• LncRNA
• chondrocytes
• inflammation
• osteoarthritis
• pro-inflammatory factors

• The work was supported by Gansu University of Chinese Medicine to introduce a talent research start-up fund
• Gansu Basic Research Program-Natural Science Funds-Youth Science and Technology Fund

• FUT1
• Osteoarthritis
• chondrocyte
• inflammatory injury
• long intergenic nonprotein coding RNA 00511
• microRNA-9-5p

• Chondrocytes/metabolism
• Pyroptosis
• NLR Family, Pyrin Domain-Containing 3 Protein/metabolism
• NLR Family, Pyrin Domain-Containing 3 Protein/genetics
• MicroRNAs/genetics
• MicroRNAs/metabolism
• RNA, Long Noncoding/genetics
• RNA, Long Noncoding/metabolism
• Fucosyltransferases/genetics
• Fucosyltransferases/metabolism
• Inflammasomes/metabolism
• Lipopolysaccharides
• Humans
• Cell Line
• Animals
• Mice
• Cell Survival
• Interleukin-1beta/metabolism
• Interleukin-18/metabolism
• Interleukin-18/genetics
• Caspase 1/metabolism
• Caspase 1/genetics

• 3D bioprinting
• Arthritis
• Chondrocytes
• Decoction
• Osteoblasts

• 81920108032 National Natural Science Foundation
• 2022JC005 New interdisciplinary research Project of Shanghai Municipal Health Commission
• 2022CX001 Innovation team project of scientific research of traditional Chinese medicine of Shanghai Health Committee
• 2022ZZ01009 Shanghai TCM Medical Center of Chronic Disease

• Cancer
• Immune cell-derived lncRNA
• Immune cells
• lncRNA

• RNA, Long Noncoding/genetics
• Humans
• Neoplasms/immunology
• Neoplasms/genetics
• Animals
• Gene Expression Regulation, Neoplastic
• Neovascularization, Pathologic/genetics
• Neovascularization, Pathologic/immunology
• Cell Proliferation

• Atherosclerosis
• Cardiovascular diseases
• IncRNAs
• Inflammation
• NF-kB

• Humans
• NF-kappa B
• RNA, Long Noncoding/genetics
• Signal Transduction
• Atherosclerosis
• Cardiovascular Diseases

• THRIL
• carotid artery restenosis
• diagnosis
• prognosis
• proliferation

• FOXO1
• atherosclerosis
• cholesterol efflux
• inflammation
• lipid accumulation

• Childhood asthma
• exacerbation
• lncRNA THRIL
• miR-125b
• miR-34a

Osteoarthritis (OA) is a prevalent inflammatory joint disorder. microRNAs (miRNAs) are increasingly involved in OA.

Our study is proposed to clarify the role of miR-124-3p in chondrocyte pyroptosis and cartilage injury in OA.

OA mouse model was established via the treatment of destabilization of the medial meniscus (DMM), and the in vitro cell model was also established as mouse chondrocytes were induced by lipopolysaccharide (LPS). Mouse cartilage injury was assessed using safranin-O-fast green staining, hematoxylin–eosin staining, and OARSI grading method. Expressions of miR-124-3p, MALAT1, KLF5, and CXCL11 were determined. Cartilage injury (MMP-13, osteocalcin), inflammation (IL-6, IL-2, TNF-, IL-1β, and IL-18)- and pyroptosis-related factors (Cleaved Caspase-1 and GSDMD-N) levels were detected. Mechanically, MALAT1 subcellular localization was confirmed. The binding relationships of miR-124-3p and MALAT1 and MALAT1 and KLF5 were verified. MALAT1 half-life period was detected. Then, miR-124-3p was overexpressed using agomiR-124-3p to perform the rescue experiments with oe-MALAT1 or oe-CXCL11.

