scholarly journals Hsa_circ_0024093/miR-4677-3p/miR-889-3p/USP9X/YAP1 axis accelerates proliferation and migration but inhibits apoptosis of VSMCs in the in vitro model of arteriosclerosis obliterans of the lower extremities

Author(s):  
Xue Zhang ◽  
Peng Wang ◽  
Kai Yuan ◽  
Maoran Li ◽  
Yiting Shen ◽  
...  
Placenta ◽  
2016 ◽  
Vol 45 ◽  
pp. 124
Author(s):  
Jessica E. Davies ◽  
Hannah EJ. Yong ◽  
Anthony J. Borg ◽  
Shaun P. Brennecke ◽  
Padma Murthi

2018 ◽  
Vol 17 (4) ◽  
pp. 105-112
Author(s):  
Jade Marie Lasiste ◽  
Pablo Zoroquiain ◽  
Denise Miyamoto ◽  
Miguel Burnier

Purpose: To determine the activity of metformin in an in vitro model of posterior capsule opacification (PCO).Design: Experimental laboratory research. Methods: The HLE-B3 lens epithelial cell line was treated with PCO induction media (PCOM) supplemented with transforming growth factor-beta (TGF-β) and fibroblast growth factor (FGF). Different metformin concentrations (0-100 mM) were used. The following cellular parameters were assessed: (1) survival, using a viability assay; (2) morphology, via microscopy and image analysis; (3) migration, using the wound assay; (4) and expression of epithelial (Pax6, E-cadherin) and mesenchymal (α-smooth muscle actin or α-SMA, fibronectin) markers via Western blot. Expression of the uptake receptor SLC22A1 was evaluated in HLE-B3 and in human donor eyes with Western blot and immunohistochemistry, respectively. Statistical analysis of variance (ANOVA) with Tukey post-hoc test was done for analysis of cytotoxicity, morphology and migration data. Results: Metformin was lethal to half (LC50) of the cells at 30 mM, and a decrease in viability (P<0.05) was noted at 5 mM. LECs in PCOM treated with 1 mM metformin showed increased Pax6 and E-cadherin and decreased α-SMA and fibronectin expression. LECs in PCOM treated with metformin also maintained epithelial morphology. Migration was inhibited with 0.5 mM metformin (P<0.05). Both HLE-B3 and the lens epithelium in donor eyes were found to express SLC22A1.Conclusion: Metformin decreased survival and migration in LECs, maintaining epithelial phenotype and reducing mesenchymal marker expression. Metformin therefore has potential as an adjunct in PCO prevention.Financial Disclosures: This work was partially funded by Mitacs Canada.


2016 ◽  
Vol 2016.28 (0) ◽  
pp. _2F23-1_-_2F23-4_
Author(s):  
Taihei Onishi ◽  
Yujie Li ◽  
Shusaku Oppata ◽  
Tadashi Idei ◽  
Makoto Ohta

2021 ◽  
Vol 22 (9) ◽  
pp. 4581
Author(s):  
Yu-Jin Lee ◽  
Song-Hee Park ◽  
Hye-Ree Park ◽  
Young Lee ◽  
Hoon Kang ◽  
...  

Mesenchymal stem cell therapy (MSCT) has been shown to be a new therapeutic option for treating alopecia areata (AA). Outer root sheath cells (ORSCs) play key roles in maintaining the hair follicle structure and supporting the bulge area. In human ORSCs (hORSCs), the mechanism for this process has not been extensively studied. In this study, we aimed to examine the influence of human hematopoietic mesenchymal stem cells (hHMSCs) in the hORSCs in vitro model of AA and determine the mechanisms controlling efficacy. Interferon-gamma (IFN-γ) pretreatment was used to induce an in vitro model of AA in hORSCs. The effect of MSCT on the viability and migration of hORSCs was examined using co-cultures, the MTT assay, and migration assays. We investigated the expression of molecules related to the Wnt/β-catenin pathway, JAK/STAT pathway, and growth factors in hHMSC-treated hORSCs by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analyses. hHMSCs increased hORSC viability and migration when they were co-cultured. hHMSCs reverted IFN-γ-induced expression—including NLRP3, ASC, caspase-1, CXCL-9 through 11, IL-1β, and IL-15—and upregulated several growth factors and hair stem cell markers. hHMSCs activated several molecules in the Wnt/β-catenin signaling pathway, such as in the Wnt families, β-catenin, phosphorylated GSK-3β and cyclin D1, and suppressed the expression of DKK1 induced by IFN-γ in hORSCs. hHMSCs suppressed the phosphorylation of JAK1 to 3, STAT1, and STAT3 compared to the controls and IFN-γ-pretreated hORSCs. These results demonstrate that hHMSCs increased hORSC viability and migration in the in vitro AA model. Additionally, MSCT definitely stimulated anagen survival and hair growth in an HF organ culture model. MSCT appeared to be associated with the Wnt/β-catenin and JAK/STAT pathways in hORSCs.


