1,721,076 research outputs found
Immunocytochemical evidence of PDGF- and TGF-beta-like molecules in invertebrate and vertebrate immunocytes: An evolutionary approach
No full textImmunoreactive platelet-derived growth factor-AB and transforming growth factor-beta 1 were demonstrated in invertebrate and vertebrate immunocytes by an immunocytochemical procedure. These factors are only present in phagocytic cells among invertebrate immunocytes, whereas in vertebrate immunocytes they are found in monocytes, granulocytes, lymphocytes, thrombocytes and platelets. These results, in agreement with previous reports, represent further evidence in favour of the hypothesis that Nature has followed a conservative strategy in using a common pool of signal molecules that have been highly conserved throughout evolution
Presence and role of cytokines and growth factors in invertebrates
No full textAvailable data from our and other laboratories on the presence and biological functions of cytokine- and growth factor-like molecules in invertebrates are reviewed. It appears that IL-1 alpha-, IL-1 beta-, IL-2-, IL-6-, TNF-alpha-like molecules and haemokinin are present in several cell types from molluscs, insects, annelids, echinodems and tunicates. In most cases, these molecules are present in cells with phagocytic activity and they modulate cell motility. PDGF-, TGF-beta-, EGF- and NGF-like molecules, growth promoting factors and the hemolymph trophic factor are present in several cell types from molluscs, insects and annelids. These molecules are probably involved in the control of cell proliferation. Both cytokines and growth factors appear to be highly ancestral and biologically very important molecules, as evident from their continuous presence from invertebrates to vertebrates. It also appears that cytokines are functionally conserved molecules, which during evolution have also maintained their pleiotropicity, redundancy in mode of action and the promiscuity of their receptors
PDGF and TGF-beta induce cell shape changes in invertebrate immunocytes via specific cell surface receptors
No full textThe presence of PDGF receptor-alpha- and -beta- and TGF-beta-receptor (type II)-like molecules on the plasma membranes of the immunocytes of the mollusc Mytilus galloprovincialis was demonstrated by an immunocytochemical procedure. Furthermore, the present study provides evidence that PDGF-AB and TGF-beta 1 provoke cell shape changes in immunocytes via interactions with the respective receptors and that these extracellular signals are transduced along the phosphoinositide signaling pathway
Platelet-derived growth factor and transforming growth factor-β induce shape changes in invertebrate immunocytes via multiple signalling pathways and provoke the expression of Fos-, Jun- and SMAD-family members
No full textRecently, we have found that platelet-derived growth factor (PDGF)-AB and transforming growth factor (TGF)-β1 induce shape changes in the immunocytes of the mollusc Mytilus galloprovincialis. Here we report that calphostin C and H-89, which specifically inhibit PKC and PKA, respectively, completely or in part inhibit the above effect. These data indicate the involvement of both pathways in growth factor-induced conformational changes in molluscan immunocytes. Furthermore, we show the presence of immunoreactive molecules for the Fos B, Jun D and Smad4 transcription factors. Stimulation by PDGF-AB or TGF-β1 up-regulate the intranuclear levels of these factors. Copyright (C) 1999 Elsevier Science Inc
Involvement of PI 3-kinase, PKA and PKC in PDGF- and TGF-β-mediated prevention of 2-deoxy-D-ribose-induced apoptosis in the insect cell line, IPLB-LdFB
No full textActivation of phosphatidylinositol (PI) 3-kinase, protein kinase A (PKA) and protein kinase C (PKC) is associated with the survival effect elicited by PDGF-AB and TGF-β1 against the apoptotic inducer 2-deoxy-D-ribose (dRib) in the fat body cell line, IPLB-LdFB, from the insect Lymantria dispar. dRib induces apoptosis and provokes mitochondrial membrane depolarization (MMD). The antioxidant N-acetyl-L-cysteine annuls only the first effect. These findings suggest that apoptosis and MMD are provoked by two different mechanisms, and that dRib induces apoptosis by oxidative stress. © 2001 Academic Press
The growth-inhibitory block of TGF-beta is located close to the G1/S border in the cell cycle
