TGFBI gene transcript is transforming growth factor-ß1-responsive and cell density-dependent in a human corneal epithelial cell line

Wang, Ming X.; Munier, Francis L.; Araki-Saski, Kaoru

doi:10.1076/opge.23.4.237.13884

Cited by 11 publications

(5 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A number of these differentially expressed genes like transforming growth factor, h-induced (Tgfbi) and BMP-1, have been studied in the past and have been shown to be TGF-h1 responsive. In human corneal epithelial cells, the Tgfbi gene transcript has been shown to be up-regulated by TGF-h1 in a cell density-dependent manner (Wang et al, 2002). Consistent with that, our microarray analysis results showed Tgfbi gene expression to be up-regulated {differential expression=+3.4} in MC3T3-E1 cells on treatment with TGFh1.…”

Section: Discussionsupporting

confidence: 89%

Collagen, type V, α1 (COL5A1) is regulated by TGF-β in osteoblasts

et al. 2004

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 89%

Collagen, type V, α1 (COL5A1) is regulated by TGF-β in osteoblasts

et al. 2004

View full text Add to dashboard Cite

“…46,47 Taken together with the present results, it suggests that a complex regulation existing between EGFR signaling, cell-cell interaction, and EMMPRIN to regulate the prolif-erative and migratory state of the basal epithelial cell. In addition, cell density, which has previously been shown to regulate the functional expression of TGF-␤ receptors in corneal epithelial cells, 48 also appears to be an important regulatory mechanism controlling EMMPRIN levels.…”

Section: Discussionmentioning

confidence: 98%

Differential Expression of Extracellular Matrix Metalloproteinase Inducer (CD147) in Normal and Ulcerated Corneas

Gabison

Mourah

Steinfels

et al. 2005

The American Journal of Pathology

112

116

View full text Add to dashboard Cite

Extracellular matrix metalloproteinase inducer (EMMPRIN) was originally identified on the tumor cell surface as an inducer of matrix metalloproteinase (MMP) production in neighboring fibroblasts. Here we demonstrate a role for EMMPRIN in MMP induction during corneal wound healing. MMP and EMMPRIN expression was analyzed in normal and ulcerated human corneas, as well as in corneal epithelial and stromal cells in culture using confocal microscopy, zymography, immunoblots, and real-time polymerase chain reaction. In normal cornea EMMPRIN was predominantly expressed in the epithelium but was markedly induced in the anterior stroma of ulcerated corneas. This coincided with MMP-2 induction that co-localized with EMMPRIN at the epithelio-stromal boundary. The role of epithelial-stromal interaction in MMP induction was investigated in an in vitro co-culture system and demonstrated an induction and co-localization of EMMPRIN and MMP-2 in the fibroblasts at the interface with epithelial cells. Direct contact of fibroblasts with EMMPRIN-containing purified epithelial cell membranes also induced MMP-1, MMP-2, and EMMPRIN and this was inhibited by a blocking anti-EMMPRIN antibody, suggesting that EMMPRIN was primarily responsible for this induction. These findings, and the up-regulation of EMMPRIN by epidermal growth factor and transforming growth factor-beta, demonstrate a role for EMMPRIN in wound healing and suggest that sustained local up-regulation of EMMPRIN and MMPs in chronic situations in which healing is delayed may lead to excessive matrix degradation and corneal melts.

show abstract

“…Western blotting was performed as previously described (8). Western blot analysis for TGF-␤-induced (TGFBi), a protein that is upregulated by and represents a surrogate marker of TGF-␤1 activity, was performed with a rabbit polyclonal antibody (Abcam) and normalized to actin levels (24,62). Antibodies for N-cadherin, E-cadherin, LYVE-1, fibroblast activation protein (FAP), and collagen I were all purchased from Abcam.…”

Section: Mouse Tail Irradiationmentioning

confidence: 99%