scholarly journals Collagen polarization promotes epithelial elongation by stimulating locoregional cell proliferation

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Hiroko Katsuno-Kambe ◽  
Jessica L Teo ◽  
Robert J Ju ◽  
James Hudson ◽  
Samantha J Stehbens ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Organotypic Culture ◽  
Break Symmetry ◽  
Mammary Epithelial ◽  
Erk Signaling ◽  
Cell Aggregates ◽  
Cellular Mechanisms ◽  
Multicellular Aggregates ◽  
A Cell ◽  
Structural Memory

Epithelial networks are commonly generated by processes where multicellular aggregates elongate and branch. Here we focus on understanding cellular mechanisms for elongation, using an organotypic culture system as a model of mammary epithelial anlage. Isotropic cell aggregates broke symmetry and slowly elongated when transplanted into collagen 1 gels. The elongating regions of aggregates displayed enhanced cell proliferation that was necessary for elongation to occur. Strikingly, this loco-regional increase in cell proliferation occurred where collagen 1 fibrils reorganized into bundles which were polarized with the elongating aggregates. Applying external stretch as a cell-independent way to reorganize the ECM, we found that collagen polarization stimulated regional cell proliferation to precipitate symmetry-breaking and elongation. This required b1-integrin and ERK signaling. We propose that collagen polarization supports epithelial anlagen elongation by stimulating loco-regional cell proliferation. This could provide a long-lasting structural memory of the initial axis that is generated when anlage break symmetry.

scholarly journals Collagen polarization provides a structural memory for the elongation of epithelial anlage

2021 ◽  
Author(s):  
Hiroko Katsuno-Kambe ◽  
Jessica L. Teo ◽  
Robert J. Ju ◽  
James E. Hudson ◽  
Samantha J. Stehbens ◽  
...  
Keyword(s):  
Break Symmetry ◽  
Mammary Epithelial ◽  
The Body ◽  
Erk Signaling ◽  
Organotypic Cultures ◽  
Multicellular Aggregates ◽  
Basement Membrane Extract ◽  
A Cell ◽  
Membrane Extract ◽  
Structural Memory

AbstractBranched epithelial networks are fundamental features of many organs in the body. The biogenesis of these networks involves distinct processes where multicellular aggregates elongate and branch. In this report we focus on understanding how the extracellular matrix contributes to the process of elongation. Using mammary epithelial organotypic cultures we found that collagen 1, but not a basement membrane extract, induces the formation of elongated multicellular aggregates. Indeed, isotropic aggregates, used as models of epithelial anlage, broke symmetry and elongated when transplanted into collagen 1 gels; this was accompanied by reorganization of collagen fibrils into bundles that were polarized around the elongating aggregates. By applying external stretch as a cell-independent way to reorganize the ECM gels, we found that collagen polarization itself can induce and guide the direction of aggregate elongation. This critically involves cell proliferation, which is selectively enhanced in the regions of anlage that elongate, and requires β1-integrin and ERK signaling. We propose that collagen polarization promotes anlage elongation by providing a structural memory of the initial axis that is generated when aggregates break symmetry.

scholarly journals microRNAs: fine tuning of erythropoiesis

2013 ◽  
Vol 18 (1) ◽  
Author(s):  
Marcin Listowski ◽  
Elżbieta Heger ◽  
Dżamila Bogusławska ◽  
Beata Machnicka ◽  
Kazimierz Kuliczkowski ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Regulation Of Gene Expression ◽  
Fine Tuning ◽  
Quantitative Composition ◽  
Transcriptional Level ◽  
Cellular Mechanisms ◽  
Cell Proliferation And Differentiation ◽  
A Cell ◽  
Mirna Pathway

