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Journal articles on the topic 'MiR-198'

Author: Grafiati

Published: 6 September 2023

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1

Ray, Jessica, Christianne Hoey, Xiaoyong Huang, Paul Christopher Boutros, and Stanley K. Liu. "Microrna-198: A novel tumor suppressor in prostate cancer." Journal of Clinical Oncology 36, no. 6_suppl (February 20, 2018): 92. http://dx.doi.org/10.1200/jco.2018.36.6_suppl.92.

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92 Background: microRNAs (miRNAs) are small non-coding RNA molecules which act as repressors of gene function, and have been identified as playing substantial roles in cancer as both tumor suppressors and oncogenes. miR-198 has been reported to be down-regulated in several cancers, with low expression associated with worse overall survival. In addition, miR-198 has demonstrated tumor suppressor effects by altering several hallmarks of cancer. Despite compelling evidence in other cancers, miR-198's role in prostate cancer aggression has not yet been evaluated. Methods: Experiments were conducted by overexpressing miR-198 in three prostate cancer cell lines: DU145, LNCaP and 22RV1. To examine miR-198's effect on hallmarks of cancer in vitro, we used standard protocols to assay proliferation, colony formation, cell cycle profile, migration, and invasive potential. Gene array, qPCR, western blotting, and siRNA knockdown experiments were used to establish miR-198 downstream targets. Results: Overexpression of the candidate tumor suppressor miR-198 diminished proliferation in all prostate cancer cell lines and significantly impaired colony formation in soft agar. Subsequently, miR-198 expression was also demonstrated to reduce growth and tumor formation in vivo using LNCaP xenografts. Gene arrays and in silico target prediction identified several candidate targets, none of which have been previously linked to miR-198. MIB1, an E3 ubiquitin ligase, was the only target we have since identified to be reduced with miR-198 overexpression at both the RNA and protein levels. Knockdown of MIB1 recapitulated miR-198's effects on proliferation and colony formation, and further experiments are underway to demonstrate a direct binding relationship. An additional gene array with MIB1 siRNA will be performed to highlight pathways through which MIB1/miR-198 suppress tumorigenesis. Conclusions: Our evidence supports miR-198 as an important tumor suppressor in prostate cancer, with elevated expression impairing proliferation, colony formation, and in vivo tumor formation. This investigation into miR-198 highlights a potential role as a prostate cancer biomarker, or as a potential target of therapeutics to restore miRNA activity.

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2

Li, Siqi, Junmei Yang, Xiaoting Liu, Rui Guo, and Ruidong Zhang. "circITGA7 Functions as an Oncogene by Sponging miR-198 and Upregulating FGFR1 Expression in Thyroid Cancer." BioMed Research International 2020 (June 22, 2020): 1–8. http://dx.doi.org/10.1155/2020/8084028.

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Background. Emerging evidence has indicated that circular RNAs (circRNAs), recognized as functional noncoding transcripts in eukaryotic cells, may be involved in regulating many physiological or pathological processes. However, the regulation and function of circular RNA circITGA7 in thyroid cancer (TC) remains unknown. Methods. In this study, we found that circITGA7 is upregulated in TC cell lines. We then performed functional analyses in the cell lines to support clinical findings. Mechanistically, we demonstrated that circITGA7 can directly bind to miR-198 and reduce the inhibition effect of miR-198 on target FGFR1 expression. Results. We reported an upregulation of circITGA7 in patients with TC. Silencing of circITGA7 inhibits metastasis and proliferation of TC cell lines in vitro. In addition, in the TC cell lines, the knockdown of circITGA7 or overexpression of miR-198 significantly suppressed FGFR1 levels. Mechanistically, we found that circITGA7 acts as miR-198 competitive endogenous RNA (ceRNA) to regulate FGFR1 expression. Conclusions. In summary, circRNA circITGA7 may play a regulatory role in TC and may be a potential marker for TC diagnosis or progression.

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3

Sundaram, Gopinath M., Hisyam M. Ismail, Mohsin Bashir, Manish Muhuri, Candida Vaz, Srikanth Nama, Ghim Siong Ow, et al. "EGF hijacks miR-198/FSTL1 wound-healing switch and steers a two-pronged pathway toward metastasis." Journal of Experimental Medicine 214, no. 10 (August 21, 2017): 2889–900. http://dx.doi.org/10.1084/jem.20170354.

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Epithelial carcinomas are well known to activate a prolonged wound-healing program that promotes malignant transformation. Wound closure requires the activation of keratinocyte migration via a dual-state molecular switch. This switch involves production of either the anti-migratory microRNA miR-198 or the pro-migratory follistatin-like 1 (FSTL1) protein from a single transcript; miR-198 expression in healthy skin is down-regulated in favor of FSTL1 upon wounding, which enhances keratinocyte migration and promotes re-epithelialization. Here, we reveal a defective molecular switch in head and neck squamous cell carcinoma (HNSCC). This defect shuts off miR-198 expression in favor of sustained FSTL1 translation, driving metastasis through dual parallel pathways involving DIAPH1 and FSTL1. DIAPH1, a miR-198 target, enhances directional migration through sequestration of Arpin, a competitive inhibitor of Arp2/3 complex. FSTL1 blocks Wnt7a-mediated repression of extracellular signal–regulated kinase phosphorylation, enabling production of MMP9, which degrades the extracellular matrix and facilitates metastasis. The prognostic significance of the FSTL1-DIAPH1 gene pair makes it an attractive target for therapeutic intervention.

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4

Gao, Xueying, Ying Tang, and Yunping Ma. "Bone Marrow Mesenchymal Stem Cells (BMSCs)-Triggered Up-Regulation of miR-198 Impedes the Aggressive Migration and Invasion of Cervical Cancer Cells." Journal of Biomaterials and Tissue Engineering 12, no. 7 (July 1, 2022): 1285–92. http://dx.doi.org/10.1166/jbt.2022.3033.

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As a subset of RNAs without protein-coding function, short non-coding RNAs (microRNAs) are reported to contribute to the progress of multiple disorders. Nevertheless, the precise function of miR-198 in human cervical cancer is still an open question. RNA sequencing between cervical cancer cell lines and normal cervical epithelial cells identified CCAR1 to be highly expressed in cervical cancer. Cells were transfected with si-CCAR1 followed by analysis of cell behaviors using clonogenic assay and transwell migrating assay. The binding of miR-198 and CCAR1 was verified by a dual-luciferase reporter gene experiment. CCAR1 was highly expressed in cervical cancer tissues and cell lines and associated with tumor staging. Knockdown of CCAR1 restrained the malignant phenotypes of cervical cancer cells. CCAR1 was a target of miR198. Co-culture with BMSCs upregulated miR-198 expression, resulting in impediment of the aggressive phenotypes of cervical cancer cells, which was mediated by suppression of CCAR1 and release of inflammatory factors. In conclusion, CCAR1 level is increased in cervical cancer tissues or cell lines. Co-culture of BMSCs can facilitate the proliferating, migrating and invading activities of cervical cancer cells but reduce the release of inflammatory factors which is possibly through manipulating the axis of miR-198/CCAR1.

