Immunolocalization patterns of histone-deacetylases in salivary glands of mice during postnatal development.

OBJECTIVE: Histone-deacetylases (HDACs) are epigenetic modulators involved in the control of gene expression. No data are available on the expression or subcellular localization of HDACs in salivary glands. The present study aims to examine the subcellular distribution of HDACs in salivary glands during postnatal development. DESIGN: The major salivary glands of C57/BL6 mice were separately removed at 10, 25, 30,60 and 90 days after birth. Hematoxylin-eosin (H&E) and immunohistochemical staining were performed for HDACs. Gene Expression of HDACs in C57BL/6. NOD-Aec1Aec2 mice salivary glands during the development of Sjögren's syndrome-like illness were also analyzed by using the gene expression datasets (GSE 15640). RESULTS: In the mice salivary gland, HDACs were found to have different localization patterns at various stages of development (10, 25, 30, 60, and 90 days). Apart from HDAC6, ductal cells of salivary glands were the primary sites for HDAC localization. HDAC2, 8, 5, 10 and 11 were expressed at high levels in the salivary gland after birth while HDAC6 showed no expression during postnatal development. This suggests that these HDAC subtypes may have different roles in salivary gland function. In the context of Sjögren's syndrome-like illness, HDAC 2, 8 and 10 showed low expression while HDAC1, 6,5,3 and 11 had relatively high expression in the salivary gland. CONCLUSIONS: This study has provided an important reference for understanding the spatiotemporal-specific expression of HDACs in the salivary gland. These results offer new clues for the experimenters and hold promise for developing innovative therapeutic strategies for salivary gland-related diseases.

Portal vein computed tomography imaging characteristics and their relationship with bleeding risk in patients with liver cirrhosis undergoing interventional therapy.

BACKGROUND: This study aimed to analyze the predictive value of multi-slice spiral computed tomography (CT) perfusion imaging for upper gastrointestinal bleeding in patients with cirrhotic portal hypertension. A total of 62 patients with cirrhotic portal hypertension and 28 healthy individuals were included. The results showed that multi-slice spiral CT perfusion imaging had a significant predictive value for upper gastrointestinal bleeding in patients with cirrhotic portal hypertension. The vascular area, number of vascular cross-sections, and gastric coronary vein diameter (GCVD) showed high predictive values, with the vascular area having the best predictive value. AIM: To investigate the predictive accuracy of multi-slice spiral CT perfusion imaging for upper gastrointestinal bleeding in patients with cirrhosis and portal hypertension. METHODS: This study included 62 patients with cirrhotic portal hypertension (disease group) and 28 healthy individuals (control group). The disease group was further divided into two subgroups: Group A (n = 27, bleeding) and group B (n = 35, no bleeding). All patients underwent multi-slice spiral CT perfusion imaging at our hospital, and we compared various parameters such as liver blood flow, vein size, number of blood vessels, and blood vessel area between the two groups. We employed statistical analysis to identify factors associated with upper gastrointestinal bleeding and created a graph comparing the predictive value of different factors for bleeding. RESULTS: We found no difference in hepatic artery (HAP) levels among the three groups (all P > 0.05). The portal vein levels in groups A and B were much lower than in the control group; group A was much lower than group B (all P < 0.05). The HAP perfusion index levels in groups A and B were much higher than in the control group; group A was much higher than group B (all P < 0.05). The portal vein diameter, splenic vein diameter, and GCVD levels in groups A and B were much higher than in the control group; those in group A were much higher than those in group B (all P < 0.05). The number of blood vessels and blood vessel area in groups A and B were much higher than in the control group; those in group A were much higher than those in group B (all P < 0.05). The statistical method showed a strong link between GCVD, number of blood vessels, blood vessel area, and upper gastrointestinal bleeding (odds ratio = 1.275, 1.346, 1.397, P < 0.05). The graph showed that GCVD, number of blood vessels, and blood vessel area could predict bleeding well, with blood vessel area having the best prediction power. CONCLUSION: That multi-slice spiral CT perfusion imaging can predict upper gastrointestinal bleeding well in patients with cirrhosis and high blood pressure in the portal vein. GCVD, number of blood vessels, and blood vessel area had high prediction power. The blood vessel area had the best prediction power, with an area under the curve of 0.831.

LncRNA LINC00534 regulates cell proliferation and migration via the miR-494-3p/PTEN axis in HTR-8/SVneo cells.

