6 results on '"Liu, Huowang"'
Search Results
2. Mir-142-3p Regulates Inflammatory Response by Contributing to Increased TNF-α in Chronic Rhinosinusitis With Nasal Polyposis.
- Author
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Qing X, Zhang Y, Peng Y, He G, Liu A, and Liu H
- Subjects
- Case-Control Studies, Cell Line, Chronic Disease, Epithelial Cells metabolism, Humans, Nasal Mucosa cytology, MicroRNAs metabolism, Nasal Polyps genetics, Rhinitis genetics, Sinusitis genetics, Tumor Necrosis Factor-alpha metabolism
- Abstract
Objective: Previous studies suggested that microRNAs played an important role in the progression of inflammation and remodeling of chronic rhinosinusitis with nasal polyposis. However, the abnormal expression of microRNAs and regulation cytokine expression in nasal polyposis are not clear., Method: The miR-142-3p and tumor necrosis factor α (TNF-α) expression levels in chronic rhinosinusitis with nasal polyposis were detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The miR-142-3p and TNF-α levels in human nasal epithelial cells (HNEpC) after stimulation by lipopolysaccharide (LPS) were detected by qRT-PCR. Moreover, HNEpCs were transfected by miR-142-3p mimics or inhibitor or cotransfected with si-TNF-α to evaluate the regulation of miR-142-3p on TNF-α which affects the production of inflammatory factors., Results: The miR-142-3p and TNF-α were significantly higher in nasal mucosa of chronic rhinosinusitis with polyps patients compared to normal human. MiR-142-3p and TNF-α expression levels were increased after LPS stimulation in a dose- and time-dependent manner. Knockdown of miR-142-3p in HNEpCs downregulated TNF-α expression at both messenger RNA and protein levels., Conclusions: It is indicated that miR-142-3p may participate in the regulation of the body's inflammatory response through the LPS-TLR-TNF-α signaling pathway in chronic rhinosinusitis with nasal polyposis.
- Published
- 2021
- Full Text
- View/download PDF
3. microRNA-18a from M2 Macrophages Inhibits TGFBR3 to Promote Nasopharyngeal Carcinoma Progression and Tumor Growth via TGF-β Signaling Pathway.
- Author
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Peng Y, Li X, Liu H, Deng X, She C, Liu C, Wang X, and Liu A
- Abstract
Objectives: Nasopharyngeal carcinoma (NPC) is a type of nasopharyngeal disease with high metastasis and invasion properties. Tumor-associated alternative activated (M2) macrophages are evidenced to connect with NPC. Based on this, this study purposes to explore the mechanism and participation of microRNA-18a (miR-18a) from M2 macrophages in NPC., Methods: Peripheral blood mononuclear cells were differentiated to macrophages and macrophages were polarized to M2 type by interleukin-4. SUNE-1 and CNE2 cells were transfected with restored or depleted miR-18a or transforming growth factor-beta III receptor (TGFBR3) to explore their roles in NPC progression with the involvement of the TGF-β signaling pathway. Next, SUNE-1 and CNE2 cells were co-cultured with M2 macrophages that had been treated with restored or depleted miR-18a or TGFBR3 to comprehend their combined roles in NPC with the involvement of the TGF-β signaling pathway., Results: MiR-18a was highly expressed and TGFBR3 was lowly expressed in NPC cells. MiR-18a restoration, TGFBR3 knockdown or co-culture with miR-18a mimics, or si-TGFBR3-transfected M2 macrophages promoted SUNE-1 cell progression, tumor growth in mice, decreased p-Smad1/t-Smad1, and elevated p-Smad3/t-Smad3. miR-18a downregulation, TGFBR3 overexpression, or co-culture with miR-18a inhibitors or OE-TGFBR3-transfected M2 macrophages depressed CNE2 cell progression, tumor growth in mice, increased p-Smad1/t-Smad1, and decreased p-Smad3/t-Smad3., Conclusion: Our study elucidates that miR-18a from M2 macrophages results in promoted NPC cell progression and tumor growth in nude mice via TGFBR3 repression, along with the Smad1 inactivation and Smad3 activation.