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5

Wu, Shujun, Hui Li, Chunya Lu, Furui Zhang, Huaqi Wang, Xinhua Lu, and Guojun Zhang. "Aberrant expression of hsa_circ_0025036 in lung adenocarcinoma and its potential roles in regulating cell proliferation and apoptosis." Biological Chemistry 399, no. 12 (November 27, 2018): 1457–67. http://dx.doi.org/10.1515/hsz-2018-0303.

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AbstractAs the most common histological subtype of lung cancer, lung adenocarcinoma remains a tremendous risk to public health, which requires ceaseless efforts to elucidate the potential diagnostic and therapeutic strategies. Circular RNAs (circRNAs) have been identified with emerging roles in tumorigenesis and development. Our preliminary work noticed that hsa_circ_0025036 was significantly upregulated in lung adenocarcinoma tissues. However, its specific roles in lung adenocarcinoma remain unclear. The results in this study revealed that hsa_circ_0025036 existed as a circular form and was aberrantly upregulated in lung adenocarcinoma tissues via quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Its expression level exhibited a close link with aggressive clinicopathological parameters including cancer differentiation, TNM stage and lymph node metastasis. hsa_circ_0025036 knockdown significantly suppressed cell proliferation and promoted cell apoptosis in A549 and Calu-3 cells. Moreover, hsa_circ_0025036/miR-198/SHMT1&TGF-αaxis was identified via bioinformatics analysis and Dual-Luciferase Reporter assays. miR-198 inhibitors reversed the function of hsa_circ_0025036 knockdown. hsa_circ_0025036 knockdown exerted similar effects with miR-198 upregulation on cell proliferation and apoptosis. In conclusion, we demonstrate that hsa_circ_0025036 regulates cell proliferation and apoptosis in lung adenocarcinoma cells probably via hsa_circ_0025036/miR-198/SHMT1&TGF-αaxis. hsa_circ_0025036 may serve as a potential prognostic biomarker and a therapeutic target for lung adenocarcinoma.

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6

LU, JIANXIN, BONNIE CHING-HA KWAN, FERNAND MAC-MOUNE LAI, LAI-SHAN TAM, EDMUND KWOK-MING LI, KAI-MING CHOW, GANG WANG, PHILIP KAM-TAO LI, and CHEUK-CHUN SZETO. "Glomerular and tubulointerstitial miR-638, miR-198 and miR-146a expression in lupus nephritis." Nephrology 17, no. 4 (April 17, 2012): 346–51. http://dx.doi.org/10.1111/j.1440-1797.2012.01573.x.

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7

Marín-Müller, Christian, Dali Li, Jian-Ming Lu, Zhengdong Liang, Osvaldo Vega-Martínez, William Fisher, Changyi Chen, and Qizhi Cathy Yao. "MiR-198 sensitizes pancreatic cancer to gemcitabine treatment through downregulation of VCP-mediated autophagy maturation." Journal of Clinical Oncology 40, no. 16_suppl (June 1, 2022): e16290-e16290. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.e16290.

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e16290 Background: The mechanism of human pancreatic ductal adenocarcinoma (PDAC) resistance to nucleoside analog and first-line chemotherapy drug gemcitabine is not clearly understood, but some studies have associated it with increased autophagy. In cancer biology, autophagy plays dual roles as it can promote tumor suppression during early stages, but in established tumors, it plays a crucial role in tumor growth by enhancing survival under metabolic and therapeutic stress. We have previously found that miR-198 acts as a tumor suppressor in PDAC through the targeting of a network of tumorigenic factors, including the Valosin-containing protein (VCP), which has been reported to play an important role in autophagy. In this study, we investigate whether the repression of VCP through miR-198 replacement disrupts the autophagy process and sensitizes PDAC cells to gemcitabine treatment. Methods: MIAPaCa2 cells with forced overexpression of mesothelin (MSLN) and AsPC-1 cell lines and, CDX and PDX mouse models were used for gemcitabine sensitization studies. For miR-198 replacement, a miR-198 expression vector-loaded lactic co-glycolic-acid-modified polyethylenimine polyplex (LPNP-p198) was used. Autophagy disruption experiments were run over miR-198 and/or VCP overexpressing cell lines. Nude mice were used for subcutaneous and orthotopic CDX models and SCID/Beige were used for the subcutaneous PDX model. Results: Cell lines were treated with LPNP-p198 in combination with gemcitabine and cell growth was significantly inhibited when compared to gemcitabine alone. Additionally, it was determined that miR-198 disrupts the autophagy maturation process and, that it is then restored by overexpression of VCP. LPNP-p198 can effectively enter tumor cells and induce tumor sensitization in vivo, resulting in an 80-90% reduction of tumor burden and metastatic spread in the LPNP-p198 plus gemcitabine group when compared to controls, with the concomitant downregulation of VCP expression in the tumor tissue. In addition, this group had the fewest mice with jaundice, ascites, and metastases to the abdominal cavity, spleen, liver, and kidney. Finally, to address the potential of the observed effect in the context of the heterogenic nature of PDAC, we confirmed our findings in a PDX mouse model, where a marked reduction in tumor burden was observed in the LPNP-p198 plus gemcitabine group compared to controls. Conclusions: Our findings indicate that miR-198 replacement disrupts the autophagy maturation process and sensitizes PDAC cells to gemcitabine through VCP repression, indicating a potential therapeutic strategy for targeting gemcitabine-resistant PDAC and, establishing the use of LPNPs as a prototype for effective nucleic acid delivery in vitro and in vivo, with potential to be used from bench to clinic.

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8

Marin-Muller, Christian, Dali Li, Jian-Ming Lü, Zhengdong Liang, Osvaldo Vega-Martínez, Sue E. Crawford, Mary K. Estes, William E. Fisher, Changyi Chen, and Qizhi Yao. "Nanoparticle-Mediated Therapy with miR-198 Sensitizes Pancreatic Cancer to Gemcitabine Treatment through Downregulation of VCP-Mediated Autophagy." Pharmaceutics 15, no. 8 (July 28, 2023): 2038. http://dx.doi.org/10.3390/pharmaceutics15082038.

