Temporal changes in peritoneal cell phenotype and neoelastic matrix induction with hyaluronan oligomers and TGF-β1 after implantation of engineered conduits

2018 ◽  
Vol 12 (6) ◽  
pp. 1420-1431 ◽  
Author(s):  
Mozhgan Shojaee ◽  
Ganesh Swaminathan ◽  
Chris A. Bashur ◽  
Anand Ramamurthi
Keyword(s):  
Temporal Changes ◽  
Peritoneal Cell ◽  
Cell Phenotype ◽  
Tgf Β1

scholarly journals Mechanotransduction and Stiffness-Sensing: Mechanisms and Opportunities to Control Multiple Molecular Aspects of Cell Phenotype as a Design Cornerstone of Cell-Instructive Biomaterials for Articular Cartilage Repair

2020 ◽  
Vol 21 (15) ◽  
pp. 5399
Author(s):  
Mischa Selig ◽  
Jasmin C. Lauer ◽  
Melanie L. Hart ◽  
Bernd Rolauffs
Keyword(s):  
Articular Cartilage ◽  
Expression Profiles ◽  
Cell Surface Receptor ◽  
Cell Phenotype ◽  
Integrin Subunit ◽  
Ample Evidence ◽  
Cell Functions ◽  
Material Stiffness ◽  
Molecular Aspects ◽  
Tgf Β1

Since material stiffness controls many cell functions, we reviewed the currently available knowledge on stiffness sensing and elucidated what is known in the context of clinical and experimental articular cartilage (AC) repair. Remarkably, no stiffness information on the various biomaterials for clinical AC repair was accessible. Using mRNA expression profiles and morphology as surrogate markers of stiffness-related effects, we deduced that the various clinically available biomaterials control chondrocyte (CH) phenotype well, but not to equal extents, and only in non-degenerative settings. Ample evidence demonstrates that multiple molecular aspects of CH and mesenchymal stromal cell (MSC) phenotype are susceptible to material stiffness, because proliferation, migration, lineage determination, shape, cytoskeletal properties, expression profiles, cell surface receptor composition, integrin subunit expression, and nuclear shape and composition of CHs and/or MSCs are stiffness-regulated. Moreover, material stiffness modulates MSC immuno-modulatory and angiogenic properties, transforming growth factor beta 1 (TGF-β1)-induced lineage determination, and CH re-differentiation/de-differentiation, collagen type II fragment production, and TGF-β1- and interleukin 1 beta (IL-1β)-induced changes in cell stiffness and traction force. We then integrated the available molecular signaling data into a stiffness-regulated CH phenotype model. Overall, we recommend using material stiffness for controlling cell phenotype, as this would be a promising design cornerstone for novel future-oriented, cell-instructive biomaterials for clinical high-quality AC repair tissue.

scholarly journals Functional cell phenotype induction with TGF-β1 and collagen-polyurethane scaffold for annulus fibrosus rupture repair

2020 ◽  
Vol 39 ◽  
pp. 1-17 ◽  
Author(s):  
J Du ◽  
◽  
RG Long ◽  
T Nakai ◽  
D Sakai ◽  
...  
Keyword(s):  
Annulus Fibrosus ◽  
Cell Phenotype ◽  
Polyurethane Scaffold ◽  
Tgf Β1

scholarly journals Matrix abnormalities in pulmonary fibrosis

2018 ◽  
Vol 27 (148) ◽  
pp. 180033 ◽  
Author(s):  
Chandak Upagupta ◽  
Chiko Shimbori ◽  
Rahmah Alsilmi ◽  
Martin Kolb
Keyword(s):  
Growth Factor ◽  
Pulmonary Fibrosis ◽  
Transforming Growth Factor ◽  
Management Strategies ◽  
Cell Phenotype ◽  
Tissue Microenvironment ◽  
Close Relationship ◽  
And Function ◽  
Stiffness Loss ◽  
Tgf Β1

Idiopathic pulmonary fibrosis (IPF) is a devastating, progressive disease, marked by excessive scarring, which leads to increased tissue stiffness, loss in lung function and ultimately death. IPF is characterised by progressive fibroblast and myofibroblast proliferation, and extensive deposition of extracellular matrix (ECM). Myofibroblasts play a key role in ECM deposition. Transforming growth factor (TGF)-β1 is a major growth factor involved in myofibroblast differentiation, and the creation of a profibrotic microenvironment. There is a strong link between increased ECM stiffness and profibrotic changes in cell phenotype and differentiation. The activation of TGF-β1 in response to mechanical stress from a stiff ECM explains some of the influence of the tissue microenvironment on cell phenotype and function. Understanding the close relationship between cells and their surrounding microenvironment will ultimately facilitate better management strategies for IPF.

Rho kinase mediates transforming growth factor-β1-induced vasculogenic mimicry formation: involvement of the epithelial–mesenchymal transition and cancer stemness activity

2020 ◽  
Vol 52 (4) ◽  
pp. 411-420 ◽  
Author(s):  
Xue Zhang ◽  
Jigang Zhang ◽  
Heming Zhou ◽  
Gaolin Liu ◽  
Qin Li
Keyword(s):  
Growth Factor ◽  
Signaling Pathway ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Vasculogenic Mimicry ◽  
Rho Kinase ◽  
Transforming Growth Factor Β1 ◽  
Cell Phenotype ◽  
Mesenchymal Transition ◽  
Tgf Β1

Abstract Vasculogenic mimicry (VM), a newly defined pattern of tumor blood supply, has been identified in several malignant tumors, including hepatocellular carcinoma (HCC). Rho kinase (ROCK) plays an important role in various types of cancers. However, whether ROCK participates in transforming growth factor-β1 (TGF-β1)-induced VM formation is unclear. Here, we evaluated the role of ROCK in TGF-β1-induced VM formation in HCC. Our findings showed that the TGF-β1/ROCK signaling pathway is involved in VM formation by inducing the epithelial–mesenchymal transition. Furthermore, TGF-β1 and ROCK were found to play distinct roles in the cancer stem cell phenotype during VM formation. These results provide insights into potential antitumor therapies for inhibiting VM by targeting the TGF-β1/ROCK signaling pathway in HCC.

