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Mechanisms regulating chondrocyte an...

The University of Western Ontario (Canada).

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Mechanisms regulating chondrocyte and fibroblast contact with the extracellular matrix.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Mechanisms regulating chondrocyte and fibroblast contact with the extracellular matrix./
Author:	Gill, Kamal S.
Description:	257 p.
Notes:	Source: Dissertation Abstracts International, Volume: 69-11, Section: B, page: 6509.
Contained By:	Dissertation Abstracts International69-11B.
Subject:	Biology, Cell. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoeng/servlet/advanced?query=NR43066
ISBN:	9780494430668

Mechanisms regulating chondrocyte and fibroblast contact with the extracellular matrix.
Gill, Kamal S.

Mechanisms regulating chondrocyte and fibroblast contact with the extracellular matrix. - 257 p.

Source: Dissertation Abstracts International, Volume: 69-11, Section: B, page: 6509.

Thesis (Ph.D.)--The University of Western Ontario (Canada), 2008.

Keywords. Chondrocytes, fibroblasts, bone sialoprotein, fibronectin, osteopontin, adhesion, spreading, insulin-like growth factor-1, focal adhesion kinase, Rho GTPases.

ISBN: 9780494430668Subjects--Topical Terms:

1017686
Biology, Cell.

Mechanisms regulating chondrocyte and fibroblast contact with the extracellular matrix.
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020 $a 9780494430668
035 $a (UMI)AAINR43066
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100 1 $a Gill, Kamal S. $3 1025302
245 1 0 $a Mechanisms regulating chondrocyte and fibroblast contact with the extracellular matrix.
300 $a 257 p.
500 $a Source: Dissertation Abstracts International, Volume: 69-11, Section: B, page: 6509.
502 $a Thesis (Ph.D.)--The University of Western Ontario (Canada), 2008.
520 $a Keywords. Chondrocytes, fibroblasts, bone sialoprotein, fibronectin, osteopontin, adhesion, spreading, insulin-like growth factor-1, focal adhesion kinase, Rho GTPases.
520 $a The extracellular matrix (ECM) does not only provide structural support for tissues but can regulate multiple cellular processes. Chondrocytes, the resident cell-type of cartilage, rely on the ECM to regulate gene expression, proliferation, differentiation and apoptosis. The purpose of this thesis is to examine mechanisms regulating chondrocyte and fibroblast contact with physiologically-relevant ECM proteins.
520 $a Fibronectin (FN) and bone sialoprotein (BSP) are ECM molecules found in cartilage. Both promoted similar levels of chondrocyte adhesion but chondrocytes had more spread area on FN compared to BSP. Focal adhesion kinase (FAK)-Src signaling regulated chondrocyte spreading on both FN and BSP and was not responsible for the observed difference. However, inhibition of Rho or ROCK increased chondrocyte spreading on BSP but not on FN. Moreover, only Rho regulated spreading of fibroblasts on BSP suggesting Rho-ROCK signaling specifically regulates chondrocyte spreading on BSP.
520 $a Chondrocyte adhesion to BSP was completely dependent on the RGD-integrin binding sequence and independent of posttranslational modifications. However, relative to BSP, the BSP-related protein osteopontin (OPN) adsorbed poorly to tissue culture polystyrene, and in its unmodified form, did not support chondrocyte adhesion. Phosphorylated OPN mimicked chondrocyte adhesion observed with BSP and bone-extracted OPN, and did not require the RGD sequence. Thus, phosphorylations are more important than the RGD sequence in mediating chondrocyte adhesion to OPN.
520 $a The growth factor IGF-1 increased cell spread area of fibroblasts on FN- and BSP-coated surfaces but did not increase spreading of chondrocytes. FAK presence was required for IGF-1-mediated spreading but FAK activation was dispensable. The intracellular signaling pathways regulating IGF-1-mediated spreading were dependent on the adhering matrix. On BSP, IGF-1 inhibited adhesion-induced activation of Rho through phosphatidylinositol 3-kinase and Rac to increase cell spreading.
520 $a In summary, we clearly demonstrate that the extent of cell contact with the ECM is dependent on two major variables: firstly, the chemical properties of the matrix that allow matrix molecules to tether cells to support structures; and second, the ability of extracellular factors to control intracellular signaling pathways that regulate the actin cytoskeleton and thus control cell morphology in a cell-type-dependent manner.
590 $a School code: 0784.
650 4 $a Biology, Cell. $3 1017686
650 4 $a Biology, Molecular. $3 1017719
650 4 $a Biology, Physiology. $3 1017816
690 $a 0307
690 $a 0379
690 $a 0719
710 2 $a The University of Western Ontario (Canada). $3 1017622
773 0 $t Dissertation Abstracts International $g 69-11B.
790 $a 0784
791 $a Ph.D.
792 $a 2008
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoeng/servlet/advanced?query=NR43066