BACKGROUND: LncRNA LINC00534 has been found to be differentially expressed in placental tissue samples of preeclampsia (PE), but the exact mechanism is still unclear. METHODS: In vitro assays were carried out in HTR-8/SVneo cells using various methods, including cell counting kit-8 (CCK-8), transwells, flow cytometry, and Western blotting (WB) and quantitative polymerase chain reaction. RNA pull-down and bioinformatics analysis were applied to examine other potential underlying mechanisms involved. RESULTS: We found that there was a high expression of LINC00534 in the placental tissues of patients with PE. LINC00534 overexpression (OE) significantly inhibited cell proliferation and migration as well as accelerated cell apoptosis in HTR8/SVneo cells. The knockdown of LINC00534 produced an opposite trend. Mechanistically, LINC00534 promoted the expressions of PTEN (Phosphatase and tensin homolog) through decreasing miR-494-3p. Further rescue studies showed that LINC00534 played a role by targeting mir-494-3p, which controlled the growth and migration of HTR-8/SVneo trophoblast cells via regulating PTEN/PI3K/AKT (Phosphatidylinositol3-kinase/protein kinase B). Moreover, lncRNA pull-down assay identified 198 potential bound proteins for LINC00534. Those proteins were mostly involved in RNA processing and modification, posttranslational modification, protein turnover, and chaperones. CONCLUSION: Overall, by suppressing HTR8/SVneo cell growth and migration via the miR-494-3p/PTEN axis and other mechanisms, LINC00534 offers new insight into PE pathogenesis.

Global, regional, and national burden of disease study of atrial fibrillation/flutter, 1990-2019: results from a global burden of disease study, 2019.

BACKGROUND: Data from the Global Burden of Disease, Injury, and Risk Factor Study 2019 (GBD 2019) was used to assess the burden and change in prevalence, incidence, deaths, disability-adjusted life years, and risk factors for atrial fibrillation/flutter in 204 countries and territories between 1990 and 2019. METHODS: Incidence, prevalence, deaths, disability-adjusted life years (DALYs), and their age-standardized rates of AF/AFL were analyzed by age, sex, socio-demographic index (SDI), and human development index (HDI) using the Global Burden of Disease study 2019 (GBD2019) results，and risk factors for AF/AFL (mainly high systolic blood pressure, high body-mass index, alcohol use, smoking and diet high in sodium) were differentially analyzed. RESULTS: There are 59.70 million (95% uncertainty interval (UI) 45.73-75.29 million) AF/AFL patients worldwide in 2019, with 4.72 million (95% uncertainty interval (UI) 3.64-5.96 million) new cases and 0.315 million deaths (95% uncertainty interval (UI) 0.268-0.361 million) and 8.39 million disability-adjusted years (95% uncertainty interval (UI) 6.69-10.54 million). The highest risk factor for deaths, DALYs attributable to AF/AFL in 2019 was high systolic blood pressure, high body-mass index, alcohol use, smoking, and diet high in sodium. It is estimated that between 2030 and 2034, the total incidence of male AF/ AFL will be 16.08 million, and the total number of deaths will be 1.01 million. For females, the total number of incidence is 16.85 million, and the total number of deaths is 1.49 million. CONCLUSIONS: AF/AFL remains a major global public health problem, although the ASR of prevalence, incidence, and DALY at the worldwide level showed a decreasing trend from 1990 to 2019(the ASR of deaths increased slightly). However, the unfavorable trend observed in this study in countries with lower SDI suggests that current prevention and treatment strategies should be reoriented. Some countries should develop more targeted and specific strategies to prevent the increase of AF/AFL.

Efficacy and safety of vernakalant for cardioversion of recent-onset atrial fibrillation: A protocol for systematic review and meta-analysis.

BACKGROUND: Atrial fibrillation (AF) is the most common tachyarrhythmia encountered in clinical practice and is associated with substantial morbidity and mortality. This study aimed to determine the efficacy and safety of vernakalant for cardioversion of recent-onset AF. METHODS: A comprehensive systematic literature search will be conducted in Cochrane Library, PubMed, Web of Science, EMBASE, for randomized controlled trials (RCTs) about the vernakalant with AF. Two reviewers will independently assess the quality of the selected studies according to the Cochrane Collaboration's tool for RCTs. The bias risk of the RCT will be assessed by the Cochrane risk of bias (ROB) tool. The quality of the evidence will be evaluated by Grading of Recommendations Assessment Development and Evaluation (GRADE) system. Results from these questions will be graphed and assessed using Review Manager 5.3. RESULTS: The results of this meta-analysis will be published in a peer-reviewed journal. CONCLUSION: This review will evaluate the safety and efficacy of vernakalant for patients with AF, provide more recommendations for patients or researchers, and high-level evidence for clinical decision-making.