No full textTransforming growth factor-beta (TGF-beta) inhibits DNA synthesis in dense cultures of young human embryonic fibroblasts and antagonizes the mitogenic action of platelet-derived growth factor (PDGF). The inhibition of the PDGF-BB action by TGF-beta was independent of the induction of mRNAs for the PDGF-A chain and PDGF-beta receptor, the predominant types of PDGF receptor in human fibroblasts. The TGF-beta-mediated inhibition did not influence the expression of various genes that are involved in the transition from the arrested (GO) state to the S phase of the cell cycle. Indeed, TGF-beta upregulated the "early" genes c-myc, c-fos, and junB and downregulated the growth arrest-specific (gas) genes. These results suggest that the inhibition of DNA synthesis by TGF-beta in human fibroblasts is independent of modulation of expression of early and gas genes, placing the TGF-beta block comparatively late in the GO to S transition. In cultures of senescent human fibroblasts TGF-beta stimulated DNA synthesis but, nevertheless, had the same effect as in young cells on the expression of PDGF chains and receptor genes, as well as on early and gas genes, with the exception of a significantly lower induction of c-fos
Dynamic interplay between breast cancer cells and normal endothelium mediates the expression of matrix macromolecules, proteasome activity and functional properties of endothelial cells
No full textBackground
Breast cancer–endothelium interactions provide regulatory signals facilitating tumor progression. The endothelial cells have so far been mainly viewed in the context of tumor perfusion and relatively little is known regarding the effects of such paracrine interactions on the expression of extracellular matrix (ECM), proteasome activity and properties of endothelial cells.
Methods
To address the effects of breast cancer cell (BCC) lines MDA-MB-231 and MCF-7 on the endothelial cells, two cell culture models were utilized; one involves endothelial cell culture in the presence of BCCs-derived conditioned media (CM) and the other co-culture of both cell populations in a Transwell system. Real-time PCR was utilized to evaluate gene expression, an immunofluorescence assay for proteasome activity, and functional assays (migration, adhesion and invasion) and immunofluorescence microscopy for cell integrity and properties.
Results
BCC-CM decreases the cell migration of HUVEC. Adhesion and invasion of BCCs are favored by HUVEC and HUVEC-CM. HA levels and the expression of CD44 and HA synthase-2 by HUVEC are substantially upregulated in both cell culture approaches. Adhesion molecules, ICAM-1 and VCAM-1, are also highly upregulated, whereas MT1-MMP and MMP-2 expressions are significantly downregulated in both culture systems. Notably, the expression and activity of the proteasome β5 subunit are increased, especially by the action of MDA-MB-231-CM on HUVEC.
Conclusions and general significance
BCCs significantly alter the expression of matrix macromolecules, proteasome activity and functional properties of endothelial cells. Deep understanding of such paracrine interactions will help to design novel drugs targeting breast cancer at the ECM level. This article is part of a Special Issue entitled Matrix-mediated cell behavior and properties
ESR2 Drives Mesenchymal-to-Epithelial Transition in Triple-Negative Breast Cancer and Tumorigenesis In Vivo
Full text linkEstrogen receptors (ERs) have pivotal roles in the development and progression of triple-negative breast cancer (TNBC). Interactions among cancer cells and tumor microenvironment are orchestrated by the extracellular matrix that is rapidly emerging as prominent contributor of fundamental processes of breast cancer progression. Early studies have correlated ERβ expression in tumor sites with a more aggressive clinical outcome, however ERβ exact role in the progression of TNBC remains to be elucidated. Herein, we introduce the functional role of ERβ suppression following isolation of monoclonal cell populations of MDA-MB-231 breast cancer cells transfected with shRNA against human ESR2 that permanently resulted in 90% reduction of ERβ mRNA and protein levels. Further, we demonstrate that clone selection results in strongly reduced levels of the aggressive functional properties of MDA-MB-231 cells, by transforming their morphological characteristics, eliminating the mesenchymal-like traits of triple-negative breast cancer cells. Monoclonal populations of shERβ MDA-MB-231 cells undergo universal matrix reorganization and pass on a mesenchymal-to-epithelial transition state. These striking changes are encompassed by the total prevention of tumorigenesis in vivo following ERβ maximum suppression and isolation of monoclonal cell populations in TNBC cells. We propose that these novel findings highlight the promising role of ERβ targeting in future pharmaceutical approaches for managing the metastatic dynamics of TNBC breast cancer
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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