miR-124-3p was downregulated in DMM mice and LPS-induced chondrocytes where cartilage injury, and increased levels of inflammation- and pyroptosis-related factors were found. miR-124-3p overexpression relieved cartilage injury and repressed chondrocyte pyroptosis. miR-124-3p bounds to MALAT1 to downregulate its stability and expression, and MALAT1 bounds to KLF5 to enhance CXCL11 transcription. Overexpression of MALAT1 or CXCL11 annulled the repressive function of miR-124-3p in chondrocyte pyroptosis.

miR-124-3p reduced MALAT1 stability and inhibited the binding of MALAT1 and KLF5 to downregulate CXCL11, thereby suppressing chondrocyte pyroptosis and cartilage injury in OA.

• Chondrocytes
• LncRNA MALAT1
• LncRNA stability
• Osteoarthritis
• Pyroptosis
• microRNA-124-3p

Inflammatory bowel disease (IBD) is a chronic inflammatory disease of the gastrointestinal tract. We aimed to investigate, for the first time, the expression profile of serum level of LncRNA THRIL and MiR-125b in IBD patients and their relations with patient’s clinical and biochemical investigations.

Our study included 210 subjects divided into 70 healthy subjects considered as control group (male and female), 70 patients with ulcerative colitis (UC), and 70 patients with Crohn’s disease (CD). Blood samples were obtained from all subjects. Expression of LncRNA THRIL and MiR-125b in serum was detected by Quantitative real time PCR (qRT-PCR).

Our results showed a significant increase in the fold change of LncRNA THRIL in UC patients (Median = 11.11, IQR; 10.21–12.45, P<0.001) and CD patients (Median = 5.87, IQR; 4.57–7.88, P<0.001) compared to controls. Meanwhile there was a significant decrease in the fold change of MiR-125b in UC patients (Median = 0.36, IQR; 0.19–0.61, P<0.001) and CD patients (Median = 0.69, IQR; 0.3–0.83, P<0.001) compared to controls. Furthermore, there was a negative significant correlation between LncRNA THRIL and MiR-125b in UC patients (r = -0.28, P = 0.016) and in CD patients (r = -0.772, P<0.001). ROC curve analysis was done showing the diagnostic value of these markers as predictors in differentiating between cases of UC, CD, and control.

Serum LncRNA THRIL and MiR-125b could be used as potential biomarkers for diagnosis and prognosis of ulcerative colitis and Crohn’s disease.

• Biomarkers
• Colitis, Ulcerative/diagnosis
• Colitis, Ulcerative/genetics
• Crohn Disease/diagnosis
• Crohn Disease/genetics
• Female
• Humans
• Inflammatory Bowel Diseases/diagnosis
• Inflammatory Bowel Diseases/genetics
• Male
• MicroRNAs/metabolism
• RNA, Long Noncoding/genetics

• Degenerative bone diseases
• Epigenetics
• Long noncoding RNAs
• Mesenchymal stromal/stem cells
• Osteoarthritis
• Osteoporosis

• ATG4D
• Autophagy
• Diabetes retinopathy
• THRIL
• miR-125b-5p

• Autophagy
• Cell Proliferation/genetics
• Endothelial Cells
• Glucose/metabolism
• Glucose/toxicity
• Humans
• MicroRNAs/genetics
• MicroRNAs/metabolism
• RNA, Long Noncoding/genetics
• RNA, Long Noncoding/metabolism
• Retina

