=0.0064) and MAS-related GPR, member F (MRGPRF)(P=0.0155 ) were both down-regulated obviously in early-onset PE. Conclusion: The different gene expression profiles suggested early- and late-onset PE are separate disease entities. Moreover, G-protein coupled receptor protein signaling pathway may contribute to the mechanism underlying early- and late-onset preeclampsia. Whole genome-wide microarray was used to describe the gene expression profiles in the placenta tissues from patients with early-(n=7; <34 weeks), late-onset (n=8; >36 weeks) PE and their controls who delivered preterm(n=5;<34 weeks) or at term(n=5; >36 weeks). Pooled controls who delivered at term were labled with cy5.
Project description:To identify lncRNA expression in placentas from patients with late-onset preeclampsia (LOPE), we have employed whole genome microarray expression profiling as a discovery platform to identify differential expression of lncRNAs in placental samples from LOPE patients and normal controls. For microarray analysis, 8 randomly and blindly selected placental samples from LOPE patients and matched controls (4 samples per group) were used to extract total RNA. The expression profiles of the placental lncRNAs were detected using the Agilent Human lncRNA Microarray V4.0(OE Biotech, Shanghai, China). The threshold for a dysregulated lncRNA was set as a fold-change (FC) value of 2.0 or greater. A totle of 163 differentially expressed lncRNAs were identified. Expression of nine lncRNAs (NONHSAT145880, ENST00000587240, NONHSAT116812, NONHSAT104536, FR339600, NONHSAG018907, TCONS_l2_00014782, NONHSAT134432 and NONHSAG024318) from this microarray was quantified n placental tissues from the LOPE patients (n = 40) and controls (n = 35) delivered by caesarean section by real-time PCR, confirming low variability between the qRT-PCR results and the microarray data.
Project description:Background: Early-onset preeclampsia (EOPE) and late-onset preeclampsia (LOPE) has been regarded as two different phenotypes with heterogeneous manifestation. The underlying mechanisms remain elusive. Aim to gain insight into the pathogenesis of the two traits, we analyzed the placental gene expression profiles in preeclampsia placentas. Methods: Whole genome-wide microarray was used to describe the gene expression profiles in the placenta tissues from patients with early-(n=7; <34 weeks), late-onset(n=8; >36 weeks) PE and their controls who delivered preterm (n=5;<34 weeks) or at term(n=5; >36 weeks) Genes were selected as differentially expressed upon a fold-change≥2 and q-value<0.05. qRT-PCR was undertaken to verify the results. Western blot was further performed to verify secreted genes at the protein level. Results: A total of 627 genes were differentially expressed in early-compared with late-onset PE. Of these, 177 genes were up-regulated and 450 genes down-regulated in early-onset PE. Go analysis showed significant alteration in several biological processes, in addition to the processes which have been found before, such as immune and inflammatory response, cell adhension, female pregnancy and blood vessel development. We also found alteration in G-protein coupled receptor protein signaling pathway, G protein-coupled receptor 124 (GPR124) (P=0.0064) and MAS-related GPR, member F (MRGPRF)(P=0.0155 ) were both down-regulated obviously in early-onset PE. Conclusion: The different gene expression profiles suggested early- and late-onset PE are separate disease entities. Moreover, G-protein coupled receptor protein signaling pathway may contribute to the mechanism underlying early- and late-onset preeclampsia.
Project description:To investigate the differentially expressed mRNAs and microRNAs in human placenta between early-onset preeclampsia (EO-PE) and preterm birth controls (PTB), next generation sequencing was performed in 5 paired EO-PE and PTB placentas.