scholarly journals The extracellular matrix as a cell survival factor.

1993 ◽  
Vol 4 (9) ◽  
pp. 953-961 ◽  
Author(s):  
J E Meredith ◽  
B Fazeli ◽  
M A Schwartz
Keyword(s):  
Extracellular Matrix ◽  
Cell Death ◽  
Cell Survival ◽  
Tyrosine Phosphatase ◽  
Cell Types ◽  
Specific Gene ◽  
Survival Factor ◽  
A Cell ◽  
Cell Growth And Differentiation ◽  
Cell Survival Factor

Programmed cell death (PCD) or apoptosis is a naturally occurring cell suicide pathway induced in a variety of cell types. In many cases, PCD is induced by the withdrawal of specific hormones or growth factors that function as survival factors. In this study, we have investigated the potential role of the extracellular matrix (ECM) as a cell survival factor. Our results indicate that in the absence of any ECM interactions, human endothelial cells rapidly undergo PCD, as determined by cell morphology, nuclei fragmentation, DNA degradation, protein cross-linking, and the expression of the PCD-specific gene TRPM-2. PCD was blocked by plating cells on an immobilized integrin beta 1 antibody but not by antibodies to either the class I histocompatibility antigen (HLA) or vascular cell adhesion molecule-1 (VCAM-1), suggesting that integrin-mediated signals were required for maintaining cell viability. Treatment of the cells in suspension with the tyrosine phosphatase inhibitor sodium orthovanadate also blocked PCD. When other cell types were examined, some, but not all, underwent rapid cell death when deprived of adhesion to the ECM. These results suggest that in addition to regulating cell growth and differentiation, the ECM also functions as a survival factor for many cell types.

scholarly journals Remembrance of Dead Cells Past: Discovering That the Extracellular Matrix Is a Cell Survival Factor

2010 ◽  
Vol 21 (4) ◽  
pp. 499-500 ◽  
Author(s):  
Martin A. Schwartz
Keyword(s):  
Cell Survival ◽  
Cancer Metastasis ◽  
Control Cell ◽  
Integrin Signaling ◽  
Tumor Resistance ◽  
Survival Factor ◽  
Response To Chemotherapy ◽  
A Cell ◽  
Resistance To Chemotherapy ◽  
Cell Survival Factor

In 1992, Jere Meredith and I followed up on a serendipitous observation and showed that matrix deprivation can lead to apoptosis. Our article in Molecular Biology of the Cell, together with work form Steve Frisch's lab, helped establish the paradigm that integrin signals control cell survival in a variety of systems. It has been a pleasure to watch that work take on a life of its own as other investigators have explored its role in processes such as cavitation, regression of the mammary gland at the end of pregnancy, cancer metastasis, and tumor resistance to chemotherapy. Recently, we described an exception to the paradigm: In some tumors, reagents that activate integrin signaling enhance apoptosis in response to chemotherapy.

scholarly journals Thyroid Hormone Induces Apoptosis in Primary Cell Cultures of Tadpole Intestine: Cell Type Specificity and Effects of Extracellular Matrix

1997 ◽  
Vol 139 (6) ◽  
pp. 1533-1543 ◽  
Author(s):  
Yuan Su ◽  
Yufang Shi ◽  
Melissa A. Stolow ◽  
Yun-Bo Shi
Keyword(s):  
Extracellular Matrix ◽  
Cell Death ◽  
Thyroid Hormone ◽  
Epithelial Cells ◽  
Mammalian Cell ◽  
Cell Types ◽  
Specific Gene ◽  
Causative Role ◽  
Cell Type Specificity

Thyroid hormone (T3 or 3,5,3′-triiodothyronine) plays a causative role during amphibian metamorphosis. To investigate how T3 induces some cells to die and others to proliferate and differentiate during this process, we have chosen the model system of intestinal remodeling, which involves apoptotic degeneration of larval epithelial cells and proliferation and differentiation of other cells, such as the fibroblasts and adult epithelial cells, to form the adult intestine. We have established in vitro culture conditions for intestinal epithelial cells and fibroblasts. With this system, we show that T3 can enhance the proliferation of both cell types. However, T3 also concurrently induces larval epithelial apoptosis, which can be inhibited by the extracellular matrix (ECM). Our studies with known inhibitors of mammalian cell death reveal both similarities and differences between amphibian and mammalian cell death. These, together with gene expression analysis, reveal that T3 appears to simultaneously induce different pathways that lead to specific gene regulation, proliferation, and apoptotic degeneration of the epithelial cells. Thus, our data provide an important molecular and cellular basis for the differential responses of different cell types to the endogenous T3 during metamorphosis and support a role of ECM during frog metamorphosis.