AbstractCell proliferation and differentiation is a complex process involving many cellular mechanisms. One of the best-studied phenomena in cell differentiation is erythrocyte development during hematopoiesis in vertebrates. In recent years, a new class of small, endogenous, non-coding RNAs called microRNAs (miRNAs) emerged as important regulators of gene expression at the post-transcriptional level. Thousands of miRNAs have been identified in various organisms, including protozoa, fungi, bacteria and viruses, proving that the regulatory miRNA pathway is conserved in evolution. There are many examples of miRNA-mediated regulation of gene expression in the processes of cell proliferation, differentiation and apoptosis, and in cancer genesis. Many of the collected data clearly show the dependence of the proteome of a cell on the qualitative and quantitative composition of endogenous miRNAs. Numerous specific miRNAs are present in the hematopoietic erythroid line. This review attempts to summarize the state of knowledge on the role of miRNAs in the regulation of different stages of erythropoiesis. Original experimental data and results obtained with bioinformatics tools were combined to elucidate the currently known regulatory network of miRNAs that guide the process of differentiation of red blood cells.

scholarly journals Dual-specificity phosphatase 5 controls the localized inhibition, propagation, and transforming potential of ERK signaling

2017 ◽  
Vol 114 (3) ◽  
pp. E317-E326 ◽  
Author(s):  
Andrew M. Kidger ◽  
Linda K. Rushworth ◽  
Julia Stellzig ◽  
Jane Davidson ◽  
Christopher J. Bryant ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Fate ◽  
Erk Signaling ◽  
Feedback Mechanisms ◽  
Extracellular Signal Regulated Kinase ◽  
Raf Kinase ◽  
Dual Specificity ◽  
Extracellular Signal ◽  
A Cell ◽  
Erk Activity

Deregulated extracellular signal-regulated kinase (ERK) signaling drives cancer growth. Normally, ERK activity is self-limiting by the rapid inactivation of upstream kinases and delayed induction of dual-specificity MAP kinase phosphatases (MKPs/DUSPs). However, interactions between these feedback mechanisms are unclear. Here we show that, although the MKP DUSP5 both inactivates and anchors ERK in the nucleus, it paradoxically increases and prolongs cytoplasmic ERK activity. The latter effect is caused, at least in part, by the relief of ERK-mediated RAF inhibition. The importance of this spatiotemporal interaction between these distinct feedback mechanisms is illustrated by the fact that expression of oncogenic BRAFV600E, a feedback-insensitive mutant RAF kinase, reprograms DUSP5 into a cell-wide ERK inhibitor that facilitates cell proliferation and transformation. In contrast, DUSP5 deletion causes BRAFV600E-induced ERK hyperactivation and cellular senescence. Thus, feedback interactions within the ERK pathway can regulate cell proliferation and transformation, and suggest oncogene-specific roles for DUSP5 in controlling ERK signaling and cell fate.

PROTECTIVE EFFECT OF POLYPEPTIDE AND AMINO ACIDS ON THE DEVELOPMENT OF THE NERVOUS TISSUE CULTURE IN THE PRESENCE OF CYCLOPHOSPHAMIDE

2017 ◽  
pp. 22-26
Author(s):  
V. B. Dolgo-Saburov ◽  
N. I. Chalisova ◽  
L. V. Lyanginen ◽  
E. S. Zalomaeva
Keyword(s):  
Amino Acids ◽  
Cell Proliferation ◽  
Tissue Culture ◽  
Protective Effect ◽  
Organotypic Culture ◽  
Inhibitory Effect ◽  
Mustard Gas ◽  
Synthesis Inhibitor ◽  
Combined Administration ◽  
The Central Nervous System

In an organotypic culture, an investigation was conducted into combined effects of cyclophosphamide DNA as synthesis inhibitor used to model a resorptive action of mustard gas, and cortexin polypeptide or each of 20 encoded amino acids on the development of cell proliferation in cerebral cortex explants of the rat. The combined administration of cyclophosphamide together with cortexin or with each of the 20 encoded amino acids, except glycine, showed suppression of the cytostatic agent inhibitory effect. Thus, cortexin and amino acids have a protective effect on cell proliferation in the tissue culture of the central nervous system under the action of mustardlike substances.

scholarly journals Wnt5A modulates integrin expression in a receptor-dependent manner in ovarian cancer cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Vajihe Azimian-Zavareh ◽  
Zeinab Dehghani-Ghobadi ◽  
Marzieh Ebrahimi ◽  
Kian Mirzazadeh ◽  
Irina Nazarenko ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cell Attachment ◽  
Ovarian Cancer Cells ◽  
Integrin Expression ◽  
Dependent Manner ◽  
Cancer Cell Proliferation ◽  
Expression Levels ◽  
Multicellular Aggregates ◽  
Focal Adhesion Kinase Activity

