scholarly journals Rho-ROCK signaling differentially regulates chondrocyte spreading on fibronectin and bone sialoprotein

2008 ◽  
Vol 295 (1) ◽  
pp. C38-C49 ◽  
Author(s):  
Kamal S. Gill ◽  
Frank Beier ◽  
Harvey A. Goldberg
Keyword(s):  
Growth Plate ◽  
Posttranslational Modifications ◽  
Rho Kinase ◽  
Cell Spreading ◽  
Dynamic Structure ◽  
Bone Sialoprotein ◽  
Growth Plate Chondrocytes ◽  
Src Signaling ◽  
Rgd Sequence ◽  
Specific Effects

The mammalian growth plate is a dynamic structure rich in extracellular matrix (ECM). Interactions of growth plate chondrocytes with ECM proteins regulate cell behavior. In this study, we compared chondrocyte adhesion and spreading dynamics on fibronectin (FN) and bone sialoprotein (BSP). Chondrocyte adhesion and spreading were also compared with fibroblasts to analyze potential cell-type-specific effects. Chondrocyte adhesion to BSP is independent of posttranslational modifications but is dependent on the RGD sequence in BSP. Whereas chondrocytes and fibroblasts adhered at similar levels on FN and BSP, cells displayed more actin-dependent spread on FN despite a 16× molar excess of BSP adsorbed to plastic. To identify intracellular mediators responsible for this difference in spreading, we investigated focal adhesion kinase (FAK)-Src and Rho-Rho kinase (ROCK) signaling. Although activated FAK localized to the vertices of adhered chondrocytes, levels of FAK activation did not correlate with the extent of spreading. Furthermore, Src inhibition reduced chondrocyte spreading on both FN and BSP, suggesting that FAK-Src signaling is not responsible for less cell spreading on BSP. In contrast, inhibition of Rho and ROCK in chondrocytes increased cell spreading on BSP and membrane protrusiveness on FN but did not affect cell adhesion. In fibroblasts, Rho inhibition increased fibroblast spreading on BSP while ROCK inhibition changed membrane protrusiveness of FN and BSP. In summary, we identify a novel role for Rho-ROCK signaling in regulating chondrocyte spreading and demonstrate both cell- and matrix molecule-specific mechanisms controlling cell spreading.

scholarly journals Expression and Functional Assessment of an Alternatively Spliced Extracellular Ca2+-Sensing Receptor in Growth Plate Chondrocytes

Endocrinology ◽  
2005 ◽  
Vol 146 (12) ◽  
pp. 5294-5303 ◽  
Author(s):  
Luis Rodriguez ◽  
Chialing Tu ◽  
Zhiqiang Cheng ◽  
Tsui-Hua Chen ◽  
Daniel Bikle ◽  
...  
Keyword(s):  
Cell Surface ◽  
Growth Plate ◽  
Inositol Phosphate ◽  
Intact Cell ◽  
Chinese Hamster ◽  
Full Length ◽  
Wild Type ◽  
Growth Plate Chondrocytes ◽  
Matrix Gene ◽  
Alternatively Spliced

The extracellular Ca2+-sensing receptor (CaR) plays an essential role in mineral homeostasis. Studies to generate CaR-knockout (CaR−/−) mice indicate that insertion of a neomycin cassette into exon 5 of the mouse CaR gene blocks the expression of full-length CaRs. This strategy, however, allows for the expression of alternatively spliced CaRs missing exon 5 [Exon5(−)CaRs]. These experiments addressed whether growth plate chondrocytes (GPCs) from CaR−/− mice express Exon5(−)CaRs and whether these receptors activate signaling. RT-PCR and immunocytochemistry confirmed the expression of Exon5(−)CaR in growth plates from CaR−/− mice. In Chinese hamster ovary or human embryonic kidney-293 cells, recombinant human Exon5(−)CaRs failed to activate phospholipase C likely due to their inability to reach the cell surface as assessed by intact-cell ELISA and immunocytochemistry. Human Exon5(−)CaRs, however, trafficked normally to the cell surface when overexpressed in wild-type or CaR−/− GPCs. Immunocytochemistry of growth plate sections and cultured GPCs from CaR−/− mice showed easily detectable cell-membrane expression of endogenous CaRs (presumably Exon5(−)CaRs), suggesting that trafficking of this receptor form to the membrane can occur in GPCs. In GPCs from CaR−/− mice, high extracellular [Ca2+] ([Ca2+]e) increased inositol phosphate production with a potency comparable with that of wild-type GPCs. Raising [Ca2+]e also promoted the differentiation of CaR−/− GPCs as indicated by changes in proteoglycan accumulation, mineral deposition, and matrix gene expression. Taken together, our data support the idea that expression of Exon5(−)CaRs may compensate for the loss of full-length CaRs and be responsible for sensing changes in [Ca2+]e in GPCs in CaR−/− mice.

