Academic literature on the topic 'Cellular Interactions (incl. Adhesion, Matrix, Cell Wall)'
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Journal articles on the topic "Cellular Interactions (incl. Adhesion, Matrix, Cell Wall)"
May, Andreas, Franz-Josef Neumann, and Klaus Preissner. "The Relevance of Blood Cell-Vessel Wall Adhesive Interactions for Vascular Thrombotic Disease." Thrombosis and Haemostasis 82, no. 08 (1999): 962–70. http://dx.doi.org/10.1055/s-0037-1615939.
Full textKuijper, PH, HI Gallardo Torres, JA van der Linden, JW Lammers, JJ Sixma, L. Koenderman, and JJ Zwaginga. "Platelet-dependent primary hemostasis promotes selectin- and integrin- mediated neutrophil adhesion to damaged endothelium under flow conditions." Blood 87, no. 8 (April 15, 1996): 3271–81. http://dx.doi.org/10.1182/blood.v87.8.3271.bloodjournal8783271.
Full textChakraborty, Biswanath. "Plant Defense Proteins." NBU Journal of Plant Sciences 2, no. 1 (2008): 1–12. http://dx.doi.org/10.55734/nbujps.2007.v02i01.001.
Full textLishko, Valeryi K., and Tatiana P. Ugarova. "Evidence That Fibrinogen Inhibits Leukocyte Adhesion to Fibrin Clot and Immobilized Fibrinogen by Binding to the Substrate but Not to Integrins." Blood 106, no. 11 (November 16, 2005): 2631. http://dx.doi.org/10.1182/blood.v106.11.2631.2631.
Full textCiciliano, Jordan, Reza Abbaspour, Caroline Wu, Muhhanad Bakir, and Wilbur A. Lam. "A Microengineered Matrix to Decouple the Biophysical and Biochemical Mechanisms of Blood Cell Interactions with Thrombi and Vascular Wall Matrices." Blood 128, no. 22 (December 2, 2016): 555. http://dx.doi.org/10.1182/blood.v128.22.555.555.
Full textSheng, Nijing, Michael B. Fairbanks, Robert L. Heinrikson, Gabriela Canziani, Irwin M. Chaiken, David M. Mosser, Hong Zhang, and Robert W. Colman. "Cleaved high molecular weight kininogen binds directly to the integrin CD11b/CD18 (Mac-1) and blocks adhesion to fibrinogen and ICAM-1." Blood 95, no. 12 (June 15, 2000): 3788–95. http://dx.doi.org/10.1182/blood.v95.12.3788.
Full textSheng, Nijing, Michael B. Fairbanks, Robert L. Heinrikson, Gabriela Canziani, Irwin M. Chaiken, David M. Mosser, Hong Zhang, and Robert W. Colman. "Cleaved high molecular weight kininogen binds directly to the integrin CD11b/CD18 (Mac-1) and blocks adhesion to fibrinogen and ICAM-1." Blood 95, no. 12 (June 15, 2000): 3788–95. http://dx.doi.org/10.1182/blood.v95.12.3788.012k47_3788_3795.
Full textLacolley, Patrick, Véronique Regnault, Patrick Segers, and Stéphane Laurent. "Vascular Smooth Muscle Cells and Arterial Stiffening: Relevance in Development, Aging, and Disease." Physiological Reviews 97, no. 4 (October 1, 2017): 1555–617. http://dx.doi.org/10.1152/physrev.00003.2017.
Full textNadif, Raja, Michael Emerson, Ulrike Mayer, Ludwig Neyses, and Elizabeth Cartwright. "Abstract 3863: Deletion Of Integrin Alpha7 Leads To Altered Cardiac Conduction And Sudden Death Associated With Connexin43 Downregulation." Circulation 118, suppl_18 (October 28, 2008). http://dx.doi.org/10.1161/circ.118.suppl_18.s_494-c.
Full textDissertations / Theses on the topic "Cellular Interactions (incl. Adhesion, Matrix, Cell Wall)"
Lucas, Anthony. "Effects of phytoestrogenic isoflavones on the process of drug transport and metabolism." 2003. http://arrow.unisa.edu.au:8081/1959.8/46666.
Full text(8917073), Clarisse Marie Fligor. "AXONAL OUTGROWTH AND PATHFINDING OF HUMAN PLURIPOTENT STEM CELL-DERIVED RETINAL GANGLION CELLS." Thesis, 2020.
Find full text(5930267), Aparna B. Shinde. "Role Of Tumor Microenvironment in Breast Cancer Metastasis." Thesis, 2019.
