scholarly journals MicroRNA-128-3p suppresses interleukin-1β-stimulated cartilage degradation and chondrocyte apoptosis via targeting zinc finger E-box binding homeobox 1 in osteoarthritis

Bioengineered ◽  
2022 ◽  
Vol 13 (1) ◽  
pp. 1736-1745
Author(s):  
Yu Sun ◽  
Xinnan Bao ◽  
Haiou Chen ◽  
Liping Zhou
Keyword(s):  
Zinc Finger ◽  
Cartilage Degradation ◽  
Interleukin 1Β ◽  
Chondrocyte Apoptosis ◽  
E Box

scholarly journals Zinc finger E-box-binding homeobox 1: its clinical significance and functional role in human thyroid cancer

2016 ◽  
pp. 1303 ◽  
Author(s):  
Yuhong Wang ◽  
Yan Zhang ◽  
Gang Liu ◽  
Shihe Wu ◽  
Futing Jiang ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Clinical Significance ◽  
Zinc Finger ◽  
Functional Role ◽  
Human Thyroid ◽  
E Box

scholarly journals Artemisinin Ameliorates Osteoarthritis by Inhibiting the Wnt/β-Catenin Signaling Pathway

2018 ◽  
Vol 51 (6) ◽  
pp. 2575-2590 ◽  
Author(s):  
Gang Zhong ◽  
Ruiming Liang ◽  
Jun Yao ◽  
Jia Li ◽  
Tongmeng Jiang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Cruciate Ligament ◽  
Interleukin 1 ◽  
Cartilage Degradation ◽  
Chondrocyte Apoptosis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cell Viability Assay ◽  
Necrosis Factor Alpha ◽  
Anti Inflammatory

Background/Aims: Current drug therapies for osteoarthritis (OA) are not practical because of the cytotoxicity and severe side-effects associated with most of them. Artemisinin (ART), an antimalarial agent, is well known for its safety and selectivity to kill injured cells. Based on its anti-inflammatory activity and role in the inhibition of OA-associated Wnt/β-catenin signaling pathway, which is crucial in the pathogenesis of OA, we hypothesized that ART might have an effect on OA. Methods: The chondro-protective and antiarthritic effects of ART on interleukin-1-beta (IL-1β)-induced and OA patient-derived chondrocytes were investigated in vitro using cell viability assay, glycosaminoglycan secretion, immunofluorescence, quantitative reverse transcription-polymerase chain reaction, and western blotting. We also used OA model rats constructed by anterior cruciate ligament transection and medial meniscus resection (ACLT+MMx) in the joints to investigate the effects of ART on OA by gross observation, morphological staining, immunohistochemistry, and enzyme-linked immunosorbent assay. Results: ART exhibited potent anti-inflammatory effects by inhibiting the expression of proinflammatory chemokines and cytokines, including interleukin (IL)-1β, IL-6, tumor necrosis factor alpha, and matrix metallopeptidase-13. It also showed favorable chondro-protective effect as evidenced by enhanced cell proliferation and viability, increased glycosaminoglycan deposition, prevention of chondrocyte apoptosis, and degeneration of cartilage. Further, ART inhibited OA progression and cartilage degradation via the Wnt/β-catenin signaling pathway, suggesting that it might serve as a Wnt/β-catenin antagonist to reduce inflammation and prevent cartilage degradation. Conclusion: In conclusion, ART alleviates IL-1β-mediated inflammatory response and OA progression by regulating the Wnt/β-catenin signaling pathway. Thereby, it might be developed as a potential therapeutic agent for OA.

scholarly journals Prolactin inhibits the apoptosis of chondrocytes induced by serum starvation

2006 ◽  
Vol 189 (2) ◽  
pp. R1-R8 ◽  
Author(s):  
C Zermeño ◽  
J Guzmán-Morales ◽  
Y Macotela ◽  
G Nava ◽  
F López-Barrera ◽  
...  
Keyword(s):  
Articular Chondrocytes ◽  
Cell Types ◽  
Cartilage Degradation ◽  
Chondrocyte Apoptosis ◽  
Heat Inactivation ◽  
Serum Starvation ◽  
Endochondral Bone Formation ◽  
Endochondral Bone ◽  
Therapeutic Value ◽  
Apoptotic Effect

The apoptosis of chondrocytes plays an important role in endochondral bone formation and in cartilage degradation during aging and disease. Prolactin (PRL) is produced in chondrocytes and is known to promote the survival of various cell types. Here we show that articular chondrocytes from rat postpubescent and adult cartilage express the long form of the PRL receptor as revealed by immunohistochemistry of cartilage sections and by RT-PCR and Western blot analyses of the isolated chondrocytes. Furthermore, we demonstrate that PRL inhibits the apoptosis of these same chondrocytes cultured in low-serum. Chondrocyte apoptosis was measured by hypodiploid DNA content determined by flow cytometry and by DNA fragmentation evaluated by the ELISA and the TUNEL methods. The anti-apoptotic effect of PRL was dose-dependent and was prevented by heat inactivation. These data demonstrate that PRL can act as a survival factor for chondrocytes and that it has potential preventive and therapeutic value in arthropathies characterized by cartilage degradation.