Airway inflammation is one of the typical pathological characteristics of asthma. MicroRNAs (miRNAs) play important roles in regulating inflammation. Nevertheless, miRNA-885-3p (miR-885-3p)’s role in asthmatic inflammation and the underlying mechanism need to be explained. In this work, miR-885-3p expression and toll-like receptor 4 (TLR4) expression in asthma patients’ plasma and lipopolysaccharide (LPS)-treated 16HBE cells were detected through quantitative real-time PCR. The interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels in 16HBE cell supernatant were examined via enzyme-linked immunosorbent assay. Cell counting kit-8 (CCK-8) assay and flow cytometry were employed to examine 16HBE cell viability and apoptosis, respectively. Western blotting was performed to examine the expression of TLR4, cleaved caspase-3, B-cell lymphoma-2 (Bcl-2), nuclear factor-kappa B (NF-κB) p65, Bcl-2-related X protein (Bax), phosphorylated (p)-NF-κB p65 and myeloid differentiation primitive-response protein 88 (MyD88) in 16HBE cells. Furthermore, the targeted relationship between TLR4 and miR-885-3p in 16HBE cells was determined through dual-luciferase reporter gene assay. Compared with healthy volunteers, miR-885-3p expression in acute asthma patients’ plasma was significantly downregulated. In 16HBE cells, the stimulation of LPS reduced miR-885-3p expression. MiR-885-3p overexpression reduced LPS-stimulated 16HBE cell injury by enhancing cell viability, and suppressing the levels of inflammatory factors and apoptosis. Furthermore, TLR4 was identified as miR-885-3p’s target gene. TLR4 overexpression weakened the impacts of miR-885-3p on LPS-stimulated cell injury and NF-κB-MyD88 signaling. In conclusion, miR-885-3p can reduce LPS-induced 16HBE cell damage, via targeting TLR4 to suppress the NF-κB-MyD88 pathway.

• Asthma
• MiR-885-3p
• NF-κB-MyD88 pathway
• TLR4
• cell injury

• Mechanism
• NF-κB
• Osteoarthritis
• Review
• ncRNAs

• Inflammation
• Long noncoding RNA
• Osteoarthritis
• Rheumatoid arthritis
• Systemic lupus erythematosus

• DNA
• RNA
• exosomes
• gene
• osteoarthritis
• platelet-rich plasma
• protein

Osteoarthritis (OS) is the most frequent degenerative condition in the joints, disabling many adults. Several abnormalities in the articular cartilage, subchondral bone, synovial tissue, and meniscus have been detected in the course of OA. Destruction of articular cartilage, the formation of osteophytes, subchondral sclerosis, and hyperplasia of synovial tissue are hallmarks of OA. More recently, several investigations have underscored the regulatory roles of non-coding RNAs (ncRNAs) in OA development. Different classes of non-coding RNAs, including long ncRNAs (lncRNAs), microRNAs (miRNAs), and circular RNAs (circRNAs), have been reported to affect the development of OA. The expression level of these transcripts has also been used as diagnostic tools in OA. In the present article, we aimed at reporting the role of these transcripts in this process. We need to give a specific angle on the pathology to provide meaningful thoughts on it.

• Animals
• Humans
• MicroRNAs
• Osteoarthritis/diagnosis
• Osteoarthritis/genetics
• RNA, Circular
• RNA, Long Noncoding

• SEMA3A
• chondrocyte apoptosis
• extracellular matrix degradation
• nrp-1
• osteoarthritis

Musculoskeletal degenerative diseases (MSDDs) are pathological conditions that affect muscle, bone, cartilage, joint and connective tissue, leading to physical and functional impairments in patients, mainly consist of osteoarthritis (OA), intervertebral disc degeneration (IDD), rheumatoid arthritis (RA) and ankylosing spondylitis (AS). Long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) are novel regulators of gene expression that play an important role in biological regulation, involving in chondrocyte proliferation and apoptosis, extracellular matrix degradation and peripheral blood mononuclear cell inflammation. Research on MSDD pathogenesis, especially on RA and AS, is still in its infancy and major knowledge gaps remain to be filled. The effects of lncRNA/circRNA-miRNA-mRNA axis on MSDD progression help us to fully understand their contribution to the dynamic cellular processes, provide the potential OA, IDD, RA and AS therapeutic strategies. Further studies are needed to explore the mutual regulatory mechanisms between lncRNA/circRNA regulation and effective therapeutic interventions in the pathology of MSDD.