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Pancreatic ductal adenocarcinoma (PDAC) remains an extremely aggressive disease characterized by rapidly acquired multi-drug resistance, including to first-line chemotherapeutic agent gemcitabine. Autophagy is a process that is often exploited by cancer and is one of several intrinsic factors associated with resistance to gemcitabine. We have previously found that miR-198 acts as a tumor suppressor in PDAC through the targeting of factors including Valosin-containing protein (VCP). VCP has been reported to play an important role in autophagic flux. In this study, we investigated whether the repression of VCP through miR-198 administration disrupts the autophagy process and sensitizes PDAC cells to gemcitabine treatment in vitro. Moreover, we used LGA-PEI (LPNP) nanoparticles to effectively administer miR-198 to tumors in vivo, inducing tumor sensitization to gemcitabine and leading to a significant reduction in tumor burden and metastases and a concomitant downregulation of VCP expression and autophagy maturation. Our results indicate a potential therapeutic strategy for targeting gemcitabine resistant PDAC and establishes the use of LPNPs for effective therapeutic delivery of nucleic acids in vitro and in vivo.

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9

Liu, Man, Yao Meng, Keren He, and Chonglin Luan. "Hsa_circ_0002060 Knockdown Ameliorates Osteoporosis by Targeting MiR-198-5p." Biological and Pharmaceutical Bulletin 44, no. 1 (January 1, 2021): 88–95. http://dx.doi.org/10.1248/bpb.b20-00643.

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10

Abhilasha, A., P. Mitra, S. Suri, I. Saxena, R. K. Shukla, and P. Sharma. "T133 Circulating levels of miR-24-3p and miR-198 in type 2 diabetes mellitus." Clinica Chimica Acta 530 (May 2022): S119. http://dx.doi.org/10.1016/j.cca.2022.04.612.

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11

Nie, Er, Xin Jin, Weining Wu, Tianfu Yu, Xu Zhou, Zhumei Shi, Junxia Zhang, Ning Liu, and Yongping You. "MiR-198 enhances temozolomide sensitivity in glioblastoma by targeting MGMT." Journal of Neuro-Oncology 133, no. 1 (April 19, 2017): 59–68. http://dx.doi.org/10.1007/s11060-017-2425-9.

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12

Liu, Lina, Luran Liu, Yunting Lu, Tianyuan Zhang, and Wenting Zhao. "Serum aberrant expression of miR-24-3p and its diagnostic value in Alzheimer’s disease." Biomarkers in Medicine 15, no. 16 (November 2021): 1499–507. http://dx.doi.org/10.2217/bmm-2021-0098.

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Aim: This study aimed to evaluate the effect of miR-24-3p in Alzheimer’s disease (AD). Materials & methods: A total of 198 participants were recruited in this study, including 104 AD patients and 94 healthy controls. Expression of miR-24-3p was detected using quantitative real-time PCR. Receiver-operating characteristic curve was used to assess the diagnostic value of miR-24-3p. In vitro AD model was established to evaluate the effect of miR-24-3p. The downstream target was detected by luciferase reporter gene assay. Results: Expression of miR-24-3p showed 1.6-fold increase in AD group compared with healthy controls, and a negative correlation of miR-24-3p with mini-mental state examination score was obtained. Receiver-operating characteristic curve showed satisfactory diagnostic accuracy. Downregulation of miR-24-3p promoted cell proliferation and inhibited cell apoptosis. KLF8 is a target gene of miR-24-3p. Conclusion: MiR-24-3p has a certain value in the diagnosis of AD and may be a potential biomarker.

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13

Lu, Zhaoan, Chuanwen Wang, Xiaolong Lv, and Wen Dai. "Hsa_circ_0010220 regulates miR-198/Syntaxin 6 axis to promote osteosarcoma progression." Journal of Bone Oncology 28 (June 2021): 100360. http://dx.doi.org/10.1016/j.jbo.2021.100360.

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14

Xu, Fei, Mengdong Ni, Jiajia Li, Jingyi Cheng, Haiyun Zhao, Jingjing Zhao, Shenglin Huang, and Xiaohua Wu. "Circ0004390 promotes cell proliferation through sponging miR-198 in ovarian cancer." Biochemical and Biophysical Research Communications 526, no. 1 (May 2020): 14–20. http://dx.doi.org/10.1016/j.bbrc.2020.03.024.

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15

Liu, Xiaoxia, Yumei Dong, Song Chen, Guangde Zhang, Mingyu Zhang, Yingzi Gong, and Xueqi Li. "Circulating MicroRNA-146a and MicroRNA-21 Predict Left Ventricular Remodeling after ST-Elevation Myocardial Infarction." Cardiology 132, no. 4 (2015): 233–41. http://dx.doi.org/10.1159/000437090.

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Objectives: MicroRNA (miR)-146a and miR-21 have been reported to participate in inflammatory reactions and fibrosis. Excessive inflammation and cardiac fibrosis may play important roles in the development of left ventricular remodeling (LVR). This study assessed whether miR-146a, miR-21 and other biomarkers could predict LVR after myocardial infarction (MI). Methods: Circulating miR-146a, miR-21 and other biomarker levels were measured in 198 patients with acute MI 5 days after primary percutaneous coronary intervention (PCI). All patients were assessed by transthoracic echocardiography on day 5 and 1 year after primary PCI. Results: Concentrations of circulating miR-146a, miR-21, C-reactive protein, creatine kinase MB type and troponin I, as well as estimated glomerular filtration rate (eGFR) and left ventricular ejection fraction (LVEF), were significantly higher in patients with than in those without LVR (p < 0.05). Multivariate logistic regression analysis showed that circulating miR-146a (odds ratio, OR = 2.127, p < 0.0001), miR-21 (OR = 1.119, p < 0.0001), eGFR (OR = 0.939, p = 0.0137) and LVEF (OR = 0.802, p = 0.0048) were independent predictors of LVR development. The area under the curve for the combination of miR-146a and miR-21 was significantly higher than for either alone. Conclusion: Circulating miR-146a and miR-21 may be novel biomarkers predictive of LVR after acute MI. Their combination may better predict LVR than either alone.

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Bakre, Abhijeet, Patricia Mitchell, Jonathan K. Coleman, Les P. Jones, Geraldine Saavedra, Michael Teng, S. Mark Tompkins, and Ralph A. Tripp. "Respiratory syncytial virus modifies microRNAs regulating host genes that affect virus replication." Journal of General Virology 93, no. 11 (November 1, 2012): 2346–56. http://dx.doi.org/10.1099/vir.0.044255-0.

