Chronic airway inflammation induced by cigarette smoke (CS) plays an essential role in the pathogenesis of chronic obstructive pulmonary disease (COPD). MALAT1 is involved in a variety of inflammatory disorders. However, studies focusing on the interaction between MALAT1 and CS-induced airway inflammation remain unknown. The present study investigated the effects and mechanisms of MALAT1 in CS-induced airway inflammation in the pathogenesis of COPD. RT-qPCR was employed to determine the mRNA levels of MALAT1, miR-30a-5p and inflammatory cytokines. Protein concentrations of IL-1β and IL-6 in cell culture supernatant and mouse bronchoalveolar lavage fluid (BALF) were assessed by ELISA assay kits. Dual-luciferase reporter assay was conducted to verify the interaction between MALAT1 and miR-30a-5p. The protein expression of JNK and p-JNK was determined by western blot (WB). MALAT1 was highly expressed in cigarette smoke extract (CSE)-treated human bronchial epithelial cells (HBECs) and COPD mice lung tissues. Knockdown of MALAT1 significantly alleviate CS-induced inflammatory response. MALAT1 directly interacted with miR-30a-5p and knockdown of miR-30a-5p significantly inhibit the protective effects of MALAT1 silencing after CS exposure. Additionally, our results showed that miR-30a-5p could regulate inflammation via modulating the activation of JNK signaling pathway. Moreover, our results demonstrated MALAT1 could activate JNK signaling pathway by sponging miR-30a-5p. Our results demonstrated MALAT1 promotes CS-induced airway inflammation by inhibiting the activation of JNK signaling pathway via sponging miR-30a-5p.

Intervertebral disc degeneration (IVDD) is a prevalent chronic condition causing spinal pain and functional impairment. This study investigates the role of extracellular vesicles (EVs) derived from human umbilical cord mesenchymal stem cells (hUCMSCs) in regulating IVDD. Using RNA-seq, we analyzed differential expressions of lncRNA and miRNA in nucleus pulposus tissues from various mouse groups. We identified key regulatory molecules, MALAT1 and miRNA-138-5p, which contribute to IVDD. Further experiments demonstrated that MALAT1 can up-regulate SLC7A11 expression by competitively binding to miR-138-5p, forming a MALAT1/miR-138-5p/SLC7A11 coexpression regulatory network. This study elucidates the molecular mechanism by which hUCMSC-derived EVs regulate IVDD and could help develop novel therapeutic strategies for treating this condition. Our findings demonstrate that hUCMSCs-EVs inhibit ferroptosis in nucleus pulposus cells, thereby improving IVDD. These results highlight the therapeutic potential of hUCMSCs-EVs in ameliorating the development of IVDD, offering significant scientific and clinical implications for new treatments.

BACKGROUND: To evaluate the role of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in the prognosis of severe community-acquired pneumonia (CAP) in children.
METHODS: According to the median MALAT1 value of 3.2 at baseline, 93 pediatric patients with severe CAP were divided into low (n = 46, median MALAT1 level = 1.9) or high (n = 47, median MALAT1 level = 4.5) MALAT1 groups. Another 93 age-, gender-, and body mass index (BMI)-matched healthy individuals were included in the control group using the propensity-score matching (PSM) method. A multivariate Cox proportional hazards model was used to explore the association of MALAT1 level with the 28-day mortality after controlling for potential confounding factors.
RESULTS: The MALAT1 expressions were significantly higher in the patients with severe CAP compared with those in the healthy controls (3.2 vs. 0.9, P < 0.01). The receiver operating characteristic (ROC) analysis showed that the area under the curve (AUC) was 0.927 when the cut-off value of MALAT1 was 1.5. Moreover, the MALAT1 expressions were substantially lower in survivals than non-survivals (3.8 vs. 2.6, P < 0.01), and the multivariate Cox regression analysis indicated a positive association between MALAT1 levels and mortality risk (HR = 3.32; 95% CI: 1.05-10.47; P = 0.04).
CONCLUSIONS: MALAT1 might be a promising marker for predicting the prognosis of severe CAP in pediatric patients.