Zinc Finger E-Box-Binding Homeobox 2

2016 ◽  
pp. 1-8
Author(s):  
Özden Akay ◽  
Kenneth Bruneel ◽  
Bieke Soen ◽  
Eva De Smedt ◽  
Niels Vandamme ◽  
...  
Keyword(s):  
Zinc Finger ◽  
E Box

scholarly journals MicroRNA-342 Prohibits Proliferation and Invasion of Melanoma Cells by Directly Targeting Zinc-Finger E-Box-Binding Homeobox 1

2018 ◽  
Vol 26 (9) ◽  
pp. 1447-1455 ◽  
Author(s):  
Quan Shi ◽  
Qi He ◽  
Jing Wei
Keyword(s):  
Cell Proliferation ◽  
Zinc Finger ◽  
Ectopic Expression ◽  
Melanoma Cells ◽  
Potential Candidate ◽  
E Box ◽  
Direct Target Gene ◽  
Direct Target ◽  
Proliferation And Invasion ◽  
Zeb1 Expression

As documented in numerous studies, microRNAs (miRNAs) play key roles in various biological processes associated with melanoma occurrence and development. In this study, we found that miRNA-342 (miR-342) was significantly downregulated in melanoma tissues and cell lines. Additionally, the ectopic expression of miR-342 prohibited the cell proliferation and invasion of melanoma. Moreover, zinc-finger E-box-binding homeobox 1 (ZEB1) was identified as a direct target gene of miR-342 in melanoma. Similar with the results induced by miR-342 overexpression, ZEB1 knockdown attenuated cell proliferation and invasion in melanoma. Furthermore, the restoration of ZEB1 expression reversed the suppressive effects of miR-342 on the proliferation and invasion of melanoma cells. These findings suggest that miR-342 may play tumor-suppressing roles in melanoma, at least partially, by directly inhibiting ZEB1 expression. Therefore, miR-342 may be developed as a potential candidate for the treatment of patients with this aggressive type of cancer.

scholarly journals The Functional Role of Zinc Finger E Box-Binding Homeobox 2 (Zeb2) in Promoting Cardiac Fibroblast Activation

2018 ◽  
Vol 19 (10) ◽  
pp. 3207 ◽  
Author(s):  
Fahmida Jahan ◽  
Natalie Landry ◽  
Sunil Rattan ◽  
Ian Dixon ◽  
Jeffrey Wigle
Keyword(s):  
Smooth Muscle ◽  
Zinc Finger ◽  
Cardiac Fibrosis ◽  
Smooth Muscle Actin ◽  
Critical Role ◽  
Cardiac Fibroblast ◽  
In Vivo Studies ◽  
Fibroblast Activation ◽  
E Box

Following cardiac injury, fibroblasts are activated and are termed as myofibroblasts, and these cells are key players in extracellular matrix (ECM) remodeling and fibrosis, itself a primary contributor to heart failure. Nutraceuticals have been shown to blunt cardiac fibrosis in both in-vitro and in-vivo studies. However, nutraceuticals have had conflicting results in clinical trials, and there are no effective therapies currently available to specifically target cardiac fibrosis. We have previously shown that expression of the zinc finger E box-binding homeobox 2 (Zeb2) transcription factor increases as fibroblasts are activated. We now show that Zeb2 plays a critical role in fibroblast activation. Zeb2 overexpression in primary rat cardiac fibroblasts is associated with significantly increased expression of embryonic smooth muscle myosin heavy chain (SMemb), ED-A fibronectin and α-smooth muscle actin (α-SMA). We found that Zeb2 was highly expressed in activated myofibroblast nuclei but not in the nuclei of inactive fibroblasts. Moreover, ectopic Zeb2 expression in myofibroblasts resulted in a significantly less migratory phenotype with elevated contractility, which are characteristics of mature myofibroblasts. Knockdown of Zeb2 with siRNA in primary myofibroblasts did not alter the expression of myofibroblast markers, which may indicate that Zeb2 is functionally redundant with other profibrotic transcription factors. These findings add to our understanding of the contribution of Zeb2 to the mechanisms controlling cardiac fibroblast activation.

scholarly journals Plasmacytoid urothelial carcinoma of renal pelvis with positive zinc finger E–box–binding homeobox 1: a case report

2020 ◽  
Author(s):  
Atsuko Takada-Owada ◽  
Yumi Nozawa ◽  
Masato Onozaki ◽  
Shuhei Noda ◽  
Tsengelumaa Jamiyan ◽  
...  
Keyword(s):  
Urothelial Carcinoma ◽  
Zinc Finger ◽  
Renal Pelvis ◽  
Plasma Cells ◽  
Epithelial Mesenchymal Transition ◽  
Resected Specimen ◽  
Mesenchymal Transition ◽  
E Box ◽  
Tumor Transformation ◽  
E Cadherin

Abstract BackgroundThe tumor transformation mechanism of a plasmacytoid urothelial carcinoma remains unexplained. We describe the case of a plasmacytoid urothelial carcinoma of the renal pelvis in which the expression of zinc finger E–box–binding homeobox 1 (ZEB1), a key nuclear transcription factor in an epithelial–mesenchymal transition, is involved in tumor transformation.Case presentationThe patient had a left nephrectomy with the clinical diagnosis of left pelvic renal cancer. The resected specimen showed that the tumor surface comprised a noninvasive papillary urothelial carcinoma with the carcinoma in situ, and the invasive area comprised a plasmacytoid urothelial carcinoma characterized by the presence of single dyscohesive malignant cells that resembled plasma cells in a loose myxoid stroma. The noninvasive urothelial carcinoma was positive for cytokeratin and E–cadherin, and negative for vimentin and ZEB1. In contrast, the invasive plasmacytoid urothelial carcinoma was positive for cytokeratin and also vimentin and ZEB1, and negative for E–cadherin. Additionally, this component was immunoreactive for CD138 and CD38 that are immunohistochemical markers for plasma cells.ConclusionWe suggest that ZEB1 is involved in the plasmacytoid transformation by repressing the E–cadherin in a plasmacytoid urothelial carcinoma.

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