scholarly journals Electrospun Polyhydroxybutyrate and Poly(L-lactide-co-ε-caprolactone) Composites as Nanofibrous Scaffolds

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Donraporn Daranarong ◽  
Rodman T. H. Chan ◽  
Nico S. Wanandy ◽  
Robert Molloy ◽  
Winita Punyodom ◽  
...  
Keyword(s):  
Cell Cycle Progression ◽  
Cell Attachment ◽  
Fibre Diameter ◽  
Nerve Tissue ◽  
Mitochondrial Activity ◽  
Cycle Progression ◽  
Support Cell ◽  
Nanofibrous Scaffolds ◽  
Average Fibre ◽  
Fibrous Membranes

Electrospinning can produce nanofibrous scaffolds that mimic the architecture of the extracellular matrix and support cell attachment for tissue engineering applications. In this study, fibrous membranes of polyhydroxybutyrate (PHB) with various loadings of poly(L-lactide-co-ε-caprolactone) (PLCL) were successfully prepared by electrospinning. In comparison to PLCL scaffolds, PLCL blends with PHB exhibited more irregular fibre diameter distributions and higher average fibre diameters but there were no significant differences in pore size. PLCL/PHB scaffolds were more hydrophilic (<120°) with significantly reduced tensile strength (ca. 1 MPa) compared to PLCL scaffolds (150.9±2.8∘and5.8±0.5 MPa). Increasing PLCL loading in PHB/PLCL scaffolds significantly increased the extension at break, (4–6-fold). PLCL/PHB scaffolds supported greater adhesion and proliferation of olfactory ensheathing cells (OECs) than those exhibiting asynchronous growth on culture plates. Mitochondrial activity of cells cultivated on the electrospun blended membranes was enhanced compared to those grown on PLCL and PHB scaffolds (212, 179, and 153%, resp.). Analysis showed that PLCL/PHB nanofibrous membranes promoted cell cycle progression and reduced the onset of necrosis. Thus, electrospun PLCL/PHB composites promoted adhesion and proliferation of OECs when compared to their individual PLCL and PHB components suggesting potential in the repair and engineering of nerve tissue.

scholarly journals Cell cycle exit and stem cell differentiation are coupled through regulation of mitochondrial activity in the Drosophila testis

2021 ◽  
Author(s):  
Diego Sainz de la Maza ◽  
Silvana Hof-Michel ◽  
Lee Phillimore ◽  
Christian Bökel ◽  
Marc Amoyel
Keyword(s):  
Cell Cycle ◽  
Stem Cells ◽  
Stem Cell ◽  
Cell Cycle Progression ◽  
Stem Cell Differentiation ◽  
Mitochondrial Activity ◽  
Self Renewal ◽  
Cycle Progression ◽  
Cell Identity ◽  
Drosophila Testis

AbstractStem cells maintain tissue homeostasis by proliferating to replace cells lost to damage or natural turnover. Whereas stem and progenitor cells proliferate, fully differentiated cells exit the cell cycle. How cell identity and cell cycle state are coordinated during this process is still poorly understood. The Drosophila testis niche supports germline stem cells and somatic cyst stem cells (CySCs), which are the only proliferating somatic cells in the testis. CySCs give rise to post-mitotic cyst cells and therefore provide a tractable model to ask how stem cell identity is linked to proliferation. We show that the G1/S cyclin, Cyclin E, is required for CySC self-renewal; however, its canonical transcriptional regulator, a complex of the E2f1 and Dp transcription factors is dispensable for self-renewal and cell cycle progression. Nevertheless, we demonstrate that E2f1/Dp activity must be silenced to allow CySCs to differentiate. We show that E2f1/Dp activity inhibits the expression of genes important for mitochondrial activity. Furthermore, promoting mitochondrial activity or biogenesis is sufficient to rescue the differentiation of CySCs with ectopic E2f1/Dp activity but not their exit from the cell cycle. Our findings together indicate that E2f1/Dp coordinates cell cycle progression with stem cell identity by regulating the metabolic state of CySCs.

Characterization of a CV-1 cell cycle. II. The role of cell-substrate attachment

1980 ◽  
Vol 42 (1) ◽  
pp. 357-365
Author(s):  
E.L. Gershey ◽  
R.M. D'Alisa
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Cell Attachment ◽  
Solid Substrate ◽  
Cycle Progression ◽  
Synchronous Cultures ◽  
Cell Substrate ◽  
Enhance Cell Attachment ◽  
Sv40 Infection

The availability of synchronous cultures of untransformed CV-I cells has allowed analysis of the role of cell-substrate attachment in cell cycle progression as well as the ability of serum and SV40 infection to override the requirement for cell-substrate attachment. Attachment to a solid substrate is required for progression through G1. Prevention of attachment results in cell cycle arrest 30 min after cytokinesis. Serum is required for attachment, but increasing the serum concentration from 2 to 20 % does not enhance cell attachment, nor obviate its need for cell cycle progression. SV40 infection does not overcome the requirement of serum for attachment nor the need of attachment for normal cycling.

scholarly journals Integrin-dependent activation of MAP kinase: a link to shape-dependent cell proliferation.