Dermatologic disorders, affecting the integumentary system, involve diverse molecular mechanisms such as cell proliferation, apoptosis, inflammation and immune responses. Long noncoding RNAs, particularly Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1), are crucial regulators of gene expression. MALAT1 influences inflammatory responses, immune cell function and signaling pathways, impacting various physiological and pathological processes, including dermatologic disorders. Dysregulation of MALAT1 is observed in skin conditions like psoriasis, atopic dermatitis and systemic lupus erythematosus. However, its precise role remains unclear. This review consolidates knowledge on MALAT1\'s impact on skin biology and pathology, emphasizing its potential diagnostic and therapeutic implications in dermatologic conditions.
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BACKGROUND: Previous studies have demonstrated the strong association of inflammatory cytokines and vitamin D (VitD) deficiency and ischemic stroke (IS) pathogenesis. Due to the negative correlation between long non-coding RNA (lncRNA) Malat1 and pro-inflammatory factors we decided to investigate the associations between Malat1 expression with serum interleukin-1β (IL-1β), and VitD levels in IS patients.
METHODS: In this cross-sectional study, 63 IS patients were included. We used enzyme-linked immunosorbent assays to evaluate the serum levels of VitD and IL-1β. Malat1 expression was evaluated by the real-time polymerase chain reaction test. The associations between Malat1expression with VitD and IL-1β were analysed with linear regression (Stepwise model) and Pearson\'s correlation analysis.
RESULTS: The Malat1 expression was inversely correlated with stroke severity (r=-0.25, P=0.043). Stepwise regression analysis showed a significant positive relationship between VitD level and Malat1 expression (Beta=0.28, P=0.02), and also showed a non-significant negative relationship between IL-1β and stroke severity. VitD level showed a positive Pearson correlation with Malat1 (r=0.28, P=0.023) and a negative correlation with IL-1β (r=-0.29, P=0.018) while it could not detect a significantly negative correlation with stroke severity.
CONCLUSIONS: For the first time the associations between Malat1 expression with IL-1β and VitD in IS patients was analyzed. We found a significant positive relationship between VitD and Malat1. This correlation needs to be investigated with a larger sample size to achieve a strong and reliable association between VitD and Malat1.

UNASSIGNED: Recent studies have addressed the possible role of long non-coding RNAs (lnc-RNAs), Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1), and Taurine Upregulated Gene 1 (TUG1), in modulating the underlying mechanisms of obesity-related metabolic abnormalities. However, studies are limited and contradictory. Hence, we sought to investigate the relationship of the transcript level of these two lnc-RNAs with metabolic syndrome (MetS)-related parameters in women with obesity and overweight.
UNASSIGNED: This cross-sectional study was conducted on 342 women with obese and overweight. We conducted assessments encompassing anthropometric measurements, body composition analysis, fasting blood sugar (FBS) levels, lipid profile analysis, insulin levels, HOMA-IR index, and liver enzyme profiling. A quantitative real-time polymerase chain reaction (PCR) was used to evaluate transcript levels of MALAT1 and TUG1. Also, a 147-question semi-quantitative food frequency questionnaire (FFQ) and the International Physical Activity Questionnaire (IPAQ) were used to evaluate food intake and physical activity, respectively.
UNASSIGNED: There was a significant association between FBS and MALAT1 transcript level (β: 0.382; 95% CI: 0.124, 0.640; P = 0.004). Also, there was a significant association between triglyceride (TG) and MALAT1 transcript level (β: 4.767; 95% CI: 2.803, 6.731; P < 0.0001). After adjusting for age, BMI, energy intake, and physical activity, an inverse significant association was observed between high-density lipoprotein cholesterol (HDL-c) and MALAT1 transcript level (β: -0.325; 95% CI: -0.644, -0.006; P = 0.046).
UNASSIGNED: Our findings indicated positive associations between mRNA levels of MALAT1 and MetS-related parameters, including FBG, TG, HDL, and systolic blood pressure in overweight and obese women. However, large prospective studies are needed to further establish this concept.
UNASSIGNED: The online version contains supplementary material available at 10.1007/s40200-023-01367-2.

