Distinct structural forms of type I collagen modulate cell cycle regulatory proteins in mesangial cells

Schöcklmann, Harald O.; Lang, Stefan; Kralewski, Martina; Hartner, Andrea; Lüdke, Andrea; Sterzel, R. Bernd

doi:10.1046/j.1523-1755.2000.00268.x

Cited by 26 publications

(17 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Many reports suggest that integrin signaling induces proliferation of cells, including mesangial cells, mammary epithelial cell, and mesenchymal cells, in the presence of ECM (Schöcklmann et al 2000, Li et al 2005, Fernandes et al 2006. Integrins comprise an a-subunit and a b-subunit that form a heterodimer.…”

Section: Discussionmentioning

confidence: 99%

Caveolin 3-mediated integrin β1 signaling is required for the proliferation of folliculostellate cells in rat anterior pituitary gland under the influence of extracellular matrix

Horiguchi¹,

Fujiwara²,

Ilmiawati³

et al. 2011

Journal of Endocrinology

View full text Add to dashboard Cite

Folliculostellate (FS) cells in the anterior pituitary gland are believed to have multifunctional properties. Using transgenic rats that express green fluorescent protein (GFP) specifically in FS cells in the anterior pituitary gland (S100b-GFP rats), we recently revealed that FS cells in primary culture exhibited marked proliferation in the presence of laminin, an extracellular matrix (ECM) component of the basement membrane. In a process referred to as matricrine action, FS cells receive ECM as a signal through their receptors, which results in morphological and functional changes. In this study, we investigated matricrine signaling in FS cells and observed that the proliferation of FS cells is mediated by integrin b1, which is involved in various signaling pathways for cell migration and proliferation in response to ECM. Then, we analyzed downstream events of the integrin b1 signaling pathway in the proliferation of FS cells and identified caveolin 3 as a potential candidate molecule. Caveolin 3 is a membrane protein that binds cholesterol and a number of signaling molecules that interact with integrin b1. Using specific small interfering RNA of caveolin 3, the proliferation of FS cells was inhibited. Furthermore, caveolin 3 drove activation of the mitogen-activated protein kinase (MAPK) signaling cascades, which resulted in upregulation of cyclin D1 in FS cells. These findings suggest that matricrine signaling in the proliferation of FS cells was transduced by a caveolin 3-mediated integrin b1 signaling pathway and subsequent activation of the MAPK pathway.

show abstract

Section: Discussionmentioning

confidence: 99%

Caveolin 3-mediated integrin β1 signaling is required for the proliferation of folliculostellate cells in rat anterior pituitary gland under the influence of extracellular matrix

Horiguchi¹,

Fujiwara²,

Ilmiawati³

et al. 2011

Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

“…Additionally, this treatment restored the changes in the cellular content and surface expression of P-selectin, VCAM-1 and MCP-1 mRNA expression detected in HuVEC seeded on this interstitial collagen. This experimental approach is normally used in this type of studies [35,36]. Pepsin removes the aminotelopeptide sequences of collagen type I, disrupts the intermolecular crosslinking between telopeptides and the triple helix structure.…”

Section: Discussionmentioning

confidence: 99%

The Leukocyte-Endothelial Cell Interactions are Modulated by Extracellular Matrix Proteins

