Literature DB >> 16720435

Cell-cell contact activation of fibroblasts increases the expression of matrix metalloproteinases.

Vappu Sirén1, Pertteli Salmenperä, Esko Kankuri, Jozef Bizik, Timo Sorsa, Taina Tervahartiala, Antti Vaheri.   

Abstract

BACKGROUND: We recently found that direct homotypic cell-cell contacts between human dermal fibroblasts induce a novel form of cell activation leading to non-apoptotic programmed cell death. As the major features of this process we identified massive induction of cyclo-oxygenase-2 and production of inflammatory prostaglandins. On the surface of the decomposing spheroids, activation of the major extracellular proteolytic cascade, plasminogen activation, associated with surface exposure of alpha-enolase, took place. AIM: To further characterize pericellular proteolysis by cell-cell contact-activated fibroblasts we studied the role of the other major extracellular proteolytic system, matrix metalloproteinases (MMPs).
METHODS: MMP expression in fibroblast clusters and monolayers was compared using mRNA microarrays and immunoblot analyses. The activities of MMPs were confirmed using MMP inhibitors and caseinolysis.
RESULTS: In microarrays MMP-1, -10, and -14 (MT1-MMP) were induced 5.8-, 106-, and 5.6-fold, respectively. These findings were confirmed by immunoblotting. Radial caseinolysis showed low level of proteolytic activity in spheroid-conditioned media; ilomastat, a general inhibitor of MMPs, suppressed 50% of the proteolytic activity thus confirming it to be at least in part due to MMPs. A cocktail of tetracycline-derived MMP inhibitors suppressed lactate dehydrogenase (LDH) release only 11%, and if combined with aprotinin 28%.
CONCLUSIONS: Cell-cell contact activation of fibroblasts induced MMP-1, -10, and MT1-MMP expression, suggesting similar signaling to that in inflammation and cancer.

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Year:  2006        PMID: 16720435     DOI: 10.1080/07853890500494999

Source DB:  PubMed          Journal:  Ann Med        ISSN: 0785-3890            Impact factor:   4.709


  5 in total

1.  Nemosis of fibroblasts is inhibited by benign HaCaT keratinocytes but promoted by malignant HaCaT cells.

Authors:  Kati Räsänen; Pertteli Salmenperä; Marc Baumann; Ismo Virtanen; Antti Vaheri
Journal:  Mol Oncol       Date:  2008-10-01       Impact factor: 6.603

2.  TAZ activation drives fibroblast spheroid growth, expression of profibrotic paracrine signals, and context-dependent ECM gene expression.

Authors:  Amy J Jorgenson; Kyoung Moo Choi; Delphine Sicard; Karry M J Smith; Samantha E Hiemer; Xaralabos Varelas; Daniel J Tschumperlin
Journal:  Am J Physiol Cell Physiol       Date:  2016-11-23       Impact factor: 4.249

3.  Inhibition of MMP activity can restore NKG2D ligand expression in gastric cancer, leading to improved NK cell susceptibility.

Authors:  Kensuke Shiraishi; Kousaku Mimura; Ley-Fang Kua; Vivien Koh; Lim Kee Siang; Shotaro Nakajima; Hideki Fujii; Asim Shabbir; Wei-Peng Yong; Jimmy So; Seiichi Takenoshita; Koji Kono
Journal:  J Gastroenterol       Date:  2016-03-22       Impact factor: 7.527

Review 4.  The ECM: To Scaffold, or Not to Scaffold, That Is the Question.

Authors:  Jonard Corpuz Valdoz; Benjamin C Johnson; Dallin J Jacobs; Nicholas A Franks; Ethan L Dodson; Cecilia Sanders; Collin G Cribbs; Pam M Van Ry
Journal:  Int J Mol Sci       Date:  2021-11-24       Impact factor: 5.923

5.  Differences in the nemosis response of normal and cancer-associated fibroblasts from patients with oral squamous cell carcinoma.

Authors:  Kati Räsänen; Ismo Virtanen; Pertteli Salmenperä; Reidar Grenman; Antti Vaheri
Journal:  PLoS One       Date:  2009-09-01       Impact factor: 3.240

  5 in total

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