1995 ◽  
Vol 6 (3) ◽  
pp. 273-282 ◽  
Author(s):  
X Zhu ◽  
R K Assoian
Keyword(s):  
Cell Cycle ◽  
Extracellular Matrix ◽  
Map Kinase ◽  
Cell Cycle Progression ◽  
Map Kinases ◽  
Kinase Activity ◽  
Cell Attachment ◽  
Cell Spreading ◽  
Cycle Progression ◽  
Dependent Cell

Adhesion to extracellular matrix mediates cell cycle progression in mid-late G1; this effect involves an integrin-dependent organization of the cytoskeleton and a consequent change in cell shape. In an effort to identify potential signal-transducing agents that are associated with integrin-dependent shape changes, we looked for kinase activities that were stimulated by long-term adhesion of G0-synchronized NIH-3T3 cells to fibronectin-coated dishes. Several kinase activities were stimulated by this procedure, two of which migrated at 42 and 44 kDa and phosphorylated myelin basic protein in vitro. Blotting with anti-phosphotyrosine and anti-mitogen-activated protein (MAP) kinase antibodies identified these enzymes as ERK 1 and ERK 2. In contrast to the rapid and transient activation of these MAP kinases by platelet-derived growth factor, stimulation of MAP kinase activity by fibronectin was gradual, persistent, and associated with cell spreading rather than cell attachment itself. Cytochalasin D blocked the activation of MAP kinase activity that was induced by the binding of cells to fibronectin. Moreover, MAP kinase was also activated by adhesion of cells to vitronectin and type IV collagen; these effects were also associated with cell spreading. These results distinguish the regulation of G1 phase MAP kinase activity by soluble mitogens and extracellular matrix. They also implicate MAP kinase in shape-dependent cell cycle progression.

scholarly journals An insight into anti-adipogenic properties of an Oroxylum indicum (L.) Kurz extract

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Tanaporn Hengpratom ◽  
Gordon M. Lowe ◽  
Griangsak Eumkeb
Keyword(s):  
Cell Cycle ◽  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Cell Cycle Progression ◽  
Inhibitory Effect ◽  
Mitochondrial Activity ◽  
Cycle Progression ◽  
Oroxylum Indicum ◽  
Glut4 Expression ◽  
Immunoblotting Assay

Abstract Background Oroxylum indicum fruit extract (OIE) has been reported to inhibit the development of adipocytes. However, the exact mechanism of its metabolic activity is not clearly defined. This study attempted to investigate whether OIE was involved in disrupting the cell cycle, glucose metabolism, and mitochondrial function in 3 T3-L1 cells. Methods The effect of the OIE on cell cycle progression was measured by flow cytometry along with observing the expression of the cycle regulator by immunoblotting. The effect of the OIE on glucose metabolism was investigated. The amount of glucose uptake (2-NBDG) influenced by insulin was determined as well as the protein tyrosine phosphorylation (PY20), and glucose transporter4 (GLUT4) expression was determined by immunoblotting assay. Mitochondria are also essential to metabolic processes. This study investigated mitochondrial activity using fluorescent lipophilic carbocyanine dye (JC-1) and mitochondria mass by MitoTracker Green (MTG) staining fluorescence dyes. Finally, cellular ATP concentration was measured using an ATP chemiluminescence assay. Results Treatment with OIE plus adipogenic stimulators for 24 h arrested cell cycle progression in the G2/M phase. Moreover, 200 μg/mL of OIE significantly diminished the expression of the insulin receptor (IR) and GLUT4 protein compared to the untreated-adipocytes (P < 0.05). The mitochondrial membrane potential (MMP) was significantly reduced (24 h) and increased (day 12) by OIE compared to untreated-adipocytes (P < 0.05). However, OIE maintained MMP and ATP at a similar level compared to the pre-adipocytes (day 12). Transmission electron microscope (TEM) results demonstrated that OIE could protect mitochondria deformation compared to the untreated-adipocytes. Conclusion These results suggest that the inhibitory effect of the OIE on adipogenesis may potentially inhibit the cell cycle and phosphorylation of IR, leading to a decrease in glucose uptake to the cells. The OIE also slows down the mitochondrial activity of the early phase of cell differentiation, which can also inhibit the development of fat cells.

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