• age-related disease
• aging
• circRNA
• degenerative musculoskeletal disorders
• lncRNA
• miRNA
• non-coding RNAs

• CCL22
• CCR4
• Cartilage degradation
• Cartilage injury
• Osteoarthritis

Osteoarthritis (OA) is a chronic bone and joint disease characterized by articular cartilage degeneration and joint inflammation and is the most common form of arthritis. The clinical manifestations of OA are chronic pain and joint activity disorder, which severely affect the patient quality of life. Long non-coding RNA (lncRNA) is a class of RNA molecules >200 nucleotides long that are expressed in animals, plants, yeast, prokaryotes and viruses. lncRNA molecules lack an open reading frame and are not translated into protein. The present review collated the results of recent studies on the role of lncRNA in the pathogenesis of OA to provide information for the prevention, diagnosis and treatment of OA.

• chondrocytes
• lncRNAs
• non‑coding RNAs
• osteoarthritis
• synoviocytes
• transcriptional regulation

Purpose: The aim of this study was to investigate the role of the tumor necrosis factor and HNRNPL related immunoregulatory long non-coding RNA (THRIL) in cerebral ischemia-reperfusion injury.

Methods: A rat middle cerebral artery occlusion/ischemia-reperfusion (MCAO/IR) model and an oxygen glucose deprivation/reoxygenation (OGD/R) cell model were constructed. THRIL was knocked down using siTHRIL. Neurological deficit score was detected based on the criteria of Zea-Longa. Brain region 2,3,5-Triphenyltetrazolium (TTC) staining and quantitative analysis of cerebral infarction volume, RT-qPCR, and fluorescence immunostaining were performed for assessing THRIL expression. MTT assay was used to detect the cell proliferation ability after transfection, TUNEL assay was applied to detect apoptosis, and western blot and ELISA detected related protein expression. A dual luciferase reporter system and RIP assay were used to confirm the target relationship.

Results: THRIL was upregulated in both in vitro and in vivo models of brain ischemia-reperfusion injury. Knockdown of THRIL attenuated OGD/R neuronal apoptosis and OGD/R-induced inflammation. THRIL targeted and regulated the expression of miR-24-3p/neuropilin-1 (NRP1) axis. THRIL silencing significantly improved the neurological functioning of rats in the MCAO/R model by miR-24-3p/NRP1/NF-κB p65 signaling pathway.

Conclusion: THRIL could aggravate cerebral ischemia-reperfusion injury by competitively binding to miR-24-3p to promote the upregulation of NRP1 and further promoted the activation of the NF-κB p65 signaling pathway.

• TNF and HNRNPL related immunoregulatory lncRNA
• cerebral ischemia-reperfusion injury
• miR-24-3p
• neuropilin-1
• nuclear factor κB p65 signaling

To confirm the role of long noncoding RNA differentiation antagonizing non‐protein coding RNA (DANCR) in chondrocyte inflammatory injury in osteoarthritis (OA) in vitro, as well as its molecular mechanism.

Human primary chondrocytes were treated with lipopolysaccharide (LPS) to construct a chondrocyte inflammatory injury in human OA cell model. Gene expression was detected using real‐time quantitative polymerase chain reaction. Cell inflammatory injury was evaluated by Cell Counting Kit‐8 assay, flow cytometry, and enzyme‐linked immunosorbent assay. The interplay between miRNA‐19a‐3p (miR‐19a) and DANCR was validated by dual‐luciferase reporter assay and RNA immunoprecipitation.

Expression of DANCR was upregulated, and miR‐19a was downregulated in human OA cartilage and LPS‐treated primary chondrocytes in vitro. Moreover, DANCR expression was inversely correlated with miR‐19a in OA patients. LPS reduced cell viability and increased the apoptotic rate and secretion of interleukin (IL)‐1β, IL‐6, IL‐8, as well as tumor necrosis factor (TNF)‐α in primary chondrocyte cells in vitro, suggesting an inflammatory injury model of OA. Functionally, knockdown of DANCR could attenuate LPS‐induced apoptosis and inflammatory response, as evidenced by improved cell viability, and reduced apoptotic rate and products of IL‐1β, IL‐6, IL‐8, and TNF‐α. Notably, DANCR negatively regulated miR‐19a expression, presumably via sponging. Furthermore, miR‐19a deletion eliminated the effect of DANCR knockdown on apoptosis and the inflammatory response of primary chondrocytes under LPS stress.