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Respiratory syncytial virus (RSV) causes substantial morbidity and life-threatening lower respiratory tract disease in infants, young children and the elderly. Understanding the host response to RSV infection is critical for developing disease-intervention approaches. The role of microRNAs (miRNAs) in post-transcriptional regulation of host genes responding to RSV infection is not well understood. In this study, it was shown that RSV infection of a human alveolar epithelial cell line (A549) induced five miRNAs (let-7f, miR-24, miR-337-3p, miR-26b and miR-520a-5p) and repressed two miRNAs (miR-198 and miR-595), and showed that RSV G protein triggered let-7f expression. Luciferase–untranslated region reporters and miRNA mimics and inhibitors validated the predicted targets, which included cell-cycle genes (CCND1, DYRK2 and ELF4), a chemokine gene (CCL7) and the suppressor of cytokine signalling 3 gene (SOCS3). Modulating let-7 family miRNA levels with miRNA mimics and inhibitors affected RSV replication, indicating that RSV modulates host miRNA expression to affect the outcome of the antiviral host response, and this was mediated in part through RSV G protein expression.

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17

Wang, Jian, Guorong Dan, Tao Shangguan, Han Hao, Ran Tang, Kaige Peng, Jiqing Zhao, Huiqin Sun, and Zhongmin Zou. "miR-198 Represses the Proliferation of HaCaT Cells by Targeting Cyclin D2." International Journal of Molecular Sciences 16, no. 8 (July 27, 2015): 17018–28. http://dx.doi.org/10.3390/ijms160817018.

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18

Liu, Yingguang, JeongMin Natalie Kim, Glynn B. Reno, Jiayi Li, Osvaldo Vega-Martinez, Peter Heeckt, Andrew Mearns-Spragg, Christian Marin-Müller, and Anthony J. Bauer. "Sa1112: THERAPEUTIC POTENTIAL OF MIR-198 TO SUPPRESS MC38 COLONIC ADENOCARCINOMA GROWTH." Gastroenterology 162, no. 7 (May 2022): S—310. http://dx.doi.org/10.1016/s0016-5085(22)60739-x.

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19

Kaushik, Pankhuri, and Arun Kumar. "Emerging role and function of miR-198 in human health and diseases." Pathology - Research and Practice 229 (January 2022): 153741. http://dx.doi.org/10.1016/j.prp.2021.153741.

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20

Che, Jianpeng, Mingming Liu, and Hongwei Lv. "Dexmedetomidine disrupts esophagus cancer tumorigenesis by modulating circ_0003340/miR-198/HMGA2 axis." Anti-Cancer Drugs 33, no. 5 (March 23, 2022): 448–58. http://dx.doi.org/10.1097/cad.0000000000001284.

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21

Walston, S. A., M. Bloomston, J. Salloum, E. J. Wuthrick, and T. M. Williams. "Expression Levels of MiR-198 Predict Clinical Outcomes in Resected Pancreatic Adenocarcinoma." International Journal of Radiation Oncology*Biology*Physics 93, no. 3 (November 2015): S155. http://dx.doi.org/10.1016/j.ijrobp.2015.07.369.

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22

Ralfkiaer, Ulrik, Peter H. Hagedorn, Nannie Bangsgaard, Marianne B. Løvendorf, Charlotte B. Ahler, Lars Svensson, Katharina L. Kopp, et al. "Diagnostic microRNA profiling in cutaneous T-cell lymphoma (CTCL)." Blood 118, no. 22 (November 24, 2011): 5891–900. http://dx.doi.org/10.1182/blood-2011-06-358382.

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AbstractCutaneous T-cell lymphomas (CTCLs) are the most frequent primary skin lymphomas. Nevertheless, diagnosis of early disease has proven difficult because of a clinical and histologic resemblance to benign inflammatory skin diseases. To address whether microRNA (miRNA) profiling can discriminate CTCL from benign inflammation, we studied miRNA expression levels in 198 patients with CTCL, peripheral T-cell lymphoma (PTL), and benign skin diseases (psoriasis and dermatitis). Using microarrays, we show that the most induced (miR-326, miR-663b, and miR-711) and repressed (miR-203 and miR-205) miRNAs distinguish CTCL from benign skin diseases with > 90% accuracy in a training set of 90 samples and a test set of 58 blinded samples. These miRNAs also distinguish malignant and benign lesions in an independent set of 50 patients with PTL and skin inflammation and in experimental human xenograft mouse models of psoriasis and CTCL. Quantitative (q)RT-PCR analysis of 103 patients with CTCL and benign skin disorders validates differential expression of 4 of the 5 miRNAs and confirms previous reports on miR-155 in CTCL. A qRT-PCR–based classifier consisting of miR-155, miR-203, and miR-205 distinguishes CTCL from benign disorders with high specificity and sensitivity, and with a classification accuracy of 95%, indicating that miRNAs have a high diagnostic potential in CTCL.

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23

Liu, Jun, Jianwen Zhao, Guang Feng, Rui Li, and Jianhang Jiao. "Silencing of circ-CDK14 suppresses osteosarcoma progression through the miR-198/E2F2 axis." Experimental Cell Research 414, no. 1 (May 2022): 113082. http://dx.doi.org/10.1016/j.yexcr.2022.113082.

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24

Zhang, Zhaohui, Hao Hu, Qian Li, Fumei Yi, and Yan'e Liu. "A Novel Circular RNA circPTCD3 Promotes Breast Cancer Progression Through Sponging miR-198." Cancer Management and Research Volume 13 (November 2021): 8435–43. http://dx.doi.org/10.2147/cmar.s256091.

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25

Liu, Weiwei, Ji Zhao, Mingming Jin, and Ming Zhou. "circRAPGEF5 Contributes to Papillary Thyroid Proliferation and Metastatis by Regulation miR-198/FGFR1." Molecular Therapy - Nucleic Acids 14 (March 2019): 609–16. http://dx.doi.org/10.1016/j.omtn.2019.01.003.

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26

Xu, Xi-Qiu, Biao Zhang, Le Guo, Yu Liu, Feng-Zhen Meng, Xu Wang, Wen-Hui Hu, Adil I. Khan, and Wen-Zhe Ho. "Exosomes Transport Anti-Human Immunodeficiency Virus Factors from Human Cervical Epithelial Cells to Macrophages." Journal of Innate Immunity 13, no. 5 (2021): 269–79. http://dx.doi.org/10.1159/000514886.