AbstractWnt5A signals through various receptors that confer versatile biological functions. Here, we used Wnt5A overexpressing human ovarian SKOV-3 and OVCAR-3 stable clones for assessing integrin expression, cell proliferation, migration, invasion, and the ability of multicellular aggregates (MCAs) formation. We found here, that Wnt5A regulates differently the expression of its receptors in the stable Wnt5A overexpressing clones. The expression levels of Frizzled (FZD)-2 and -5, were increased in different clones. However ROR-1, -2 expression levels were differently regulated in clones. Wnt5A overexpressing clones showed increased cell proliferation, migration, and clonogenicity. Moreover, Wnt5A overexpressing SKOV-3 clone showed increased MCAs formation ability. Cell invasion had been increased in OVCAR-3-derived clones, while this was decreased in SKOV-3-derived clone. Importantly, αv integrin expression levels were increased in all assessed clones, accompanied by increased cell attachment to fibronectin and focal adhesion kinase activity. Moreover, the treatment of clones with Box5 as a Wnt5A/FZD5 antagonist abrogates ITGAV increase, cell proliferation, migration, and their attachment to fibronectin. Accordingly, we observed significantly higher expression levels of ITGAV and ITGB3 in human high-grade serous ovarian cancer specimens and ITGAV correlated positively with Wnt5A in metastatic serous type ovarian cancer. In summary, we hypothesize here, that Wnt5A/FZD-5 signaling modulate αv integrin expression levels that could be associated with ovarian cancer cell proliferation, migration, and fibronectin attachment.

Cellular mechanisms involved in the melatonin inhibition of HT-29 human colon cancer cell proliferation in culture

2007 ◽  
Vol 43 (2) ◽  
pp. 195-205 ◽  
Author(s):  
Ana García-Navarro ◽  
Cristina González-Puga ◽  
Germaine Escames ◽  
Luis C. López ◽  
Ana López ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Human Colon ◽  
Colon Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Human Colon Cancer Cell ◽  
Cellular Mechanisms ◽  
Human Colon Cancer ◽  
Ht 29

scholarly journals GnRH as a Cell Proliferation Regulator: Mechanism of Action and Evolutionary Implications

2004 ◽  
Vol 21 (10) ◽  
pp. 1005-1013 ◽  
Author(s):  
Masahiro Enomoto ◽  
Min Kyun Park
Keyword(s):  
Cell Proliferation ◽  
Mechanism Of Action ◽  
A Cell

scholarly journals Rel Induces Interferon Regulatory Factor 4 (IRF-4) Expression in Lymphocytes

2000 ◽  
Vol 191 (8) ◽  
pp. 1281-1292 ◽  
Author(s):  
Raelene J. Grumont ◽  
Steve Gerondakis
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Nuclear Factor Κb ◽  
Wild Type ◽  
Cell Type ◽  
Regulatory Factor ◽  
Specific Manner ◽  
A Cell ◽  
Cell Type Specific ◽  
Interferon Regulatory Factor 4

In lymphocytes, the Rel transcription factor is essential in establishing a pattern of gene expression that promotes cell proliferation, survival, and differentiation. Here we show that mitogen-induced expression of interferon (IFN) regulatory factor 4 (IRF-4), a lymphoid-specific member of the IFN family of transcription factors, is Rel dependent. Consistent with IRF-4 functioning as a repressor of IFN-induced gene expression, the absence of IRF-4 expression in c-rel−/− B cells coincided with a greater sensitivity of these cells to the antiproliferative activity of IFNs. In turn, enforced expression of an IRF-4 transgene restored IFN modulated c-rel−/− B cell proliferation to that of wild-type cells. This cross-regulation between two different signaling pathways represents a novel mechanism that Rel/nuclear factor κB can repress the transcription of IFN-regulated genes in a cell type–specific manner.

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