BACKGROUND: Erectile dysfunction (ED) is a common male sexual dysfunction, with an increasing incidence, and the current treatment is often ineffective.
METHODS: Vascular endothelial growth factor (VEGFA) was used to treat bone marrow-derived mesenchymal stem cells (BM-MSCs), and their cell migration rates were determined by Transwell assays. The expression of the von Willebrand Factor (vWF)VE-cadherin, and endothelial nitric oxide synthase(eNOS) endothelial markers was determined by qRT‒PCR and Western blot analyses. The MALAT1-induced differentiation of BM-MCs to ECs via the CDC42/PAK1/paxillin pathway was explored by transfecting VEGFA-induced BM-MSC with si-MALAT1 and overexpressing CDC42 and PAK1. The binding capacity between CDC42, PAK1, and paxillin in VEGFA-treated and non-VEGFA-treated BM-MSCs was examined by protein immunoprecipitation. MiR-206 was overexpressed in VEGFA-induced BM-MSC, and the binding sites of MALAT1, miR-206, and CDC42 were identified using a luciferase assay. Sixty male Sprague‒Dawley rats were divided into six groups (n = 10/group). DMED modelling was demonstrated by APO experiments and was assessed by measuring blood glucose levels. Erectile function was assessed by measuring the intracavernosa pressure (ICP) and mean arterial pressure (MAP). Penile erectile tissue was analysed by qRT‒PCR, Western blot analysis, and immunohistochemical staining.
RESULTS: MALAT1 under VEGFA treatment conditions regulates the differentiation of BM-MSCs into ECs by modulating the CDC42/PAK1/paxillin axis. In vitro experiments demonstrated that interference with CDC42 and MALAT1 expression inhibited the differentiation of BM-MSCs to ECs. CDC42 binds to PAK1, and PAK1 binds to paxillin. In addition, CDC42 in the VEGFA group had a greater ability to bind to PAK1, whereas PAK1 in the VEGFA group had a greater ability to bind to paxillin. Overexpression of miR-206 in VEGFA-induced BM-MSCs demonstrated that MALAT1 competes with the CDC42 3\'-UTR for binding to miR-206, which in turn is involved in the differentiation of BM-MSCs to ECs. Compared to the DMED model group, the ICP/MAP ratio was significantly greater in the three BM-MSCs treatment groups.
CONCLUSIONS: MALAT1 facilitates BM-MSC differentiation into ECs by regulating the miR-206/CDC42/PAK1/paxillin axis to improve ED. The present findings revealed the vital role of MALAT1 in the repair of BM-MSCs for erectile function and provided new mechanistic insights into the BM-MSC-mediated repair of DMED.

UNASSIGNED: Hypertrophic scarring (HS) is commonly described as an abnormal post-traumatic tissue repair characterized by excessive hypercellularity and extracellular matrix (ECM) deposition. Mounting evidence suggests that MALAT1 is maladjusted in many fibrotic diseases, but its contribution to HS progression remains poorly understood. Hence, we sought to elucidate the fundamental role of MALAT1 in HS.
UNASSIGNED: The expression of MALAT1, miR-29a-3p, and Smurf2 in skin tissues and fibroblasts was assessed by RT-qPCR and Western blotting. Furthermore, lentiviruses, RNAi, or plasmids were utilized to transfect hypertrophic scar fibroblasts (HSFs) for gene overexpression or downregulation. The biological behaviors of HSFs were quantified by the CCK-8 assay, wound healing assay, transwell assay, and flow cytometry. Mechanistically, bioinformatics analysis, dual-luciferase reporter assays, and rescue experiments were performed to verify the relationship between miR-29a-3p and MALAT1 or Smurf2.
UNASSIGNED: Our data indicate that MALAT1, Smurf2 were overexpressed while miR-29a-3p was suppressed in HS tissues and fibroblasts. Downregulation of MALAT1 may lead to decreased proliferation, migration, and invasion of fibroblasts, accompanied by enhanced apoptosis, reduced TGF-β signal transduction, and ECM accumulation in HSFs, by enhancing miR-29a-3p and suppressing Smurf2 expression. Mechanistically, MALAT1 acted as a sponge for miR-29a-3p, while miR-29a-3p directly targeted Smurf2. More importantly, rescue experiments suggested that MALAT1 downregulation induced impact on the proliferation, migration, and invasion of HSFs could be partially overturned through miR-29a-3p knockdown or Smurf2 overexpression.
UNASSIGNED: MALAT1 knockdown inhibits the proliferation, migration, invasion, and collagen deposition of HSFs via targeting the miR-29a-3p/Smurf2 axis, which may reveal a promising therapeutic exploitable vulnerability to HS.