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The female reproductive tract (FRT) is a major site of HIV sexual transmission. As the outermost layer of cells in the FRT, the human cervical epithelial cells (HCEs) have direct contact with HIV or infected cells. Our early work showed that supernatant (SN) from TLR3-activated HCEs contain the antiviral factors that could potently inhibit HIV replication in macrophages. However, it remains to be determined how HCEs transport the anti-HIV factors to macrophages. This follow-up study examined the role of exosomes in HCE-mediated anti-HIV activity. We found that TLR3 activation of HCEs resulted in the release of exosomes that contained multiple IFN-stimulated genes (ISGs: <i>ISG56</i>, <i>OAS1</i>, <i>MxA,</i> and <i>Mx2</i>) and the HIV restriction microRNAs (miR-28, miR-29 family members, miR-125b, miR-150, miR-382, miR-223, miR-20a, and miR-198). The depletion of exosomes from SN of TLR3-activated HCEs diminished HCE-mediated anti-HIV activity in macrophages, indicating that HCE-derived exosomes are responsible for transporting the antiviral molecules to macrophages. These in vitro findings suggest a novel antiviral mechanism by which HCEs participate in the FRT innate immunity against HIV infection. Further in vivo studies are necessary in order to develop an exosome-based delivery system for prevention and treatment of HIV infection through sexual transmission.

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Lanza, Michele, Giuditta Benincasa, Dario Costa, and Claudio Napoli. "Clinical Role of Epigenetics and Network Analysis in Eye Diseases: A Translational Science Review." Journal of Ophthalmology 2019 (December 23, 2019): 1–11. http://dx.doi.org/10.1155/2019/2424956.

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Network medicine is a molecular-bioinformatic approach analyzing gene-gene interactions that can perturb the human interactome. This review focuses on epigenetic changes involved in several ocular diseases, such as DNA methylation, histone and nonhistone post-translational modifications, and noncoding RNA regulators. Although changes in aberrant DNA methylation play a major role in the pathogenesis of most ocular diseases, histone modifications are seldom investigated. Hypermethylation in TGM-2 and hypomethylation in MMP-2/CD24 promoter genes may play a crucial role in pterygium development; hypermethylation in regulatory regions of GSTP1 and OGG1 genes appear to be diagnostic biomarkers of cataract; hypomethylation of TGF-β1 promoter may trigger glaucoma onset; hypermethylation of the LOXL1 gene might be associated with pseudoexfoliation syndrome. A large panel of upregulated micro-RNAs (miRNAs), including hsa-hsa-miR-494, hsa-let-7e, hsa-miR-513-1, hsa-miR-513-2, hsa-miR-518c, hsa-miR-129-1, hsa-miR-129-2, hsa-miR-198, hsa-miR-492, hsa-miR-498, hsa-miR-320, hsa-miR-503, and hsa-miR-373,∗ may have a putative role in the development of retinoblastoma. Hypermethylation of H3K4 and hypomethylation of H3K27 at the TGFBIp locus are putative pathogenic mechanisms involved in corneal dystrophies. Determining how, where, and when specific epigenetic changes trigger ocular diseases may provide useful clinical biomarkers for their prevention, diagnosis, and management, as well as innovative drug targets. PF-04523655, a 19-nucleotide methylated double-stranded siRNA targeting the RTP80 gene, showed a dose-related improvement in best-corrected visual acuity (BCVA) in patients affected by diabetic macular edema. The observed results support a clinical network-based research program aimed to clarify the role of epigenetic regulators in the development of ocular diseases and personalized therapy.

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Prinz, Christian, Leonard Fehring, and Robin Frese. "MicroRNAs as Indicators of Malignancy in Pancreatic Ductal Adenocarcinoma (PDAC) and Cystic Pancreatic Lesions." Cells 11, no. 15 (August 2, 2022): 2374. http://dx.doi.org/10.3390/cells11152374.

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The dysregulation of microRNAs has recently been associated with cancer development and progression in pancreatic ductal adenocarcinoma (PDAC) and cystic pancreatic lesions. In solid pancreatic tumor tissue, the dysregulation of miR-146, miR-196a/b, miR-198, miR-217, miR-409, and miR-490, as well as miR-1290 has been investigated in tumor biopsies of patients with PDAC and was reported to predict cancer presence. However, the value of the predictive biomarkers may further be increased during clinical conditions suggesting cancer development such as hyperinsulinemia or onset of diabetes. In this specific context, the dysregulation of miR-486 and miR-196 in tumors has been observed in the tumor tissue of PDAC patients with newly diagnosed diabetes mellitus. Moreover, miR-1256 is dysregulated in pancreatic cancer, possibly due to the interaction with long non-coding RNA molecules that seem to affect cell-cycle control and diabetes manifestation in PDAC patients, and, thus, these three markers may be of special or “sentinel value”. In blood samples, Next-generation sequencing (NGS) has also identified a set of microRNAs (miR-20a, miR-31-5p, miR-24, miR-25, miR-99a, miR-185, and miR-191) that seem to differentiate patients with pancreatic cancer remarkably from healthy controls, but limited data exist in this context regarding the prediction of cancer presences and outcomes. In contrast to solid pancreatic tumors, in cystic pancreatic cancer lesions, as well as premalignant lesions (such as intraductal papillary neoplasia (IPMN) or mucinous-cystic adenomatous cysts (MCAC)), the dysregulation of a completely different expression panel of miR-31-5p, miR-483-5p, miR-99a-5p, and miR-375 has been found to be of high clinical value in differentiating benign from malignant lesions. Interestingly, signal transduction pathways associated with miR-dysregulation seem to be entirely different in patients with pancreatic cysts when compared to PDAC. Overall, the determination of these different dysregulation “panels” in solid tumors, pancreatic cysts, obtained via fine-needle aspirate biopsies and/or in blood samples at the onset or during the treatment of pancreatic diseases, seems to be a reasonable candidate approach for predicting cancer presence, cancer development, and even therapy responses.

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Wang, Guixiang, Yajun Li, Hufei Zhu, Guoqiang Huo, Jingying Bai, and Zhiyong Gao. "Circ-PRKDC Facilitates the Progression of Colorectal Cancer Through miR-198/DDR1 Regulatory Axis." Cancer Management and Research Volume 12 (December 2020): 12853–65. http://dx.doi.org/10.2147/cmar.s273484.

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Ye, Lin, Sheng Li, Dingwei Ye, Deyong Yang, Feng Yue, Yanjie Guo, Xiaochi Chen, Feng Chen, Jianing Zhang, and Xishuang Song. "Livin expression may be regulated by miR-198 in human prostate cancer cell lines." European Journal of Cancer 49, no. 3 (February 2013): 734–40. http://dx.doi.org/10.1016/j.ejca.2012.08.029.

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Wang, Ruihuan, Jie Shen, Qing Wang, and Minjuan Zhang. "Bortezomib inhibited the progression of diffuse large B-cell lymphoma via targeting miR-198." Biomedicine & Pharmacotherapy 108 (December 2018): 43–49. http://dx.doi.org/10.1016/j.biopha.2018.08.151.