Ruiz-Torres¹,

Pérez-Rivero²,

Rodrı́guez-Puyol³

et al. 2006

Cell Physiol Biochem

View full text Add to dashboard Cite

Background: Endothelium is supported, in normal conditions, by a basement membrane composed, among others, by collagen IV and laminin. Changes in the basement membrane composition could induce changes in endothelial cell modifying their interactions with leukocytes. Methods and Results: Isolated polymorphonuclear cells (PMN) and peripheral blood mononuclear cells (PBMC) were added to cultured human umbilical endothelial cells (HuVEC) previously seeded on collagen IV, collagen I or gelatin. Adhesion of leukocytes to HUVEC and specific cytotoxicity were analysed. PMN adhesion and cytotoxicity were lower whereas those from PBMC were higher when HuVEC were seeded on collagen I, as compared with cells seeded on collagen IV. To analyse the mechanisms involved in these phenomena, P-selectin, ICAM-1, VCAM-1 and MCP- 1 expression were evaluated in HuVEC seeded on the different ECM components. P-selectin and mRNA expression of VCAM-1 were lower in cells seeded on collagen I. By contrast, MCP-1 expression was higher in collagen I. Collagen I-dependent effects were partially prevented when collagen I was treated with pepsin. ILK activity was lower in cells seeded on collagen I, whereas ERK 1/2 activity was enhanced. ILK overexpression reduced ERK 1/2 phosphorylation and this could promote the reduction in P-selectin and the increase in MCP-1. Conclusion: Collagen I decreased ILK activity and this would induce an increase in ERK 1/2 activity in HuVEC. As a consequence, the P-selectin content is diminished and, by contrast, the MCP-1 content is increased. The final effect is a lower recruitment of PMN and a higher adhesion of PBMC.

show abstract

“…When polymerized into fibrils, as it is mostly found in vivo, type I collagen inhibits growth of a number of cell types including smooth muscle cells (Koyama et al, 1996), melanoma cells (Henriet et al, 2000), glomerular epithelial cells (Schocklmann et al, 2000), and hepatocytes De Smet et al, 2001), whereas adhesion to monomeric collagen stimulates cell cycle progression under similar culture conditions. Unlike loss of adhesion, however, which blocks cell cycle progression and also induces apoptosis, adhesion to collagen gels promotes survival and increased differentiated function (Ben-Ze'ev et al, 1988;Gomez-Lechon et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

“…Decreased cyclin D1 expression Schocklmann et al, 2000), and/or increased expression of cell cycle inhibitor proteins such as p21 or p27 KIP (Koyama et al, 1996;Henriet et al, 2000) have been demonstrated in various cell types in response to adhesion to fibrillar collagen. The mechanisms by which adhesion to fibrillar collagen modulates the signaling pathways that determine the expression levels of cell cycle regulatory proteins, however, are not well defined.…”

Section: Introductionmentioning

confidence: 99%

Type I Collagen Structure Regulates Cell Morphology and EGF Signaling in Primary Rat Hepatocytes through cAMP-dependent Protein Kinase A

Fassett

Tobolt

Hansen

2006

MBoC

View full text Add to dashboard Cite

Adhesion to type 1 collagen elicits different responses dependent on whether the collagen is in fibrillar (gel) or monomeric form (film). Hepatocytes adherent to collagen film spread and proliferate, whereas those adherent to collagen gel remain rounded and growth arrested. To explore the role of potential intracellular inhibitory signals responsible for collagen gel-mediated growth arrest, cAMP-dependent protein kinase A (PKA) was examined in hepatocytes adherent to collagen film or gel. PKA activity was higher in hepatocytes on collagen gel than on film during G1 of the hepatocyte cell cycle. Inhibition of PKA using H89 increased cell spreading on collagen gel in an EGF-dependent manner, whereas activation of PKA using 8-Br-cAMP decreased cell spreading on collagen film. PKA inhibition also restored ERK activation, cyclin D1 expression and G1-S progression on collagen gel, but had no effect on cells adherent to collagen film. Analysis of EGF receptor phosphorylation revealed that adhesion to collagen gel alters tyrosine phosphorylation of the EGF receptor, leading to reduced phosphorylation of tyrosine residue 845, which was increased by inhibition of PKA. These results demonstrate that fibrillar type 1 collagen can actively disrupt cell cycle progression by inhibiting specific signals from the EGF receptor through a PKA-dependent pathway.

show abstract

Distinct structural forms of type I collagen modulate cell cycle regulatory proteins in mesangial cells

Cited by 26 publications

References 36 publications

Caveolin 3-mediated integrin β1 signaling is required for the proliferation of folliculostellate cells in rat anterior pituitary gland under the influence of extracellular matrix

Caveolin 3-mediated integrin β1 signaling is required for the proliferation of folliculostellate cells in rat anterior pituitary gland under the influence of extracellular matrix

The Leukocyte-Endothelial Cell Interactions are Modulated by Extracellular Matrix Proteins

Type I Collagen Structure Regulates Cell Morphology and EGF Signaling in Primary Rat Hepatocytes through cAMP-dependent Protein Kinase A

Contact Info

Product

Resources

About