- Published
- 2020
- Full Text
- View/download PDF
4. Endoscopic endonasal transsphenoidal approach for sellar tumors beyond the sellar turcica.
- Author
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Song Y, Li H, Liu H, Li W, Zhang X, Guo L, and Tan G
- Subjects
- Adolescent, Adult, Aged, Cerebrospinal Fluid Rhinorrhea etiology, Child, Diabetes Insipidus etiology, Epistaxis etiology, Female, Humans, Hypothalamic Diseases etiology, Male, Middle Aged, Postoperative Complications etiology, Subdural Effusion etiology, Surgical Wound Infection etiology, Treatment Outcome, Young Adult, Adenoma surgery, Craniopharyngioma surgery, Endoscopy methods, Meningeal Neoplasms surgery, Meningioma surgery, Pituitary Neoplasms surgery, Sella Turcica surgery, Sphenoid Sinus surgery
- Abstract
Conclusions: The endoscopic endonasal transsphenoidal approach can be a choice for sellar tumors beyond the sellar turcica, but it is necessary to make the choice carefully because of the severe surgical risks., Objectives: To summarize our experience of removal of sellar tumors beyond the sellar turcica via the endoscopic endonasal transsphenoidal approach and to evaluate the surgical efficacy and complications., Methods: Between January 2007 and January 2012, 30 patients with sellar tumors beyond the sellar turcica underwent surgery using the endoscopic endonasal transsphenoidal approach., Results: Postoperative pathological examination demonstrated that pituitary adenoma occurred in 22 patients, craniopharyngioma in 5, and meningioma in 3. Total removal was achieved in 21 patients (70.0%) and subtotal removal was achieved in 8 patients (26.7%). After the surgery, cerebrospinal fluid leakage occurred in 3 patients, temporary diabetes insipidus occurred in 25 patients and persistent diabetes insipidus in 4 patients, intracranial infection occurred in 1 patient, frontal subdural effusion occurred in 1 patient, sinusitis occurred in 2 patients, epistaxis occurred in 3 patients, and 1 patient with a huge pituitary adenoma died of hypothalamic failure related to the operation.
- Published
- 2014
- Full Text
- View/download PDF
5. [Inflammatory cytokine expression in recurrent nasal polyps by antibody chips].
- Author
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Chen Y, Sun H, Liu H, and Chen X
- Subjects
- Adolescent, Adult, Aged, Chemokine CCL11 metabolism, Chemokines metabolism, Female, Humans, Interleukin-1beta metabolism, Interleukin-6 metabolism, Male, Middle Aged, Recurrence, Young Adult, Antibodies, Cytokines metabolism, Nasal Polyps metabolism, Protein Array Analysis methods
- Abstract
Objective: To investigate the expression of inflammatory cytokines in patients with recurrent nasal polyps by antibody chips., Methods: Proteins from the patients'nasal membrane in a nasal polyps group, a recurrent nasal polyps group, and a control group were labeled with biotin. The biotin-labeled proteins reacted with antibody chips on which the antibodies of 40 major inflammatory cytokines were prepared. The target proteins were conjugated with streptomycin antibody labeled with horseradish peroxidase (HRP),and signals were imaged by laser scanner., Results: Compared with the control group, the levels of inflammatory cytokines of nasal polyp group were notably increased, including pro-and anti-inflammatory cytokines, chemokines and certain cytokine receptors; while in recurrent nasal polyps, expression of chemokines were increased and most anti-inflammatory cytokines were decreased., Conclusion: Antibody chips demonstrate a significant change in cytokine profiles in patients with recurrent nasal polypsis, as compared with those with nasal polyps. The abnormally higher expression of chemotatic factors in the nasal mucosa may play an important role in the recurrence of human nasal polyps.
- Published
- 2009
6. [Differential proteins analysis for human nasal polyposis and normal nasal mucosa].
- Author
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He G, Sun H, Wang T, Li C, and Liu H
- Subjects
- Adult, Aged, Case-Control Studies, Electrophoresis, Gel, Two-Dimensional, Female, Humans, Male, Middle Aged, Nasal Mucosa pathology, Nasal Polyps pathology, Nasal Mucosa metabolism, Nasal Polyps metabolism, Proteomics
- Abstract
Objective: To establish two-dimensional polyacrylamide gel electrophoresis (2-DE) map with high resolution and reproducibility from human nasal polyposis and normal nasal mucosa, and to identify differential expression proteins of 2-DE map., Method: Samples of human nasal polyposis and normal nasal mucosa (each sample group containing seven cases) were obtained. The total proteins were extracted and separated by immobilized pH gradient (IPG)-based 2-DE. The silver-stained 2-DE were scanned with digital Image Scanner and analyzed with ImageMaster 2-DE Elite 4.01 software. Peptide mass fingerprint (PMF) of differential protein spots was obtained with matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS). The peptide mass fingerprints were searched in Swiss-Prot and TreMBL database by PeptIdent software, and then differential expression proteins were identified., Result: (1) 2-DE for a randomly selected 1 sample from each of the 2 groups was repeated 3 times respectively to analyze the reproductive of the method. The image analysis showed: For the polyposis tissues, the average proteins spots of three 2-DE maps were 891 +/- 67 and 767 +/- 83, spots were matched with the average matching rate of 86.1%. The average deviations of matched spot position were (1.13 +/- 0.16) mm in IEF direction and 1.45 +/- 0.21) mm in SDS-PAGE direction, respectively. For the nasal mucosa tissues, the average proteins spots of three 2-DE maps were 936 +/- 62 and 821 +/- 78, spots were matched with the average matching rate of 87.7%. Comparing the average electrophoresis profiles of the two tissues, each sample contained 7 cases. The proteins spots of nasal polyposis and nasal mucosa tissues were 1532 and 1617. A total of 1 065 proteins spots were matched between the two tissues average electrophoresis profiles. (2)Twenty dif-ferential expression protein spots were incised from silver staining gel randomly and digested in gel by TPCK Trypsin. Sixteen PMF were obtained by MALDI-TOF-MS, and 11 differential expression proteins were identified., Conclusion: In this study, the well-resolved reproducible 2-DE map of human nasal polyposis and nasal mucosa were established. Certain differential proteins were identified.
- Published
- 2006
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