Elevated high-sensitivity C-reactive protein levels predict poor outcomes among patients with acute cardioembolic stroke.

BACKGROUND: High-sensitivity C-reactive protein (hs-CRP) as a prognostic factor of stroke has been proposed and studied. However, the relationship between hs-CRP levels and outcomes among patients with cardioembolic stroke (CES) remains unclear. This study aimed to evaluate the association between hs-CRP levels in the acute phase of CES and poor patient outcomes. METHODS: We recruited 478 patients with first-onset CES. Hs-CRP and other biochemical markers were measured within 24 h after admission. Hs-CRP levels were grouped into quartiles (<2.31, 2.31 to <6.09, 6.09 to <22.30, and ≥22.30 mg/L). Stroke severity was assessed using the modified Rankin scale (mRS), with mRS scores of 0 to 2 classified as a good outcome, and scores of 3 to 6 as a poor outcome. Composite endpoints included poor outcomes, vascular death, myocardial infarction (MI), and recurrent stroke (ischemic or hemorrhagic). At 3-month and 1-year follow-ups, we used multivariate logistic regression analysis to assess the relationship between baseline hs-CRP levels, mRS scores, and composite endpoints. RESULTS: Among 478 patients with CES, the median hs-CRP level was 6.09 mg/L. Regarding the primary outcome, we found that hs-CRP levels ≥22.30 mg/L were positively correlated with poor outcomes at the 3-month and 1-year follow-ups [odds ratio (OR): 3.862, 95% confidence interval (CI): (1.675-8.904), P=0.002; and OR: 5.479, 95% CI: (1.692-17.744), P=0.005, respectively]. The secondary outcomes paralleled the results of the primary outcomes at the 3-month and 1-year follow-ups [OR: 3.381, 95% CI: (1.620-7.058), P=0.001; and OR: 3.181, 95% CI: (1.475-6.860), P=0.003, respectively]. CONCLUSIONS: Elevated hs-CRP in patients with CES is an independent predictor of poor outcomes; however, this association is particularly evident when hs-CRP ≥22.30 mg/L.

ELK1/lncRNA-SNHG7/miR-2682-5p feedback loop enhances bladder cancer cell growth.

AIMS: The purpose of this paper is to unearth the ceRNA regulatory mechanism of SNHG7 in bladder cancer (BCa). MATERIALS AND METHODS: The expression of SNHG7 in BCa cells was uncovered by qRT-PCR. The biological functions of SNHG7 in BCa cells were explored by CCK-8 assay, colony formation assay, flow cytometry analysis, wound healing assay and transwell assay. Luciferase reporter assay and RIP assay were applied to analyze the interaction of ELK1 with SNHG7 or miR-2682-5p. KEY FINDINGS: SNHG7 was conspicuously highly expressed in BCa tissues and cells. The upregulated expression of SNHG7 was related with poor prognosis in BCa patients. Moreover, SNHG7 exerted oncogenic functions in BCa through enhancing cell growth, migration and invasion. ELK1 increased the level of SNHG7 by binding with the promoter region of SNHG7. SNHG7 strengthened the expression of ELK1 via acting as a sponge of miR-2682-5p. Both ELK1 and miR-2682-5p involved in the SNHG7-mediated BCa progression. SIGNIFICANCE: ELK1/SNHG7/miR-2682-5p feedback loop enhances cell growth, migration and invasion in BCa.

Serum LUCAT1 implicates the pathogenesis of muscle-invasive bladder cancer via targeting miR-199a-5p and miR-199b-5p.