L-type calcium channels in growth plate chondrocytes participate in endochondral ossification

2007 ◽  
Vol 101 (2) ◽  
pp. 389-398 ◽  
Author(s):  
Edna E. Mancilla ◽  
Mario Galindo ◽  
Barbara Fertilio ◽  
Mario Herrera ◽  
Karime Salas ◽  
...  
Keyword(s):  
Calcium Channels ◽  
Growth Plate ◽  
Endochondral Ossification ◽  
Growth Plate Chondrocytes

scholarly journals Differential effects of insulin-like growth factor binding proteins-1, -2, -3, and -6 on cultured growth plate chondrocytes

2002 ◽  
Vol 62 (5) ◽  
pp. 1591-1600 ◽  
Author(s):  
Daniela Kiepe ◽  
Tim Ulinski ◽  
David R. Powell ◽  
Susan K. Durham ◽  
Otto Mehls ◽  
...  
Keyword(s):  
Growth Factor ◽  
Growth Plate ◽  
Binding Proteins ◽  
Insulin Like Growth Factor ◽  
Growth Plate Chondrocytes ◽  
Differential Effects ◽  
Factor Binding

Investigation of RARg Signaling in Human Growth-Plate Chondrocytes

2021 ◽  
Author(s):  
Joshua M. Abzug ◽  
Hongying Tian ◽  
Masatake Matsuoka ◽  
Danielle A. Hogarth ◽  
Casey M. Codd ◽  
...  
Keyword(s):  
Growth Plate ◽  
Human Growth ◽  
Growth Plate Chondrocytes

scholarly journals Catch-Up Growth after Hypothyroidism Is Caused by Delayed Growth Plate Senescence

Endocrinology ◽  
2008 ◽  
Vol 149 (4) ◽  
pp. 1820-1828 ◽  
Author(s):  
Rose Marino ◽  
Anita Hegde ◽  
Kevin M. Barnes ◽  
Lenneke Schrier ◽  
Joyce A. Emons ◽  
...  
Keyword(s):  
Growth Rate ◽  
Growth Inhibition ◽  
Growth Plate ◽  
Bone Growth ◽  
Structural Characteristics ◽  
Linear Growth Rate ◽  
Growth Plate Chondrocytes ◽  
Growth Plates ◽  
Catch Up ◽  
Growth Inhibiting

Catch-up growth is defined as a linear growth rate greater than expected for age after a period of growth inhibition. We hypothesized that catch-up growth occurs because growth-inhibiting conditions conserve the limited proliferative capacity of growth plate chondrocytes, thus slowing the normal process of growth plate senescence. When the growth-inhibiting condition resolves, the growth plates are less senescent and therefore grow more rapidly than normal for age. To test this hypothesis, we administered propylthiouracil to newborn rats for 8 wk to induce hypothyroidism and then stopped the propylthiouracil to allow catch-up growth. In untreated controls, the growth plates underwent progressive, senescent changes in multiple functional and structural characteristics. We also identified genes that showed large changes in mRNA expression in growth plate and used these changes as molecular markers of senescence. In treated animals, after stopping propylthiouracil, these functional, structural, and molecular senescent changes were delayed, compared with controls. This delayed senescence included a delayed decline in longitudinal growth rate, resulting in catch-up growth. The findings demonstrate that growth inhibition due to hypothyroidism slows the developmental program of growth plate senescence, including the normal decline in the rate of longitudinal bone growth, thus accounting for catch-up growth.

scholarly journals Selective enrichment of microRNAs in extracellular matrix vesicles produced by growth plate chondrocytes

Bone ◽  
2016 ◽  
Vol 88 ◽  
pp. 47-55 ◽  
Author(s):  
Zhao Lin ◽  
Nicholas E. Rodriguez ◽  
Junjun Zhao ◽  
Allison N. Ramey ◽  
Sharon L. Hyzy ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Growth Plate ◽  
Matrix Vesicles ◽  
Growth Plate Chondrocytes ◽  
Selective Enrichment

scholarly journals Cellular reactions to biodegradable magnesium alloys on human growth plate chondrocytes and osteoblasts

2013 ◽  
Vol 38 (4) ◽  
pp. 881-889 ◽  
Author(s):  
Karin Pichler ◽  
Tanja Kraus ◽  
Elisabeth Martinelli ◽  
Patrick Sadoghi ◽  
Giuseppe Musumeci ◽  
...  
Keyword(s):  
Growth Plate ◽  
Magnesium Alloys ◽  
Human Growth ◽  
Growth Plate Chondrocytes ◽  
Biodegradable Magnesium
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