Differentiation antagonizing non‐protein coding RNA silencing could protect human chondrocyte cells against LPS‐induced inflammatory injury and apoptosis through targeting miR‐19a, suggesting a vital role of the DANCR/miR‐19a axis in OA.

• DANCR
• Inflammatory injury
• Lipopolysaccharide
• Osteoarthritis
• miR-19a

Long non-coding RNAs (lncRNAs) have been demonstrated to play critical roles in various diseases. Our bioinformatics analysis showed that lncRNA TNFα and heterogenous nuclear ribonucleoprotein L (hnRNPL) related immunoregulatory LincRNA (THRIL) may interact with miR-19a, which targets TNF-α. This study aimed to explore the role of THRIL, an enhancer of LPS-induced inflammatory, in sepsis.

Research subjects of the present study included 66 sepsis patients and 66 healthy volunteers. The expression levels of THRIL, miR-19a and TNF-α in plasma samples from these participants were determined by RT-qPCR. The interaction between THRIL and miR-19a was explored by performing overexpression experiments in human bronchial epithelial cells (HBEpCs). The roles of THRIL, miR-19a and TNF-α in regulating the apoptosis of HBEpCs were analyzed by cell apoptosis assay.

We found that THRIL was upregulated in sepsis patients. THRIL is predicted to interact with miR-19a, and the interaction was confirmed by dual-luciferase activity assay. However, THRIL and miR-19a did not affect the expression of each other. Instead, overexpression of THRIL resulted in the increased expression levels of TNF-α, a downstream target of miR-19a in HBEpCs. In HBEpCs, LPS treatment induced the overexpression of THRIL. Cell apoptosis analysis showed that overexpression of THRIL and TNF-α promoted the apoptosis of HBEpCs induced by LPS, while overexpression of miR-19a played an opposite role. Overexpression of THRIL attenuated the effects of overexpression of miR-19a.

Therefore, THRIL is upregulated in sepsis and may sponge miR-19a to upregulate TNF-α, thereby promoting lung cell apoptosis.

• Apoptosis
• Sepsis
• TNF-α
• lncRNA THRIL
• miR-19a

• Apoptosis
• Inflammatory response
• Lung injury
• Sepsis
• lncRNA THRIL

• Acute Lung Injury/diagnosis
• Acute Lung Injury/immunology
• Acute Lung Injury/pathology
• Animals
• Apoptosis/genetics
• Apoptosis/immunology
• Bronchoalveolar Lavage Fluid/cytology
• Bronchoalveolar Lavage Fluid/immunology
• Cell Line
• Disease Models, Animal
• Endothelial Cells
• Endothelium, Vascular/cytology
• Gene Knockdown Techniques
• Humans
• Lipopolysaccharides/immunology
• Lung/blood supply
• Lung/immunology
• Lung/pathology
• Male
• Mice
• MicroRNAs/metabolism
• Microvessels/cytology
• RNA, Long Noncoding/metabolism
• Sepsis/complications
• Sepsis/immunology
• Signal Transduction/genetics
• Signal Transduction/immunology
• Up-Regulation/genetics
• Up-Regulation/immunology
• rho-Associated Kinases/genetics