Muscle-invasive bladder cancer (MIBC) is a common malignancy of urinary system cancers, accounting for about 1/3 of all newly diagnosed bladder cancer cases. Due to its strong metastasis, the 5-year survival of MIBC is less than 50%, and in serious cases, the overall survival of metastatic bladder cancer patients is about 1.3 years. LncRNAs, a type of non-coding RNAs defined as the transcripts exceeding 200 nucleotides in length, are frequently aberrant in multiple cancers including cervical, ovarian, breast and bladder cancers. Recently, LUCAT1 (short for lung cancer-associated transcript 1), a lncRNA first reported to be involved in smoking-related lung cancer, has been observed to exhibit crucial roles in the epithelial-to-mesenchymal transition (EMT), migration and invasion processes of clear cell renal cell carcinoma (ccRCC) and colorectal cancer. However, whether it involves in the pathogenesis of MIBC remains underexplored. In the present study, LUCAT1 was up-regulated in the serum samples of MIBC patients and bladder cancer cell lines, as assessed using real-time PCR. Our in vitro data (including wound healing and trans-well assays) showed that LUCAT1 was required for the proliferation, EMT, migration and invasion processes of T24 cells. Moreover, LUCAT1 directly targeted miR-199a-5p and miR-199b-5p, as affirmed using the luciferase reporter assay, and manipulation of LUCAT1 significantly suppressed miR-199a-5p and miR-199b-5p. Collectively, our findings highlight an axis of LUCAT1/miR-199a/b-5p in MIBC pathogenesis. Therefore, LUCAT1 may possibly be a promising candidate for diagnostic biomarker and therapeutic target of MIBC.

The long noncoding RNA uc.294 is upregulated in early-onset pre-eclampsia and inhibits proliferation, invasion of trophoblast cells (HTR-8/SVneo).

Recently, a large number of long noncoding RNAs (lncRNAs) have been reported in human diseases that are evolutionarily conserved and are likely to play a role in many biological events including pre-eclampsia. In our previous research, we selected thousands of lncRNAs for their relationship with early-onset pre-eclampsia. Among these lncRNAs, a lncRNA named uc.294 attracted our attention, was once reported to specifically be expressed at a high level in the early-onset of pre-eclampsia. This study aims to investigate the function of uc.294 in early-onset pre-eclampsia and the possible mechanism. The uc.294 expression level in early-onset pre-eclampsia or in normal placenta tissues was evaluated by quantitative real-time polymerase chain reaction. To detect the proliferation, invasion, and apoptosis capacity of the trophoblast cells, we performed the Cell Counting Kit-8 assay, transwell assay, and flow cytometry, respectively. Here we report, for the first time, that uc.294 inhibits proliferation, invasion, and promotes apoptosis of trophoblast cells HTR-8/SVneo by working in key aspects of biological behaviors. However, how uc.294 acts to regulate gene functions in early-onset pre-eclampsia needs further exploration.

Effects of Pyrazine Derivatives and Substituted Positions on the Photoelectric Properties and Electromemory Performance of D⁻A⁻D Series Compounds.

Pyrazine derivatives quinoxaline and pyridopyrazine were selected as the acceptors, and benzocarbazole was used as the donor to synthesize four different D⁻A⁻D compounds. The results showed that 2,3-bis(decyloxy)pyridine[3,4-b]pyrazine (DPP) exhibited stronger electron-withdrawing ability than that of 2,3-bis(decyloxy)quinoxaline (DPx), because DPP possesses one more nitrogen (N) atom, resulting in a red-shift of the intramolecular charge transfer (ICT) absorption bands and fluorescent emission spectra for compounds with DPP as the acceptor compared with those that use DPx as the acceptor. The band-gap energy (Eg) of the four D⁻A⁻D compounds were 2.82 eV, 2.70 eV, 2.48 eV, and 2.62 eV, respectively, for BPC-2DPx, BPC-3DPx, BPC-2DPP, and BPC-3DPP. The solvatochromic effect was insignificant when the four compounds were in the ground state, which became significant in an excited state. With increasing solvent polarity, a 30⁻43 nm red shift was observed in the emissive spectra of the compounds. The thermal decomposition temperatures of the four compounds between 436 and 453 °C had very high thermal stability. Resistor-type memory devices based on BPC-2DPx and BPC-2DPP were fabricated in a simple sandwich configuration, Al/BPC-2DPx/ITO or Al/BPC-2DPP/ITO. The two devices showed a binary non-volatile flash memory, with lower threshold voltages and better repeatability.

Prediction of vaginal birth after cesarean delivery in Chinese parturients.

