scholarly journals Genistein Mitigates High Glucose-Induced Podocyte Adhesion Injury by Modulating Autophagy via Mtor Signal

2021 ◽  
Author(s):  
Yuhang Lian ◽  
Zhixia Tian ◽  
Haiyan Cao ◽  
Zhonghui Jia ◽  
Tiekun Yan ◽  
...  
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Western Blot ◽  
High Glucose ◽  
Potential Mechanism ◽  
Mtor Signaling Pathway ◽  
Integrin Β1 ◽  
Related Factors ◽  
Migration Assay ◽  
Adhesion Ability

Abstract Purpose: The study aimed to investigate the characteristics of autophagy on podocyte under high glucose (HG) conditions and further explore the effect of Genistein on podocyte autophagy，adhesion and the potential mechanism.Materials and methods: CCK-8 was used to detect the viability of podocyte. The level of autophagy was mainly detected by western blot and immunofluorescence. The expression of autophagy related factors and podocyte adhesion markers, including LC3-II, p62, p-mTOR and integrin β1-MF, were detected by immunofluorescence at 0，6，12，24，36，48，72h. The expression levels of proteins in the LC3-II, p62, p-mTOR/mTOR, integrin β1-MF were further investigated by western blot. Wound healing test and cell migration assay were used to detect podocyte adhesion ability.Results: The present study showed that HG-induced podocyte viability was reduced significantly for 6 h. Decreased integrin β1-MF, LC3-II, increased p62 and abnormal activation of the mTOR signal was detected in podocyte under HG conditions. Genistein restored podocyte viability and up-regulated integrin β1-MF, LC3-II expression, down-regulated p62, p-mTOR expression. Moreover, the HG-induced podocyte adhesion injury was abrogated by treatment with Genistein.Conclusion：Our results demonstrated that podocyte adhesion injury in HG environment was related to the decrease of autophagy level. Genistein activated podocyte autophagy by inhibiting the mTOR signaling pathway, regulated the renewal expression of integrin β1-MF, and finally reduced HG-induced podocyte adhesion injury.

scholarly journals M2 macrophage-derived exosomal microRNAs inhibit cell migration and invasion in gliomas through PI3K/AKT/mTOR signaling pathway

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Jie Yao ◽  
Zefen Wang ◽  
Yong Cheng ◽  
Chao Ma ◽  
Yahua Zhong ◽  
...  
Keyword(s):  
Cell Migration ◽  
Western Blot ◽  
Signaling Pathway ◽  
Target Gene ◽  
Glioma Cells ◽  
Mtor Signaling ◽  
Migration And Invasion ◽  
M2 Macrophage ◽  
Mtor Signaling Pathway ◽  
Cell Migration And Invasion

Abstract Background Glioma, the most common primary brain tumor, account Preparing figures for 30 to 40% of all intracranial tumors. Herein, we aimed to study the effects of M2 macrophage-derived exosomal microRNAs (miRNAs) on glioma cells. Methods First, we identified seven differentially expressed miRNAs in infiltrating macrophages and detected the expression of these seven miRNAs in M2 macrophages. We then selected hsa-miR-15a-5p (miR-15a) and hsa-miR-92a-3p (miR-92a) for follow-up studies, and confirmed that miR-15a and miR-92a were under-expressed in M2 macrophage exosomes. Subsequently, we demonstrated that M2 macrophage-derived exosomes promoted migration and invasion of glioma cells, while exosomal miR-15a and miR-92a had the opposite effects on glioma cells. Next, we performed the target gene prediction in four databases and conducted target gene validation by qRT-PCR, western blot and dual luciferase reporter gene assays. Results The results revealed that miR-15a and miR-92a were bound to CCND1 and RAP1B, respectively. Western blot assays demonstrated that interference with the expression of CCND1 or RAP1B reduced the phosphorylation level of AKT and mTOR, indicating that both CCND1 and RAP1B can activate the PI3K/AKT/mTOR signaling pathway. Conclusion Collectively, these findings indicate that M2 macrophage-derived exosomal miR-15a and miR-92a inhibit cell migration and invasion of glioma cells through PI3K/AKT/mTOR signaling pathway.

Multi-scale modeling of a wound-healing cell migration assay

2007 ◽  
Vol 245 (3) ◽  
pp. 576-594 ◽  
Author(s):  
Anna Q. Cai ◽  
Kerry A. Landman ◽  
Barry D. Hughes
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Cell Migration Assay ◽  
Migration Assay ◽  
Multi Scale ◽  
Scale Modeling ◽  
Multi Scale Modeling

Design and Fabrication of Microfluidic-Based 3D Microphysiological Systems for Studying Cell Migration and Invasion Behaviors

2021 ◽  
Vol 11 (9) ◽  
pp. 1698-1706
Author(s):  
Xi Wang ◽  
Qingling He ◽  
Qianyin Li ◽  
Yuan Li ◽  
Shoma Suresh ◽  
...  
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Microfluidic Device ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Migration Assay ◽  
Fibroblast Migration ◽  
Raw264.7 Macrophages ◽  
3D Microenvironment