• Exosomes
• LncRNA
• MicroRNA
• Osteoarthritis

Osteoarthritis (OA), the most common chronic joint disease in the elderly, has become a significant economic burden for families and societies worldwide. Although treatments are continually improving, current drugs only target joint pain, with no effective therapies modifying OA progression. Long noncoding RNAs (lncRNAs), which have received increasing attention in recent years, are abnormally expressed in OA cartilage. In the present study, weighted coexpression network analysis (WGCNA) was applied to identify modules related to certain OA clinical traits. In total, 4404 coding genes and 161 lncRNAs were differentially expressed based on two OA expression profile data sets and normal control samples. Subsequently, 11 independent modules were acquired, and the green module, with a total of 49 hub genes, was identified as the most relevant to OA. These hub genes were validated using the GSE12021 data set. There was only one lncRNA among the hub genes, namely, NONHSAG034351. Thus, we further explored the function of NONHSAG034351‐related genes in the network. Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed that NONHSAG034351‐associated genes are involved in the response to lipopolysaccharide, angiogenesis, tumour necrosis factor (TNF) signalling, and mitogen‐activated protein kinase (MAPK) signalling pathways. In conclusion, we identified modules through WGCNA related to OA clinical traits. NONHSAG034351, the only hub‐lncRNA, was downregulated in OA synovial tissue and might play a significant role in the pathological progression of this disease. Our findings have important clinical implications and could provide novel biomarkers that indicate the molecular mechanisms of OA and act as potential therapeutic targets.

Long noncoding RNAs (lncRNAs) have been reported to be abnormally expressed in osteoarthritis (OA), which is the most common chronic joint disease among the elderly. In the present study, we report the expression profiles of lncRNAs in OA and the identification of modules through WGCNA related to OA clinical traits. NONHSAG034351, the only hub‐lncRNA identified to be downregulated in the synovial tissue of OA patients, might play a significant role in the pathological progression of OA. Furthermore, our findings provide novel biomarkers associated with the molecular mechanisms underlying OA pathogenesis, thus implying potential therapeutic targets with important clinical implications.

• NONHSAG034351
• WGCNA
• hub gene
• lncRNA
• osteoarthritis

This study aimed to investigate the role of long non‐coding RNA (lncRNA) THRIL in coronary heart disease (CHD) patients.

A total of 420 patients who underwent coronary arteriography due to suspected symptoms of CHD were enrolled, in which 220 were diagnosed as CHD and 200 were set as control subjects. LncRNA THRIL in plasma samples of CHD patients and control subjects was detected by reverse transcription‐quantitative polymerase chain reaction. Gensini score and biochemical indexes were evaluated in CHD patients and control subjects. Plasma inflammatory cytokines were detected, and major adverse cardiovascular events (MACE) were recorded in CHD patients.

Both before and after adjustment by age/gender, lncRNA THRIL was increased in CHD patients compared with control subjects (both P < .001), and it well predicted enhanced CHD risk by receiver operating characteristic curves. For coronary artery stenosis, it was positively correlated with Gensini score (P < .001, r = .430). For clinical characteristics, lncRNA THRIL was positively correlated with diabetes mellitus occurrence (P < .001) and fasting blood glucose (FBG) level (P = .029, r = .147). For inflammation, it was positively associated with CRP (P < .001, r = .374), TNF‐α (P < .001, r = .249), IL‐1β (P = .001, r = .222), IL‐8 (P < .001, r = .254), and IL‐17 (P = .011, r = .172), while negatively correlated with IL‐10 (P < .001, r = −.244). For prognosis, lncRNA THRIL was positively associated with MACE accumulating rate (P = .037) in CHD patients.

Long non‐coding RNA THRIL was increased in CHD patients and well predicted elevated CHD risk. Moreover, it was correlated with enhanced coronary stenosis, systematic inflammation, FBG level, and MACE risk in CHD patients.

• coronary heart disease
• disease risk
• inflammation
• long non-coding RNA THRIL
• major adverse cardiovascular events

• apoptosis
• autophagy
• chondrocytes
• noncoding RNA
• osteoarthritis

The immunosuppressive facet and tumorigenic role of TNF-α have been revealed in osteosarcoma (OS). Long noncoding RNA THRIL is identified to regulate TNF-α expression and participates in immune response. Thus, investigations on the clinical expression pattern of THRIL/TNF-α signal in OS would provide a potential target premise for OS patients.