There is an urgent need in China to better predict vaginal birth after cesarean (VBAC) to face the challenge of the second child policy. We aimed to validate a widely used VBAC prediction model (Grobman's model) and a modified version of this model in a Chinese population. In this retrospective cohort study, 444 women with one cesarean delivery and at least one subsequent attempt for a trial of labor in Nanjing, China were included. The considered potential VBAC predictors included Grobman's background variables and five new variables. Overall, a total of 370 women had VBAC, with a success rate of 83.3%. The new background variables "maternal height" and "estimated fetal weight" were considered as two additional predictors for VBAC. The AUC of Grobman's model was 0.831 (95%CI = 0.775-0.886) while the AUC of our modified model with two new variables added was 0.857 (sensitivity = 72.2%, specificity = 83.8%). However, the difference between the AUC of the two models was not significant (Z = -1.69, P = 0.091). We confirmed that Grobman's model was accepted in the Chinese population. A modified model that is supplemented with maternal height and estimated fetal weight needs to be further studied in the Chinese population.

Downregulation of caveolin-1 increased EGFR-TKIs sensitivity in lung adenocarcinoma cell line with EGFR mutation.

Although epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), including gefitinib and erlotinib, have shown notable effects in lung adenocarcinoma patients harboring EGFR mutations, there are significant differences between individual patients in the degree of benefits provided by EGFR-TKIs. Some evidence supports a role for caveolin-1 (Cav-1) in modulating drug sensitivity. This study aimed to investigate whether Cav-1 plays an important role in sensitivity to EGFR-TKIs in lung adenocarcinoma cells. Downregulation of Cav-1 in PC-9 cells were performed to investigate changes in sensitivity to EGFR-TKIs in vitro and in vivo. Knockdown of Cav-1 dramatically enhanced sensitivity to EGFR-TKIs by down-regulating phosphorylation of EGFR. These results suggest that Cav-1 may be a predictor of the poor efficacy of EGFR-TKIs treatment in lung adenocarcinoma with EGFR mutations.

Peptidome Analysis of Human Serum From Normal and Preeclamptic Pregnancies.

Preeclampsia is a kind of disease that severely harms the health of pregnant women and infants. To better understand the molecular mechanisms involved in preeclampsia, we used liquid chromatography-mass spectrometry/mass spectrometry (LC-MS/MS) to construct a comparative peptidomic profiling of human serum between normal and preeclamptic pregnancies. A total of 201 peptides were confidently identified, with 21 up-regulated and three down-regulated. Further analysis indicated that these differentially expressed peptides correlate with enzyme regulator activity, biological regulation, and coagulation cascades occurring during pathological changes of preeclampsia. The identification of key peptides in serum may serve not only as a basis for better understanding and further exploring the etiology and pathogenesis of PE, but also as potential biomarkers and in providing targets for future therapy in PE, especially in early onset severe PE (sPE). J. Cell. Biochem. 118: 4341-4348, 2017. © 2017 Wiley Periodicals, Inc.

Dysregulation of LncRNAs in Placenta and Pathogenesis of Preeclampsia.

BACKGROUND: Preeclampsia, a gestational disease characterized by hypertension and proteinuria twenty weeks into pregnancy, is one of the leading causes of fetal and maternal mortality. Although multiple genetic and environmental factors are found to be related to the preeclampsia risk, the pathogenic pathways remain largely undefined. The placenta plays a critical role in the fetal development by carrying out the barrier, fetal-maternal exchange, and endocrine functions during pregnancy. Accumulated data indicated that the expression of multiple long noncoding RNA (LncRNA) is dysregulated in preeclamptic placentas. Moreover, manipulation of LncRNA expression led to functional alterations in trophoblast cell cultures, including changes in proliferation, differentiation, apoptosis, and migration. OBJECTIVE: This article reviews published data on this subject and provides detailed information on the regulation and function of LncRNAs IGF2/H19, MEG3, SPRY4-IT1, HOTAIR, MALAT1, and FLT1P1 and CEACAMP8 in placental trophoblasts. The potential mechanisms underlying the action of these LncRNAs are also discussed to facilitate a better understanding on the potential role of these LncRNAs for the pathogenesis of preeclampsia. CONCLUSION: It is elaborated that some lncRNAs probably contribute to the pathogenesis of preeclampsia through methylation, Notch-EGFL7 signaling pathway and Wnt/ß-catenin pathway.

Using the BITOLA system to identify candidate molecules in the interaction between oral lichen planus and depression.