Find full textMetastasis of primary
mammary tumors to vital secondary organs is the primary cause of breast cancer-associated
death, with no effective treatment. Metastasis is a highly selective process
that requires cancer cells to overcome multiple barriers to escape the primary
tumor, survive in circulation, and eventually colonize distant secondary
organs. One of the important aspects of metastatic cancers is the ability to
undergo epithelial-mesenchymal transition (EMT) and the reverse process
mesenchymal-epithelial transition (MET) process. Constant interconversion of
tumor cells between these phenotypes creates epithelial-mesenchymal heterogeneity
(EMH) and interaction between these tumor cell types and the stromal cell
compartment is clearly important to metastasis. In healthy tissues, stromal
cells maintain the composition and structure of the tissue through the production
of extracellular matrix (ECM) proteins and paracrine signaling with epithelial
cells. However, little is known about how EMH
promotes changes in the ECM to promote breast cancer progression and
metastasis. Cancer cells also secret exosomes, nano-size extracellular
vesicles, to establish intercellular communication with distant organs in order
to induce metastasis. These exosomes contain a plethora of different proteins
including extracellular matrix proteins and matrix crosslinking enzymes.
Fibronectin, an important ECM protein, plays an active role in tumor
progression and is often crosslinked by tissue transglutaminase 2 (TGM2) to
promote fibrosis in cancer. Both FN and TGM2 exist in exosomes and are
expressed by heterogenous breast tumors. Although FN and TGM2 have been
reported to play essential roles in cancer, their involvement in metastasis
remains unclear. This work utilizes a variety of approaches to investigate the
role of tumor heterogeneity and ECM proteins in promoting breast cancer
metastasis. In this dissertation, we establish that mesenchymal cells
expressing intracellular FN are held in a stable non-metastatic mesenchymal
phenotype and produce cellular fibrils containing functionalized FN capable of
supporting the growth of metastatic competent epithelial cells. We introduce a
novel 3D culture system consisting of a tessellated scaffold which is capable
of recapitulating cellular and matrix phenotypes in vivo. Further, we
also demonstrate breast tumor cells secrete exosomes containing TGM2
crosslinked FN fibrils to promote premetastatic niche formation and induction
of metastasis. Using genetic approaches, we establish TGM2 is essential
and sufficient to drive metastasis. Finally, we demonstrate pharmacological
inhibition of TGM2 offers a potential therapeutic strategy to treat metastatic
breast cancer. Altogether, our research provides insights into the mechanism
through which TGM2 promotes metastatic breast cancer. This work will help in
developing new drugs to target TGM2 aimed at reducing breast cancer metastasis.
(11022450), Jonathan Mark LaCombe. "DYRK1A-RELATED TRABECULAR DEFECTS IN MALE TS65DN MICE EMERGE DURING A CRITICAL DEVELOPMENTAL WINDOW." Thesis, 2021.
Find full textDown syndrome (DS) is a complex genetic disorder caused by the triplication of human chromosome 21 (Hsa21). The presence of an extra copy of an entire chromosome greatly disrupts the copy number and expression of over 350 protein coding genes. This gene dosage imbalance has far-reaching effects on normal development and aging, leading to cognitive and skeletal defects that emerge earlier in life than the general population.
The present study begins by characterizing skeletal development in young male Ts65Dn mice to test the hypothesis that skeletal defects in male Ts65Dn mice are developmental in nature.Femurs from young mice ranging from postnatal day 12- to 42-days of age (P12-42) were measured and analyzed by microcomputed tomography (μCT). Cortical defects were present generally throughout development, but trabecular defects emerged at P30 and persisted until P42.
The gene Dual-specificity tyrosine-regulated kinase 1a (Dyrk1a) is triplicated in both DS and in Ts65Dn mice and has been implicated as a putative cause of both cognitive and skeletal defects. To test the hypothesis that trisomic Dyrk1a is related to the emergence of trabecular defects at P30, expression of Dyrk1a in the femurs of male Ts65Dn mice was quantified by qPCR. Expression was shown to fluctuate throughout development and overexpression generally aligned with the emergence of trabecular defects at P30.
The growth rate in trabecular measures between male Ts65Dn and euploid littermates was similar between P30 and P42, suggesting a closer look into cellular mechanisms at P42. Assessment of proliferation of BMSCs, differentiation and activity of osteoblasts showed no significant differences between Ts65Dn and euploid cellular activity, suggesting that the cellular microenvironment has a greater influence on cellular activity than genetic background.
These data led to the hypothesis that reduction of Dyrk1a gene expression and pharmacological inhibition of DYRK1A could be executed during a critical period to prevent the emergence of trabecular defects at P30. To tests this hypothesis, doxycycline-induced cre-lox recombination to reduce Dyrk1a gene copy number or the DYRK1A inhibitor CX-4945 began at P21. The results of both genetic and pharmacological interventions suggest that trisomic Dyrk1a does not influence the emergence of trabecular defects up to P30. Instead, data suggest that the critical window for the rescue of trabecular defects lies between P30 and P42.