Temporal changes in renal endoglin and TGF-β1 expression following ureteral obstruction in rats

2005 ◽  
Vol 61 (3) ◽  
pp. 457-467 ◽  
Author(s):  
M. Prieto ◽  
A. B. Rodríguez-Peña ◽  
A. Düwel ◽  
J. V. Rivas ◽  
N. Docherty ◽  
...  
Keyword(s):  
Ureteral Obstruction ◽  
Temporal Changes ◽  
Tgf Β1

l-Thyroxine promotes a proliferative airway smooth muscle phenotype in the presence of TGF-β1

2015 ◽  
Vol 308 (3) ◽  
pp. L301-L306 ◽  
Author(s):  
Bart G. J. Dekkers ◽  
Saeideh Naeimi ◽  
I. Sophie T. Bos ◽  
Mark H. Menzen ◽  
Andrew J. Halayko ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Thyroid Hormones ◽  
Protein Expression ◽  
Airway Smooth Muscle ◽  
Transforming Growth Factor ◽  
Airway Remodeling ◽  
Contractile Protein ◽  
Cell Phenotype ◽  
Minor Effect ◽  
Tgf Β1

Hypothyroidism may reduce, whereas hyperthyroidism may aggravate, asthma symptoms. The mechanisms underlying this relationship are largely unknown. Since thyroid hormones have central roles in cell growth and differentiation, we hypothesized that airway remodeling, in particular increased airway smooth muscle (ASM) mass, may be involved. To address this hypothesis, we investigated the effects of triiodothyronine (T3) and l-thyroxine (T4) in the absence and presence of the profibrotic transforming growth factor (TGF)-β1 on human ASM cell phenotype switching. T3 (1–100 nM) and T4 (1–100 nM) did not affect basal ASM proliferation. However, when combined with TGF-β1 (2 ng/ml), T4 synergistically increased the proliferative response, whereas only a minor effect was observed for T3. In line with a switch from a contractile to a proliferative ASM phenotype, T4 reduced the TGF-β1-induced contractile protein expression by ∼50%. Cotreatment with T3 reduced TGF-β1-induced contractile protein expression by ∼25%. The synergistic increase in proliferation was almost fully inhibited by the integrin αvβ3 antagonist tetrac (100 nM), whereas no significant effects of the thyroid receptor antagonist 1–850 (3 μM) were observed. Inhibition of MEK1/2, downstream of the integrin αvβ3, also inhibited the T4- and TGF-β1-induced proliferative responses. Collectively, the results indicate that T4, and to a lesser extent T3, promotes a proliferative ASM phenotype in the presence of TGF-β1, which is predominantly mediated by the membrane-bound T4 receptor αvβ3. These results indicate that thyroid hormones may enhance ASM remodeling in asthma, which could be of relevance for hyperthyroid patients with this disease.

scholarly journals The neutrophil antimicrobial peptide cathelicidin promotes Th17 differentiation

2020 ◽  
Author(s):  
Danielle Minns ◽  
Katie J Smith ◽  
Virginia Alessandrini ◽  
Gareth Hardisty ◽  
Lauren Melrose ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Subset ◽  
Cell Phenotype ◽  
Dependent Manner ◽  
Adaptive Immune ◽  
Aryl Hydrocarbon ◽  
Th17 Differentiation ◽  
Deficient Mice ◽  
Tgf Β1

ABSTRACTThe host defence peptide cathelicidin (LL-37 in humans, mCRAMP in mice) is released from neutrophils by de-granulation, NETosis and necrotic cell death; it has potent antibacterial, antiviral and antifungal activity as well as being a powerful immunomodulator. It is released in proximity to CD4+ T cells during inflammatory and infectious disease but its impact on T cell phenotype is scarcely understood. Here we demonstrate that cathelicidin is a powerful Th17 potentiating factor which increases expression of the aryl hydrocarbon receptor (AHR) and the RORγt transcription factor, in a TGF-β1-dependent manner. We show that cathelicidin induces IL-17F production in particular, and that its induction of IL-17A+F+ double producing cells is dependent on AHR while its induction of IL-17F single producing cells is not. In the presence of TGF-β1, cathelicidin profoundly suppressed IL-2 and down-regulated T-bet, specifically directing T cells away from Th1 and into a Th17 phenotype. Strikingly, Th17, but not Th1 cells were protected from apoptotic death by cathelicidin, in the first example of a neutrophil-released mediator inducing survival of a T cell subset. Finally, we show that cathelicidin is released by neutrophils in mouse lymph nodes following inoculation of heat-killed Salmonella typhimurium and that cathelicidin-deficient mice have suppressed Th17 responses during inflammation, but not at steady state. We propose that the release of cathelicidin by neutrophils is required for maximal Th17 differentiation and IL-17 production by CD4+ T cells, and that this is one method by which early neutrophilia directs subsequent adaptive immune responses with some sophistication.

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