Monday, August 23, 2010

Integrin Beta4 and other integrins

Downregulation of Integrin Beta4 has been reported to inhibit chondrogenesis in TGF-beta3 inhibits chondrogenesis of cultured chick leg bud mesenchymal cells via downregulation of connexin 43 and integrin beta4. and upregulation was related to enhanced chondrogenesis in TiO2 nanotube stimulate chondrogenic differentiation of limb mesenchymal cells by modulating focal activity.  LSJL decreases Integrin Beta 4 expression.

Integrin signaling and cell spreading alterations by rottlerin treatment of chick limb bud mesenchymal cells.

"Endochondral skeletal development begins with the formation of a cartilaginous template where mesenchymal cells aggregate and increase in density prior to their overt differentiation into chondrocytes. Prechondrogenic condensation, in which mesenchymal cells aggregate, requires cell migration and proliferation. Rottlerin suppresses migration and cell surface expression of integrin beta1 in chondrogenic progenitors. Perturbation of integrin beta1 function using an anti-integrin beta1 blocking antibody suppressed the migration of wing bud mesenchymal cells. Phosphorylation levels of Src and focal adhesion kinase (FAK) were decreased by rottlerin treatment. Cell treatment with PP2, an inhibitor of Src family kinase, or electroporation of FAK specific siRNA, suppressed cell migration in a wound-healing assay. Cells treated with rottlerin showed decreased phosphorylation of Akt, independent of PKCdelta inhibition. In addition, an Akt inhibitor suppressed the migration of chick limb bud mesenchymal cells[LSJL increases Akt-p]. Rottlerin may act as a negative regulator for cell migration, an essential step for prechondrogenic condensation, by regulating integrin beta1 signaling at focal adhesion complexes via modulation of Akt activity."

"intimate cell–cell interactions promote [mesenchymal] condensation. Condensation begins by chondroprogenitor cell–cell homophilic adhesions with an increased number of intercellular contacts occurring through gap junctions"

"Hyaluronic acid[up in LSJL], fibronectin and type I collagen[up in LSJL] all increase, and overt differentiation begins at the center of this precartilage with a subsequent increase in the production of type II collagen."

"members of the integrin family, including the α5β1 fibronectin (FN) receptor, α2β1 and α3β1, and the vitronectin receptor αvβ3 interact reversibly with both ECM proteins and cytoskeletal structures"

Integrins and extracellular matrix proteins in the human childhood and adolescent growth plate.

"[We] compare the expression of integrins (alpha1, alpha2, alpha3, alpha5, alpha6, alphav, beta1, beta3, and beta5 subunits) together with matching binding proteins in human childhood and adolescent growth plate cartilage. Integrin beta1 was detected in all chondrocytes of the growth plate cartilage, beta3 only in osteoclasts of the opening zone, and beta5 in hypertrophic chondrocytes and osteoblasts. Integrin alpha1, alpha2, and alpha5 subunits were expressed by chondrocytes in the proliferative and hypertrophic zone as well as in osteoblasts and osteoclasts. Integrin av and alpha6 subunits were present in chondrocytes of all zones, alpha3 only in osteoclasts. Collagen type II{up} and fibronectin were seen throughout the growth plate, collagen type X{up} in the hypertrophic zone, collagen type I in the ossifying trabecules. Laminin was expressed by chondrocytes in the resting zone and more weakly in the proliferative zonecollagen VI was present in the pericellular and interterritorial matrix in all zones of the growth plate. There was no difference in integrin expression in children before and during puberty. Integrin expression is not influenced by endocrine factors during sexual maturation."

Chondrosarcoma cells under mechanical strain increased expressed of a5 when adhering to fibronectin and a2 when adhering to collagen 2A1.

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