2017 ◽  
Vol 18 (5) ◽  
pp. 415-418 ◽  
Author(s):  
María Guembe ◽  
María Jesús Pérez Granda ◽  
Raquel Cruces ◽  
Luis Alcalá ◽  
Emilio Bouza

Introduction Neutral-valve closed-system connectors can reduce the frequency of catheter colonization. Commercially available closed system connectors need to be tested and compared with each other to assess how they protect against contamination. We aimed to compare, in vitro, the efficacy of connectors NeutraClear® and MicroClave® against contamination under conditions of daily clinical practice. Methods The model consisted of a set of 200 blood culture bottles (BCBs) with a cannula inserted (100 closed with NeutraClear® and 100 closed with MicroClave®) that were assessed in two experiments while instilling 1 mL of saline: manipulation based on the standard of care and manipulation using gloves impregnated with a 0.05 McFarland Staphylococcus aureus solution. The BCBs were incubated in a BACTEC System at 37°C under continuous shaking for up to 7 days. When a bottle turned positive, 100 µL of the fluid was cultured. The positivity rate and time to positivity of the BCB in each experiment was compared. Results In the aseptic model in the NeutraClear® and MicroClave® groups, only 1 BCB and 2 BCBs were positive, respectively, (p = 0.55). In the contaminated model, all BCBs were positive in both groups at the end of the incubation time. We did not find differences for the MTP between NeutraClear® and MicroClave® (36.04 vs. 20.13 hours, p = 0.09). Conclusions The NeutraClear® needleless connector proved to be as efficient as the MicroClave® connector in the prevention of catheter colonization and migration of S. aureus from the surface to the inside of the hub in an in vitro model.


2003 ◽  
Vol 64 (10) ◽  
pp. 1205-1212 ◽  
Author(s):  
Anna K. Rotting ◽  
David E. Freeman ◽  
Jo Ann C. Eurell ◽  
Peter D. Constable ◽  
Matthew Wallig

2006 ◽  
Vol 14 (2) ◽  
pp. 203-209 ◽  
Author(s):  
Caroline A. Harrison ◽  
Martin J. Heaton ◽  
Christopher M. Layton ◽  
Sheila Mac Neil

Author(s):  
Hoda Keshmiri Neghab ◽  
Mohammad Hasan Soheilifar ◽  
Gholamreza Esmaeeli Djavid

Abstract. Wound healing consists of a series of highly orderly overlapping processes characterized by hemostasis, inflammation, proliferation, and remodeling. Prolongation or interruption in each phase can lead to delayed wound healing or a non-healing chronic wound. Vitamin A is a crucial nutrient that is most beneficial for the health of the skin. The present study was undertaken to determine the effect of vitamin A on regeneration, angiogenesis, and inflammation characteristics in an in vitro model system during wound healing. For this purpose, mouse skin normal fibroblast (L929), human umbilical vein endothelial cell (HUVEC), and monocyte/macrophage-like cell line (RAW 264.7) were considered to evaluate proliferation, angiogenesis, and anti-inflammatory responses, respectively. Vitamin A (0.1–5 μM) increased cellular proliferation of L929 and HUVEC (p < 0.05). Similarly, it stimulated angiogenesis by promoting endothelial cell migration up to approximately 4 fold and interestingly tube formation up to 8.5 fold (p < 0.01). Furthermore, vitamin A treatment was shown to decrease the level of nitric oxide production in a dose-dependent effect (p < 0.05), exhibiting the anti-inflammatory property of vitamin A in accelerating wound healing. These results may reveal the therapeutic potential of vitamin A in diabetic wound healing by stimulating regeneration, angiogenesis, and anti-inflammation responses.


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