Autoantibodies to p75/LEDGF, a cell survival factor, found in patients with atypical retinal degeneration

2006 ◽  
Vol 27 (1) ◽  
pp. 17-27 ◽  
Author(s):  
Marian S. Chin ◽  
Rafael C. Caruso ◽  
Barbara Detrick ◽  
John J. Hooks
Keyword(s):  
Cell Survival ◽  
Retinal Degeneration ◽  
Survival Factor ◽  
A Cell ◽  
Cell Survival Factor

scholarly journals Whole Transcriptome Profiling Identifies CD93 and Other Plasma Cell Survival Factor Genes Associated with Measles-Specific Antibody Response after Vaccination

PLoS ONE ◽  
2016 ◽  
Vol 11 (8) ◽  
pp. e0160970 ◽  
Author(s):  
Iana H. Haralambieva ◽  
Michael T. Zimmermann ◽  
Inna G. Ovsyannikova ◽  
Diane E. Grill ◽  
Ann L. Oberg ◽  
...  
Keyword(s):  
Antibody Response ◽  
Cell Survival ◽  
Plasma Cell ◽  
Specific Antibody ◽  
Transcriptome Profiling ◽  
Specific Antibody Response ◽  
Survival Factor ◽  
Whole Transcriptome ◽  
Cell Survival Factor

Abstract 143: A Novel TAK1 Signaling Network Regulating Programmed Necrosis and Myocardial Remodeling

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Qinghang Liu ◽  
Lei Li ◽  
Yi Chen ◽  
Jessica Doan ◽  
Jeffery Molkentin
Keyword(s):  
Heart Failure ◽  
Cell Death ◽  
Cell Survival ◽  
Cardiac Fibrosis ◽  
Signaling Network ◽  
Specific Gene ◽  
Caspase 8 ◽  
Programmed Necrosis ◽  
Genetic Ablation ◽  
Cell Death Pathway

We recently identified a novel signaling molecule, TAK1 (TGFβ-activated kinase 1, also known as MAP3K7), as a key regulator of the hypertrophic signaling network. Importantly, TAK1 is activated in mouse models of heart failure as well as in diseased human myocardium. Here, we defined a previously unidentified, novel role for TAK1 in promoting cardiac cell survival and homeostasis using cardiac-specific gene-targeted mice. Indeed, cardiac-specific ablation of TAK1 in mice using a Cre-LoxP system showed enhanced pathological cardiac remodeling and massive cell death, and these mice gradually developed heart failure and spontaneous death. Remarkably, ablation of TNF receptor 1 (TNFR1) largely rescued the pathological phenotype of TAK1-deficient mice, preventing early lethality and cardiac fibrosis, suggesting that TNFR1 signaling is critical in mediating adverse remodeling and heart failure associated with TAK1 deficiency. Genetic or pharmacological inactivation of TAK1 in cardiomyocytes markedly induced programmed necrosis and apoptosis in response to TNFα. Conversely, overexpression of the constitutively active TAK1 mutant, or TAK1 plus its activator TAB1, protected cardiomyocytes from TNFα-induced cell death. Mechanistically, inactivation of TAK1 promoted formation of the necroptotic cell death complex consisting of RIP1, RIP3, caspase 8, and FADD. Genetic ablation of RIP1, RIP3, caspase 8, or FADD largely blocked TNFα-induced cell death in TAK1-deficient cells, whereas deletion of Bax/Bak or cyclophilin D showed no effects. Further, IKK/NFκB-mediated cell survival signaling was greatly impaired in TAK1-deficient cardiomyocytes. Taken together, our data indicate that TAK1 functions as a critical “molecular switch” in TNFα-induced programmed necrosis in cardiomyocytes, by interacting with the RIP1/3-caspase 8-FADD cell death pathway as well as the IKK-NFκB cell survival pathway. These findings thus define an important TAK1-mediated cardio-protective signaling network in the heart, which may suggest new therapeutic strategies in the treatment of heart disease.