Long noncoding RNAs (lncRNAs) participate in transcriptional, epigenetic, and post-transcriptional regulation of gene expression and may influence carcinogenesis. MALAT1 is a lncRNA that is expressed in endocrine and many other neoplasms and it has been shown to have oncogenic and/or tumor suppressor effects in tumor development. Olfactory neuroblastomas arise in the nasal cavity while sympathetic neuroblastomas are present mainly in the adrenal and periadrenal regions. These neoplasms have overlapping histopathological features. Rare cases of sympathetic neuroblastomas metastatic to the nasal cavity have been reported. PHOX2B has been shown to be relatively specific for sympathetic neuroblastomas, but only a limited number of cases of olfactory neuroblastomas have been examined for PHOX2B expression. This study aimed to explore the potential utilization of MALAT1 and PHOX2B in distinguishing these two entities. Tissue microarrays (TMA) were created for olfactory neuroblastomas (n = 26) and sympathetic neuroblastomas (n = 52). MALAT1 lncRNA expression was assessed by in situ hybridization using RNAScope technology. TMA slides were scanned by Vectra multispectral imaging system and image analysis and quantification were performed with inForm software. PHOX2B expression was analyzed by immunohistochemistry. MALAT1 showed predominantly nuclear expression in both tumor types and MALAT1 expression was 2-fold higher in olfactory neuroblastomas compared to sympathetic neuroblastomas (p < 0.0001). PHOX2B showed nuclear staining in most sympathetic neuroblastomas (51/52, 98 %) while only 1 olfactory neuroblastoma (3.8 %) was focally positive for this marker. These findings suggest immunostaining of PHOX2B could be an excellent marker in distinguishing between these two tumor types.

Sepsis commonly occurs in patients with serious infections. It severely threatens the health of patients and has very high mortality rates. Urosepsis is a type of sepsis in which the serious infection originates from the urinary system. Early diagnosis of the occurrence and severity of urogenital sepsis is crucial for improving patient prognosis. Long noncoding RNAs (LncRNAs) play important roles in the occurrence of a number of diseases, including sepsis, and can be potential biomarkers that predict disease development. The present study aimed to discover potential LncRNAs that can predict the occurrence of urosepsis. RNA-sequence data from patients with sepsis from the GEO database was analyzed and LncRNAs associated with sepsis were identified. The expression of LncRNAs associated with sepsis was tested in clinical urosepsis samples. Finally, the value of these LncRNAs in predicting urosepsis was verified using clinical samples. From the GEO database a total of nine LncRNAs (MALAT1, NEAT1, RMRP, LncIRX5, LINC01742, DSCR4, C22ORF34, LINC00381, and LINC01102) were identified that had expression changes corresponding with the occurrence of sepsis. Specifically, MALAT1, NEAT1 and DSCR4 revealed differential expression in patients with urosepsis. Moreover, MALAT1, and DSCR4 were shown to be significant risk indicators for urosepsis, and NEAT1 was shown to reflect disease severity. Therefore, the present study indicated that the LncRNAs, MALAT1, NEAT1 and DSCR4 can reflect the occurrence and severity of urosepsis and may act as potential biomarkers.