Exacerbations of oral lichen planus (OLP) have been linked to the periods of psychological stress, anxiety and depression. The specific mechanism of the interaction is unclear. The aim of this study was to explore the candidate genes or molecules that play important roles in the interaction between OLP and depression. The BITOLA system was used to search all intermediate concepts relevant to the "Gene or Gene Product" for OLP and depression, and the gene expression data and tissue-specific gene data along with manual checking were then employed to filter the intermediate concepts. Finally, two genes (NCAM1, neural cell adhesion molecule 1; CD4, CD4 molecule) passed the follow-up inspection. By using the text mining can formulate a new hypothesis: NCAM1 and CD4 were identified as involved or potentially involved in the interaction between OLP and depression. These results offer a new clue for the experimenters and hold promise for developing innovative therapeutic strategies for these two diseases.

Long non-coding RNA RPAIN regulates the invasion and apoptosis of trophoblast cell lines via complement protein C1q.

Long non-coding RNAs (lncRNAs) are key regulatory molecules that are involved in a variety of biological processes and human diseases. Their impact on early onset preeclampsia remains unclear. In this study, we tested the expression of RPAIN (transcript variant 12 of RPA interacting protein, a non-coding RNA, NR_027683.1) in placenta tissues derived from 25 pregnant women with PE and 15 healthy pregnant women using quantitative real-time PCR. The effect of RPAIN on trophoblast proliferation, invasion, and apoptosis and the underlying mechanisms were examined in trophoblast cell lines (HTR-8/SVneo). The results showed that RPAIN expression levels were significantly increased in early onset preeclamptic placentas compared to normal controls. The proliferation and invasive abilities of the trophoblast cells were significantly inhibited, and the apoptosis abilities of the trophoblast cells were significantly promoted when RPAIN was overexpressed. In addition, the overexpression of RPAIN inhibited the expression of complement protein C1q. Furthermore, C1q overexpression rescued the decreased cell invasion and enhanced cell apoptosis in RPAIN-overexpressing trophoblast cells. Our results suggest that increased RPAIN levels may contribute to the development of preeclampsia through regulating trophoblast invasion and apoptosis via C1q. Therefore, we proposed RPAIN as a novel lncRNA molecule, which might contribute to the development of PE (preeclampsia) and might compose a potential diagnostic and therapeutic target for this disease.

Celecoxib targets breast cancer stem cells by inhibiting the synthesis of prostaglandin E2 and down-regulating the Wnt pathway activity.

Pharmacological targeting of breast cancer stem cells (CSCs) is highly promising for the treatment of breast cancer, as the small population of CSCs is responsible for tumor initiation, progression, recurrence and chemo-resistance. Celecoxib is one of the most commonly used non-steroidal anti-inflammatory drugs (NSAIDs), which have chemo-preventive activity against cancers, including breast cancer and colorectal cancer. However, the mechanisms by which NSAIDs exert its cancer prevention effects have yet been completely understood. In the present study, we investigated for the first time the effect of celecoxib on breast CSCs inhibition and its potential molecular mechanisms. Our results demonstrated that celecoxib suppresses CSC self-renewal, sensitizes chemo-resistance, inhibits epithelial to mesenchymal transition (EMT), and attenuates metastasis and tumorigenesis. Further exploring the underlying mechanism revealed that celecoxib targets breast CSCs by inhibiting the synthesis of prostaglandin E2 and down-regulating the Wnt pathway activity. Our findings suggest that celecoxib, by targeting CSCs, may be used as an adjuvant chemotherapy drug to improve breast cancer treatment outcomes.

Distinct expression profiles of lncRNAs between early-onset preeclampsia and preterm controls.

Early-onset preeclampsia (EOPE), which is the most severe form of the syndrome, confers a high risk of neonatal morbidity and perinatal death. We aim to study the roles of long non-coding RNAs (lncRNAs) in the pathogenesis of early-onset preeclampsia (EOPE). Therefore, we examined the expression profiles of lncRNAs between early-onset preeclampsia and preterm controls using microarray analysis. Quantitative real-time PCR (qRT-PCR) was performed to verify the selected differentially expressed lncRNAs. In total, we identified 15,646 upregulated and 13,178 downregulated lncRNAs in the placenta of EOPE patients compared to the preterm controls. Gene ontology and pathway analysis revealed that compared to the preterm controls, many of the processes over-represented in the EOPE patients were related to cell migration and cell motility. A selection of the differentially expressed lncRNA transcripts was confirmed using qRT-PCR, particularly RP11-465L10.10, which is associated with the MMP9 gene. These data may offer a background/reference resource for future functional studies of lncRNAs related to EOPE.