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Raj Christian, Simon Durai, Krishnaraj Thirugnanasambantham, Mohamed Ibrahim Hairul Islam, Mathan Kumar Sudalaimuthu, Sandhya Sundaram, Ganapathy Ashok, Venugopal Senthilkumar, Senguttuvan Muralidaran, and Saravanan Subramanian. "Identification of Expressed miRNAs in Human Rheumatoid Arthritis Using Computational Approach – Discovery of a New miR-7167 from Human." MicroRNA 8, no. 2 (February 26, 2019): 147–54. http://dx.doi.org/10.2174/2211536608666181204111438.

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Background: Rheumatoid Arthritis (RA) is a chronic inflammatory and autoimmune disease leading to bones and joints destruction. It is one of the major causes of lifetime disability and mortality among humans in the developing and developed countries. It was evident that epigenetic dysregulation is related to the pathogenesis of RA. MicroRNAs (miRNAs) are small non-coding RNAs that are epigenetic regulators for diverse biological processes and also provided novel molecular insights in the formation of arthritis. Objective: The influences of miRNAs in the alteration of gene regulation during the pathogenesis of arthritis were exposed in recent years. Method: The computational approach to identify miRNA through EST-based homology is more powerful, economical and time-efficient. In this study, we applied EST-based homology search to identify miRNAs responsible for the development of arthritis in human beings. Results: Our study on 36519 ESTs in human RA condition revealed the expression of four miRNAs, HSA-miR-198, HSA-miR-4647, has-miR-7167-5p and has-miR-7167-3p. The present study is the first report about has-miR-7167 that was homologous to Macaca mulatta. Conclusion: The predicted targets of these identified miRNAs revealed many biological functions in the pathogenesis of RA. Further elaborated studies on these miRNAs will help to understand their function in the development of RA and the use of miRNAs as therapeutic targets in the future.

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Elfimova, Natalia, Elisabeth Sievers, Hannah Eischeid, Monika Kwiecinski, Andrea Noetel, Heike Hunt, Diana Becker, et al. "Control of mitogenic and motogenic pathways by miR-198, diminishing hepatoma cell growth and migration." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1833, no. 5 (May 2013): 1190–98. http://dx.doi.org/10.1016/j.bbamcr.2013.01.023.

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Wu, Shujun, Guojun Zhang, Ping Li, Shanshan Chen, Furui Zhang, Juan Li, Chenyang Jiang, et al. "miR-198 targets SHMT1 to inhibit cell proliferation and enhance cell apoptosis in lung adenocarcinoma." Tumor Biology 37, no. 4 (November 9, 2015): 5193–202. http://dx.doi.org/10.1007/s13277-015-4369-z.

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Huang, Kai, Xi Fan, Yuwen Jiang, Sheng Jin, Jiechun Huang, Liewen Pang, Yiqing Wang, Yuming Wu, and Xiaotian Sun. "Integrative identification of hub genes in development of atrial fibrillation related stroke." PLOS ONE 18, no. 3 (March 23, 2023): e0283617. http://dx.doi.org/10.1371/journal.pone.0283617.

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Background As the most common arrhythmia, atrial fibrillation (AF) is associated with a significantly increased risk of stroke, which causes high disability and mortality. To date, the underlying mechanism of stroke occurring after AF remains unclear. Herein, we studied hub genes and regulatory pathways involved in AF and secondary stroke and aimed to reveal biomarkers and therapeutic targets of AF-related stroke. Methods The GSE79768 and GSE58294 datasets were used to analyze AF- and stroke-related differentially expressed genes (DEGs) to obtain a DEG1 dataset. Weighted correlation network analysis (WGCNA) was used to identify modules associated with AF-related stroke in GSE66724 (DEG2). DEG1 and DEG2 were merged, and hub genes were identified based on protein–protein interaction networks. Gene Ontology terms were used to analyze the enriched pathways. The GSE129409 and GSE70887 were applied to construct a circRNA-miRNA-mRNA network in AF-related stroke. Hub genes were verified in patients using quantitative real-time polymerase chain reaction (qRT-PCR). Results We identified 3,132 DEGs in blood samples and 253 DEGs in left atrial specimens. Co-expressed hub genes of EIF4E3, ZNF595, ZNF700, MATR3, ACKR4, ANXA3, SEPSECS-AS1, and RNF166 were significantly associated with AF-related stroke. The hsa_circ_0018657/hsa-miR-198/EIF4E3 pathway was explored as the regulating axis in AF-related stroke. The qRT-PCR results were consistent with the bioinformatic analysis. Conclusions Hub genes EIF4E3, ZNF595, ZNF700, MATR3, ACKR4, ANXA3, SEPSECS-AS1, and RNF166 have potential as novel biomarkers and therapeutic targets in AF-related stroke. The hsa_circ_0018657/hsa-miR-198/EIF4E3 axis could play an important role regulating the development of AF-related stroke.

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Zhou, Changluan, Lei Tan, Yingjie Sun, Xusheng Qiu, Chunchun Meng, Ying Liao, Cuiping Song, Weiwei Liu, Venugopal Nair, and Chan Ding. "Exosomes Carry microRNAs into Neighboring Cells to Promote Diffusive Infection of Newcastle Disease Virus." Viruses 11, no. 6 (June 6, 2019): 527. http://dx.doi.org/10.3390/v11060527.

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Newcastle disease virus (NDV), an avian paramyxovirus, was shown to prefer to replicate in tumor cells instead of normal cells; however, this mechanism has not been fully elucidated. Exosomes play a crucial role in intercellular communication due to the bioactive substances they carry. Several studies have shown that exosomes are involved in virus infections. However, the effect that exosomes have on NDV-infected tumor cells is not known. In this study, we focus on the role of exosomes secreted by NDV-infected HeLa cells in promoting NDV replication. Three miRNA candidates (miR-1273f, miR-1184, and miR-198) embraced by exosomes were associated with enhancing NDV-induced cytopathic effects on HeLa cells. Furthermore, luciferase assays, RT-qPCR, and enzyme-linked immunosorbent assay (ELISA) all demonstrated that these miRNAs could suppress interferon (IFN)-β gene expression. Enhanced NDV replication in HeLa cells was identified by Western blot and plaque assays. Based on these results, we speculate that NDV employed exosomes entry into neighboring cells, which carry miRNAs, resulting in inhibition of the IFN pathway and promotion of viral infection. To our knowledge, this is the first report on the involvement of NDV-employed exosomes in tumor cells, and as such, it provides new insights into the development of anti-tumor therapies.