Analyses of cellular multimerin 1 receptors: in vitro evidence of binding mediated by αΙΙbβ3 and αvβ3

2005 ◽  
Vol 94 (11) ◽  
pp. 1004-1011 ◽  
Author(s):  
Frédéric Adam ◽  
Shilun Zheng ◽  
Nilesh Joshi ◽  
David Kelton ◽  
Amin Sandhu ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Cell Types ◽  
Factor V ◽  
Cellular Activation ◽  
Fiber Assembly ◽  
Expression Studies ◽  
Additional Cell ◽  
A Cell ◽  
Rgd Site

SummaryMultimerin 1 (MMRN1) is a large, soluble, polymeric, factor V binding protein and member of the EMILIN protein family.In vivo, MMRN1 is found in platelets, megakaryocytes, endothelium and extracellular matrix fibers, but not in plasma. To address the mechanism of MMRN1 binding to activated platelets and endothelial cells, we investigated the identity of the major MMRN1 receptors on these cells using wild-type and RGE-forms of recombinant MMRN1. Ligand capture, cell adhesion, ELISA and flow cytometry analyses of platelet-MMRN1 binding, indicated that MMRN1 binds to integrins αIIbβ3 and αvβ3. Endothelial cell binding to MMRN1 was predominantly mediated by αvβ3 and did not require the MMRN1 RGD site or cellular activation. Like many other αvβ3 ligands, MMRN1 had the ability to support adhesion of additional cell types, including stimulated neutrophils. Expression studies, using a cell line capable of endothelial-like MMRN1 processing, indicated that MMRN1 adhesion to cellular receptors enhanced its extracellular matrix fiber assembly. These studies implicate integrin-mediated binding in MMRN1 attachment to cells and indicate that MMRN1 is a ligand for αIIbβ3 and αvβ3.

scholarly journals Inducible cell-specific mouse models for paired epigenetic and transcriptomic studies of microglia and astroglia

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Ana J. Chucair-Elliott ◽  
Sarah R. Ocañas ◽  
David R. Stanford ◽  
Victor A. Ansere ◽  
Kyla B. Buettner ◽  
...  
Keyword(s):  
Gene Expression ◽  
Affinity Purification ◽  
Regulation Of Gene Expression ◽  
Cell Types ◽  
Tissue Level ◽  
Cell Phenotype ◽  
Specific Gene ◽  
Cell Type ◽  
A Cell ◽  
Cell Type Specific

AbstractEpigenetic regulation of gene expression occurs in a cell type-specific manner. Current cell-type specific neuroepigenetic studies rely on cell sorting methods that can alter cell phenotype and introduce potential confounds. Here we demonstrate and validate a Nuclear Tagging and Translating Ribosome Affinity Purification (NuTRAP) approach for temporally controlled labeling and isolation of ribosomes and nuclei, and thus RNA and DNA, from specific central nervous system cell types. Analysis of gene expression and DNA modifications in astrocytes or microglia from the same animal demonstrates differential usage of DNA methylation and hydroxymethylation in CpG and non-CpG contexts that corresponds to cell type-specific gene expression. Application of this approach in LPS treated mice uncovers microglia-specific transcriptome and epigenome changes in inflammatory pathways that cannot be detected with tissue-level analysis. The NuTRAP model and the validation approaches presented can be applied to any brain cell type for which a cell type-specific cre is available.

Lens Epithelium-Derived Growth Factor (LEDGF/p75) is a cancer cell survival factor that controls the expression of decoy TRAIL-receptor 2 (DcR2)

Apmis ◽  
2008 ◽  
Vol 116 (5) ◽  
pp. 413-413
Author(s):  
Lou Klitgaard Povlsen ◽  
Mads Daugaard ◽  
Mikkel Rohde ◽  
Jakob E. Larsen ◽  
Marja Jäättelä
Keyword(s):  
Growth Factor ◽  
Cell Survival ◽  
Cancer Cell ◽  
Lens Epithelium ◽  
Trail Receptor ◽  
Survival Factor ◽  
Cancer Cell Survival ◽  
Cell Survival Factor
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