Words similar to cell-matrix
Example sentences for: cell-matrix
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Previously, studies of phenotypes in this laboratory have shown that SPARC-null mice develop osteopenia around 2.5 months of age [ 19 ] in bones where SPARC is normally the most abundant non-collagenous glycoprotein [ 3 ] . The second phenotype thus far uncovered is in the lens where SPARC is normally produced by lens epithelial cells [ 20 21 ] and is a component of the lens capsule [ 20 22 ] . SPARC-null mice show progressive cataract formation beginning approximately 1.5 months after birth [ 14 21 ] . Electron microscopy of the SPARC-null lens revealed abnormality at the lens cell-ECM (capsule) interface with an intrusion of cellular processes into the basement membrane of the lens capsule, whereas wild-type lens exhibited a precise border at the cell-matrix interface [ 23 ] . In the present study, we show for the first time that SPARC plays a role in wound repair in vivo and in vitro.
One of the established in vivo substrates of PTEN, FAK, is known to play a major role in growth-regulatory signal transduction initiated by cell surface integrin receptors [ 48 49 ] . As we observe a correlation between increased PTEN activity and decreased levels of FAK phosphorylation (compare Figure 4Band Figure 5), it is likely that the dephosphorylation of FAK in response to the disruption of cell-matrix interactions is accomplished by increased PTEN activity.
In view of PTEN's potent growth-inhibitory capacity, we conclude that its induction after cell-matrix disruptions contributes to the maintenance of the anchorage-dependent phenotype of normal cells.
TSP-1 is a homotrimeric multidomain glycoprotein synthesized and secreted by numerous cell types, including platelets, vascular smooth muscle cells and keratinocytes [ 4 ] . Due to its interaction with a wide variety of proteins, TSP-1 has been implicated in a number of biological processes including coagulation, cell adhesion, the modulation of cell-cell and cell-matrix interactions, control of tumor growth and metastasis, and angiogenesis [ 10 ] . Inhibition of tumor cell proliferation has been achieved in vivo by systemic treatment with TSP-1 peptide mimetics [ 11 ] , but a correlation between primary tumor TSP-1 expression and poor prognosis has not been clearly established [ 12 ] . While there are reports that these molecules can originate from tumor cells [ 13 ] , the majority of reports have suggested that the major source of both TSP-1 and OPN is tumor-associated stroma [ 14 ] or infiltrating macrophages and lymphocytes [ 15 ] .
This protein acts as inhibitor of cyclin-dependent kinases (the "cell cycle engine" [ 50 ] ), and its elevated expression has been consistently demonstrated in different cell types after the disruption of cell-matrix interactions (compare Figure 1and [ 31 32 51 52 ] ). Furthermore, p27 Kip1is an established target of PTEN signaling, i.e., its activity has been found increased after the forced expression of exogenous PTEN [ 53 54 55 56 ] . In combination with the data presented in this manuscript, it therefore appears that PTEN contributes to anchorage-dependent growth control by a two-fold approach: the dephosphorylation of the signaling molecule FAK in combination with the stimulation of the cell cycle inhibitor p27 Kip1.
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