We collected OS (n=83), nontumor tissues (n=37) and serum samples (n=83 for OS and n=40 for healthy control) to determine the expressions and clinical significance of THRIL/TNF-α signal. Knockdown of THRIL in OS cell lines MG63 and Saos2 in vitro and in vivo was performed to confirm its function in the development of OS.

Elevated expression of THRIL was associated with increased TNF-α levels in OS tissues and serum samples. Combination of THRIL and TNF-α in tissues showed a more efficient diagnostic value for OS patients than either of them. Moreover, high-expressed THRIL was associated with larger tumor size, advanced Enneking stage and lung metastasis, whereas high TNF-α expression was found in patients with high histologic grade and patients who simultaneously harbor high THRIL and TNF-α showed the worst overall survival and metastasis-free survival. TNF-α signals increased OS cell vitalities in vitro but knockdown of THRIL inhibited TNF-α expressions, leading to impaired cell vitality, increased apoptosis and also downregulated epithelial to mesenchymal transition (EMT) phenotype and the ability of invasion, but these processes were restored by the treatment of TNF-α. The oncogenic role of THRIL/TNF-α signal was also confirmed in the xenograft model of MG63 cells.

Overexpressed THRIL and TNF-α promoted OS progression with efficient diagnostic and prognostic value. THRIL/TNF-α signal supported cell growth and EMT phenotype of OS cells in vitro and in vivo.

• THRIL
• TNF-α
• growth
• lncRNA
• osteosarcoma

• Cancer
• Chronic disease
• LncRNA
• NF-κB
• Non-coding RNA

• Animals
• Disease Models, Animal
• Gene Expression Regulation
• Genetic Predisposition to Disease/genetics
• Humans
• MicroRNAs/genetics
• NF-kappa B/genetics
• Neoplasms/genetics
• Neoplasms/pathology
• RNA, Long Noncoding/genetics
• Signal Transduction/genetics

• K22 CA197074 NCI NIH HHS
• P30 CA036727 NCI NIH HHS

LPS can induce an inflammatory immune response in the intestine, and long non-coding RNA (lncRNA) is involved in the process of inflammatory disease. However, the biological role of lncRNA in the intestinal inflammation of piglets remains unclear. In this study, the lncRNA expression profile of the ileal mucosa of piglets challenged by LPS was analysed using lncRNA sequencing. In total, 112 novel lncRNAs were predicted, of which 58 were up-regulated and 54 down-regulated following LPS challenge. Expression of 15 selected lncRNAs was validated by quantitative PCR. We further investigated the target genes of lncRNA that were enriched in the signalling pathways involved in the inflammatory immune response by utilising Gene Ontology and Kyoto Encyclopaedia of Genes and Genomes analysis, with cell adhesion molecules and mTOR signalling pathway identified. In addition, the co-expression networks between the differentially expressed lncRNAs and the target mRNAs were constructed, with seven core lncRNAs identified, which also demonstrated that the relationship between lncRNAs and the target genes was highly correlated. Our study offers important information about the lncRNAs of the mucosal immune system in piglets and provides new insights into the inflammatory mechanism of LPS challenge, which might serve as a novel target to control intestinal inflammation.

• Long non-coding RNA
• cam signalling pathway
• intestinal inflammation
• lipopolysaccharide
• mTOR signalling pathway

• Animals
• Cell Adhesion/genetics
• Gene Ontology
• Inflammation/genetics
• Intestinal Mucosa/physiology
• Intestines/physiology
• Lipopolysaccharides/immunology
• RNA, Long Noncoding/genetics
• Signal Transduction/genetics
• Swine
• TOR Serine-Threonine Kinases/genetics
• Transcriptome

• National Natural Science Foundation of China
• the Hubei Provincial Department of Education