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Georges, Steven, Lidia Rodriguez Calleja, Camille Jacques, Melanie Lavaud, Brice Moukengue, Fernando Lecanda, Thibaut Quillard, et al. "Loss of miR-198 and -206 during primary tumor progression enables metastatic dissemination in human osteosarcoma." Oncotarget 9, no. 87 (November 6, 2018): 35726–41. http://dx.doi.org/10.18632/oncotarget.26284.

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Lü, Jian-Ming, Zhengdong Liang, Dongliang Liu, Bin Zhan, Qizhi Yao, and Changyi Chen. "Two Antibody-Guided Lactic-co-Glycolic Acid-Polyethylenimine (LGA-PEI) Nanoparticle Delivery Systems for Therapeutic Nucleic Acids." Pharmaceuticals 14, no. 9 (August 25, 2021): 841. http://dx.doi.org/10.3390/ph14090841.

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We previously reported a new polymer, lactic-co-glycolic acid-polyethylenimine (LGA-PEI), as an improved nanoparticle (NP) delivery for therapeutic nucleic acids (TNAs). Here, we further developed two antibody (Ab)-conjugated LGA-PEI NP technologies for active-targeting delivery of TNAs. LGA-PEI was covalently conjugated with a single-chain variable fragment antibody (scFv) against mesothelin (MSLN), a biomarker for pancreatic cancer (PC), or a special Ab fragment crystallizable region-binding peptide (FcBP), which binds to any full Ab (IgG). TNAs used in the current study included tumor suppressor microRNA mimics (miR-198 and miR-520h) and non-coding RNA X-inactive specific transcript (XIST) fragments; green fluorescence protein gene (GFP plasmid DNA) was also used as an example of plasmid DNA. MSLN scFv-LGA-PEI NPs with TNAs significantly improved their binding and internalization in PC cells with high expression of MSLN in vitro and in vivo. Anti-epidermal growth factor receptor (EGFR) monoclonal Ab (Cetuximab) binding to FcBP-LGA-PEI showed active-targeting delivery of TNAs to EGFR-expressing PC cells.

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Araga, S., F. S. Galin, M. Kishimoto, A. Adachi, and J. B. Blalock. "Prevention of experimental autoimmune myasthenia gravis by a monoclonal antibody to a complementary peptide for the main immunogenic region of the acetylcholine receptors." Journal of Immunology 157, no. 1 (July 1, 1996): 386–92. http://dx.doi.org/10.4049/jimmunol.157.1.386.

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Abstract We have previously reported that a complementary peptide (denoted RhCA 67-16), encoded by RNA complementary to that of the Torpedo acetylcholine receptor (AChR) main immunogenic region (MIR), AChR residues alpha 61-76, induces polyclonal and monoclonal Ab reactive with Ig against the AChR MIR. RhCA 67-16 vaccination also protected against the development of experimental autoimmune myasthenia gravis (EAMG) in Lewis rats. In the present report, we found that a mAb (denoted TCM 240, IgG1 kappa) against RhCA 67-16 recognized three different idiotypic Ab (mAb 6, mAb 35, and mAb 198), which were previously reported by others to recognize the AChR MIR and to cause EAMG. Based on these results, TCM 240 was tested for prophylactic effects in EAMG. EAMG induced passively by mAb 35 was inhibited by simultaneous injection with TCM 240. The disease severity was inversely paralleled by the ratio of mAb 35 to TCM 240. EAMG induced by immunization with purified native Torpedo AChR was also inhibited by TCM 240, but not a control mAb. The inhibitory effect of TCM 240 on actively induced EAMG occurred without significantly lowering the overall AChR Ab levels, which indicates a limited repertoire of disease-causing Ab in EAMG and perhaps MG. Such findings suggest the existence of an EAMG-associated Id and also support the concept of an MIR. In a more general sense, these results demonstrate that prophylactic and perhaps diagnostic mAb for autoimmune diseases can be produced by immunization with complementary peptides for disease-associated epitopes.

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Chen, Gang, Wenting Huang, Hanlin Wang, Hong Yang, Fang-Hui Ren, Yi-Huan Luo, Chun-Qin Huang, Yue-Ya Liang, Hai-Wei Liang, and Yiwu Dang. "Lower expressed miR-198 and its potential targets in hepatocellular carcinoma: a clinicopathological and in silico study." OncoTargets and Therapy Volume 9 (August 2016): 5163–80. http://dx.doi.org/10.2147/ott.s108828.

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Marin-Muller, C., U. Bharadwaj, M. Li, C. Chen, and Q. Yao. "A Reciprocal Repression Between Tumor Suppressor MiR-198 and Mesothelin Regulates Proliferation and Metastasis in Pancreatic Cancer." Journal of Surgical Research 172, no. 2 (February 2012): 233. http://dx.doi.org/10.1016/j.jss.2011.11.358.

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Tan, Sheng, Rui Li, Keshuo Ding, Peter E. Lobie, and Tao Zhu. "miR-198 inhibits migration and invasion of hepatocellular carcinoma cells by targeting the HGF/c-MET pathway." FEBS Letters 585, no. 14 (June 3, 2011): 2229–34. http://dx.doi.org/10.1016/j.febslet.2011.05.042.

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Hu, Yingbin, Ziyuan Tang, Bonian Jiang, Juying Chen, and Zhongpin Fu. "miR-198 functions as a tumor suppressor in breast cancer by targeting CUB domain-containing protein 1." Oncology Letters 13, no. 3 (February 2, 2017): 1753–60. http://dx.doi.org/10.3892/ol.2017.5673.

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Han, Hye-Suk, Jieun Yun, Sung-nam Lim, Joung-Ho Han, Ki Hyeong Lee, Seung Taik Kim, Min-Ho Kang, et al. "Downregulation of cell-free miR-198 as a diagnostic biomarker for lung adenocarcinoma-associated malignant pleural effusion." International Journal of Cancer 133, no. 3 (February 25, 2013): 645–52. http://dx.doi.org/10.1002/ijc.28054.

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Bellone, M., F. Tang, R. Milius, and B. M. Conti-Tronconi. "The main immunogenic region of the nicotinic acetylcholine receptor. Identification of amino acid residues interacting with different antibodies." Journal of Immunology 143, no. 11 (December 1, 1989): 3568–79. http://dx.doi.org/10.4049/jimmunol.143.11.3568.