The cell migration and invasion behaviors play pivotal roles in tissue regeneration. For the skin repair process, a directed inflammatory response that regulates fibroblasts is critical for efficient wound healing. In this study, the authors present the design and fabrication of a microfluidic-based three-dimensional (3D) microphysiological system and how it impacts in controlling fibroblast migration and invasion under the induction of differently polarized macrophages. The microfluidic device had two chambers on opposite sides of a 1 mm micochannel, providing directed induction and sufficient width for long-term observation. The test cells could be seeded with or without matrix gel, cultured in a 2D or 3D microenvironment according to experiment settings. The microchannel allowed for any sorts of matrix filling and was on-demanding for continuous surveillance. Herein, our microfluidic device reserved the advantages of traditional methods using transwell chamber or scratch wound healing assay. In addition, it even came with more superiority such as retrievability, dynamic observation, and 3D environment simulation. The migration and invasion pattern of NIH3T3 modulated by RAW264.7 macrophages in different polarization status was demonstrated as an example. The results of the migration assay corresponded with that of the proliferation and gene expression experiments, verifying that our device was fully capable of restoring in vivo microenvironment and presenting cellular motility behaviors.

scholarly journals High-Glucose Inhibits Human Fibroblast Cell Migration in Wound Healing via Repression of bFGF-Regulating JNK Phosphorylation

PLoS ONE ◽  
2014 ◽  
Vol 9 (9) ◽  
pp. e108182 ◽  
Author(s):  
Yuan Hu Xuan ◽  
Bin Bin Huang ◽  
Hai Shan Tian ◽  
Li Sha Chi ◽  
Yuan Meng Duan ◽  
...  
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
High Glucose ◽  
Human Fibroblast ◽  
Fibroblast Cell ◽  
Human Fibroblast Cell

scholarly journals Cutaneous Regeneration Mechanism of β-Sheet Silk Fibroin in a Rat Burn Wound Healing Model

Polymers ◽  
2021 ◽  
Vol 13 (20) ◽  
pp. 3537
Author(s):  
Kai-Chieh Chou ◽  
Chun-Ting Chen ◽  
Juin-Hong Cherng ◽  
Ming-Chia Li ◽  
Chia-Cheng Wen ◽  
...  
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Cell Adhesion ◽  
Silk Fibroin ◽  
Dermal Fibroblasts ◽  
Integrin Β1 ◽  
Burn Wound ◽  
Ecm Proteins ◽  
Β Sheet

Therapeutic dressings to enhance burn wound repair and regeneration are required. Silk fibroin (SF), a natural protein, induces cell migration and serves as a biomaterial in various dressings. SF dressings usually contain α-helices and β-sheets. The former has been confirmed to improve cell proliferation and migration, but the wound healing effect and related mechanisms of β-sheet SF remain unclear. We investigated the effects of β-sheet SF in vivo and in vitro. Alcohol-treated α-helix SF transformed into the β-sheet form, which promoted granulation formation and re-epithelialization when applied as lyophilized SF dressing (LSFD) in a rat burn model. Our in vitro results showed that β-sheet SF increased human dermal fibroblast (HDF) migration and promoted the expression of extracellular matrix (ECM) proteins (fibronectin and type III collagen), matrix metalloproteinase-12, and the cell adhesion molecule, integrin β1, in rat granulation tissue and HDFs. This confirms the role of crosstalk between integrin β1 and ECM proteins in cell migration. In summary, we demonstrated that β-sheet SF facilitates tissue regeneration by modulating cell adhesion molecules in dermal fibroblasts. LSFD could find clinical application for burn wound regeneration. Moreover, β-sheet SF could be combined with anti-inflammatory materials, growth factors, or antibiotics to develop novel dressings.

scholarly journals Overexpression of osmosensitive Ca2+-activated channel TMEM63B promotes migration in HEK293T cells

2019 ◽  
Author(s):  
Marta C. Marques ◽  
Inês S. Albuquerque ◽  
Sandra H. Vaz ◽  
Gonçalo J. L. Bernardes
Keyword(s):  
Wound Healing ◽  
Plasma Membrane ◽  
Cell Migration ◽  
Plant Cells ◽  
Active Cell ◽  
Mechanosensitive Channels ◽  
Potential Mechanism ◽  
Cell Homeostasis ◽  
Mammalian Homologue

AbstractThe recent discovery of the osmosensitive calcium (Ca2+) channel OSCA has revealed the potential mechanism by which plant cells sense diverse stimuli. Osmosensory transporters and mechanosensitive channels can detect and respond to osmotic shifts that play an important role in active cell homeostasis. TMEM63 family of proteins are described as the closest homologues of OSCAs. Here, we characterize TMEM63B, a mammalian homologue of OSCAs, recently classified as mechanosensitive. In HEK293T cells TMEM63B localizes to the plasma membrane and is associated to F-actin. This Ca2+-activated channel specifically induces Ca2+ influx across the membrane in response to extracellular Ca2+ concentration and hyperosmolarity. In addition, overexpression of TMEM63B in HEK293T cells significantly enhanced cell migration and wound healing. The link between Ca2+ osmosensitivity and cell migration might help to establish TMEM63B’s pathogenesis, for example in cancer in which it is frequently overexpressed.

A simple microfluidic strategy for cell migration assay in an in vitro wound-healing model

2013 ◽  
Vol 21 (6) ◽  
pp. 897-903 ◽  
Author(s):  
Min Zhang ◽  
Hongjing Li ◽  
Huipeng Ma ◽  
Jianhua Qin
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Cell Migration Assay ◽  
Migration Assay ◽  
Wound Healing Model ◽  
Healing Model
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