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Abstract In myasthenia gravis a highly conserved area of the nicotinic receptor (AcChR) dominates the autoantibody response (main immunogenic region, MIR), and it is formed by residues within the sequence segment 67-76 of the AcChR alpha-subunit. We have studied the binding of eight anti-MIR mAb to synthetic peptides containing the sequence segment 67-76 of the human alpha-subunit, and peptide analogues containing single residue substitutions of this sequence. We used also a peptide where both Asp70 and Asp71 were substituted by glycine residues. The binding of six anti-MIR mAb was strongly influenced by several substitutions. All these mAb required residues Asn68, and Pro69 for binding. Five of them required also Asp71 and Tyr72. Substitution of Asp70, which is an Ala residue in Torpedo AcChR, was irrelevant for the binding of an anti-Torpedo and an anti-Electrophorus mAb, and moderately reduced the binding of an anti-human mAb (no. 203). Substitution of Trp67 moderately reduced the binding of some of these mAbs. A mAb of this group (the antihuman mAb no. 198) bound in a manner only slightly influenced by ionic strength, whereas the binding of the other five mAb of this group was very sensitive to the ionic strength. Two anti-Electrophorus MIR mAb bound similarly to all peptide analogues in low ionic strength. At high ionic strength only the peptide analogue where Asp 70 was changed to a Gly residue bound significantly. This may indicate that the Electrophorus MIR has an uncharged residue at this position, as does Torpedo AcChR. Residues at position 73, 74, 75, and 76 were of little or no importance for the binding of all anti-MIR mAb. A free amino terminus was essential for the binding of most mAb. The results of competition experiments between different peptides and native AcChR for mAb binding were consistent with those obtained in direct binding experiments.

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Zheng, Yuanyuan, Ping Li, Jianghui Ma, Chengxi Yang, Saimin Dai, and Changyong Zhao. "Cancer-derived exosomal circ_0038138 enhances glycolysis, growth, and metastasis of gastric adenocarcinoma via the miR-198/EZH2 axis." Translational Oncology 25 (November 2022): 101479. http://dx.doi.org/10.1016/j.tranon.2022.101479.

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Vorobiev, D., A. Maillet, J. O. Fortrat, L. Pastushkova, A. M. Allevard, D. Sigaudo, R. Cartier, et al. "Blood volume regulating hormones, fluid and electrolyte modifications during 21 and 198-day space flights (Altair-MIR 1993)." Acta Astronautica 36, no. 8-12 (October 1995): 733–42. http://dx.doi.org/10.1016/0094-5765(95)00164-6.

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Duan, Xiaohui, Bo Jiang, Jianhui Yang, Lixue Zhou, Bingzhang Tian, and Xianhai Mao. "FOXP3 inhibits MYC expression via regulating miR-198 and influences cell viability, proliferation and cell apoptosis in HepG2." Cancer Medicine 7, no. 12 (October 30, 2018): 6182–92. http://dx.doi.org/10.1002/cam4.1780.

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Ludwig, Nicole, Tanja Rädle-Hurst, Andreas Keller, Lars Motsch, Ina Marsollek, Mohammed El Rahman, Masood Abu-Halima, Hashim Abdul-Khaliq, and Eckart Meese. "Characterization of micro-RNA Profile in the Blood of Patients with Marfan's Syndrome." Thoracic and Cardiovascular Surgeon 66, no. 01 (July 5, 2017): 116–24. http://dx.doi.org/10.1055/s-0037-1604083.

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Background Marfan's syndrome (MFS) is an autosomal dominant inheritance disorder with a 1/5,000 live-birth prevalence. It is characterized by a wide range of clinical manifestations with more than 3,000 mutations identified in the FBN1 gene. In this study, we aimed to determine if specific patterns of circulating micro-RNAs (miRNAs) are associated with MFS-associated with cardiovascular diseases. Methods Microarray-based miRNA profiling was performed on blood samples of 12 MFS patients, and 12 healthy volunteers (HVs) controls and the differences in miRNA abundance between the two groups were validated using independent cohorts of 22 MFS and of 22 HV controls by real-time quantitative polymerase chain reaction (RT-qPCR). Enrichment analyses of altered miRNA abundance were predicted using bioinformatics tools. Results Altered miRNA abundance levels were determined between MFS (n = 34) and HVs (n = 34). In a screening phase, we analyzed 12 patients with MFS and 12 HVs by miRNA microarray. We found 198 miRNAs that were significantly altered in MFS patients as compared with HVs, including 16 miRNAs with a more than 1.5-fold change. Out of these 16 miRNAs, 10 showed a decreased abundance and 6 showed an increased abundance. In the validation phase, we analyzed independent cohorts of 22 MFS and of 22 HV controls by RT-qPCR. We confirmed the direction of abundance changes and the significance of different abundances between MFS patients and HVs for four miRNAs, namely, miR-362–5p, miR-339–3p, miR-340–5p, and miR-210–3p. Only the miR-150–5p showed a significant correlation with mitral valve prolapse (p = 0.010). The predicted targets for the validated miRNAs were associated with signal transduction, tissue remodeling, and cellular interaction pathways. Conclusion The altered abundance level of different miRNAs in whole blood of MFS patients lays the ground to the development of novel diagnostic approaches with altered miRNAs levels associated with MFS with manifestations associated with cardiovascular diseases.

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Raitoharju, Emma, Niku Oksala, and Terho Lehtimäki. "MicroRNAs in the Atherosclerotic Plaque." Clinical Chemistry 59, no. 12 (December 1, 2013): 1708–21. http://dx.doi.org/10.1373/clinchem.2013.204917.

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BACKGROUND MicroRNAs (miRNA, miR) are noncoding RNAs that regulate gene expression by hindering translation. miRNA expression profiles have been shown to differ in vivo and in vitro in many cellular processes associated with cardiovascular diseases (CVDs). The progression of CVDs has also been shown to alter the blood miRNA profile in humans. CONTENT We summarize the results of animal and cell experiments concerning the miRNA profile in the atherosclerotic process and the changes which occur in the blood miRNA profile of individuals with CVD. We also survey the relationship of these CVD-related miRNAs and their expression in the human advanced atherosclerotic plaque, thereby providing more insight into miRNA function in human atherosclerotic lesions. The miRNAs miR-126, -134, -145, -146a, -198, -210, -340*, and -92a were found to be expressed differently in the blood of individuals affected and unaffected by CVD. These differences paralleled those seen in tissue comparisons of miRNA expression in advanced atherosclerotic plaques and healthy arteries. Furthermore, several miRNAs associated with atherosclerosis in in vitro studies (such as miR-10a, -126, -145, -146a/b, -185, -210, and -326) were expressed in plaques in a similar pattern as was predicted by the in vitro experiments. The clinical implications of miRNAs in atherosclerosis as biomarkers and as possible drug targets are also reviewed. SUMMARY miRNA profiles in in vitro and in vivo studies as well as in human peripheral blood are quite representative of the miRNA expression in human atherosclerotic plaques. miRNAs appear promising in terms of future clinical applications.

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