Am. J. Respir. Cell Mol. Biol., Volume 18, Number 6, June, 1998 813-822

Cell-Matrix Interactions Modulate 92-kD Gelatinase Expression by Human Bronchial Epithelial Cells

Pin Mei Yao, Christophe Delclaux, Marie Pia d'Ortho, Bernard Maitre, Alain Harf, and Chantal Lafuma

INSERM Unité U296 and Département de Physiologie, Faculté de Médecine, Créteil, France

We have previously reported that primary human bronchial epithelial cells (HBECs) cultured on types I + III collagen were able to differentially regulate the production of major constitutive 92-kD gelatinase, minor 72-kD gelatinase, and their tissue-specific inhibitor, tissue inhibitor of metalloproteinase-1 (TIMP-1) in response to lipopolysaccharide (LPS) or proinflammatory cytokines, suggesting that HBECs may be involved in vivo in the active remodeling of the underlying extracellular matrix (ECM). In this study, we examined the possible effects of specific type IV collagen as compared with types I + III collagen on HBEC behavior and function. We investigated 92-kD gelatinase and TIMP-1 expression with zymography and reverse zymography, respectively, at the protein level, and with quantitative reverse transcription-polymerase chain reaction (RT-PCR) at the mRNA level. Results showed similar morphologic features and identical proliferation rates of HBECs in response to the two matrix substrates. Nevertheless, differences at the protein and mRNA levels between HBEC cultures on type IV collagen and on types I + III collagen included: (1) a lower basal level of 92-kD gelatinase production; (2) less upregulation of 92-kD gelatinase in response to LPS endotoxin or to the proinflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor- (TNF-); and (3) loss of activation of the proforms of the 92-kD and 72-kD gelatinases. These findings, together with the maintenance of TIMP-1 expression, strongly suggest that type IV collagen used as a matrix substratum is associated with a homeostatic HBEC phenotype, and limits the ability of HBECs to degrade the matrix. In contrast, types I + III collagen may be associated with a matrix resorption phenotype corresponding to active matrix remodeling and repair. Thus, the ECM underlying HBECs may modulate matrix remodeling by HBECs, particularly in response to inflammatory processes during acute lung injury.

This article has been cited by other articles:

				P. Chen, J. K. McGuire, R. C. Hackman, K.-H. Kim, R. A. Black, K. Poindexter, W. Yan, P. Liu, A. J. Chen, W. C. Parks, et al. Tissue Inhibitor of Metalloproteinase-1 Moderates Airway Re-Epithelialization by Regulating Matrilysin Activity Am. J. Pathol., May 1, 2008; 172(5): 1256 - 1270. [Abstract] [Full Text] [PDF]

				P. T. Elkington, J. A. Green, J. E. Emerson, L. D. Lopez-Pascua, J. J. Boyle, C. M. O'Kane, and J. S. Friedland Synergistic Up-Regulation of Epithelial Cell Matrix Metalloproteinase-9 Secretion in Tuberculosis Am. J. Respir. Cell Mol. Biol., October 1, 2007; 37(4): 431 - 437. [Abstract] [Full Text] [PDF]

				K. J. Greenlee, D. B. Corry, D. A. Engler, R. K. Matsunami, P. Tessier, R. G. Cook, Z. Werb, and F. Kheradmand Proteomic Identification of In Vivo Substrates for Matrix Metalloproteinases 2 and 9 Reveals a Mechanism for Resolution of Inflammation J. Immunol., November 15, 2006; 177(10): 7312 - 7321. [Abstract] [Full Text] [PDF]

				E. Lechapt-Zalcman, V. Pruliere-Escabasse, D. Advenier, S. Galiacy, C. Charriere-Bertrand, A. Coste, A. Harf, M.-P. d'Ortho, and E. Escudier Transforming growth factor-beta1 increases airway wound repair via MMP-2 upregulation: a new pathway for epithelial wound repair? Am J Physiol Lung Cell Mol Physiol, June 1, 2006; 290(6): L1277 - L1282. [Abstract] [Full Text] [PDF]

				B. Doornaert, V. Leblond, S. Galiacy, G. Gras, E. Planus, V. Laurent, D. Isabey, and C. Lafuma Negative impact of DEP exposure on human airway epithelial cell adhesion, stiffness, and repair Am J Physiol Lung Cell Mol Physiol, January 1, 2003; 284(1): L119 - L132. [Abstract] [Full Text] [PDF]

				T. Okamoto, G. Valacchi, K. Gohil, T. Akaike, and A. van der Vliet S-Nitrosothiols Inhibit Cytokine-Mediated Induction of Matrix Metalloproteinase-9 in Airway Epithelial Cells Am. J. Respir. Cell Mol. Biol., October 1, 2002; 27(4): 463 - 473. [Abstract] [Full Text] [PDF]

				J.-C. Lacherade, A. Van De Louw, E. Planus, E. Escudier, M.-P. D'Ortho, C. Lafuma, A. Harf, and C. Delclaux Evaluation of basement membrane degradation during TNF-{alpha}-induced increase in epithelial permeability Am J Physiol Lung Cell Mol Physiol, July 1, 2001; 281(1): L134 - L143. [Abstract] [Full Text] [PDF]

				T. Betsuyaku, Y. Fukuda, W. C. Parks, J. M. Shipley, and R. M. Senior Gelatinase B Is Required for Alveolar Bronchiolization after Intratracheal Bleomycin Am. J. Pathol., August 1, 2000; 157(2): 525 - 535. [Abstract] [Full Text] [PDF]

				C. Legrand, C. Gilles, J.-M. Zahm, M. Polette, A.-C. Buisson, H. Kaplan, P. Birembaut, and J.-M. Tournier Airway Epithelial Cell Migration Dynamics: MMP-9 Role in Cell–Extracellular Matrix Remodeling J. Cell Biol., July 26, 1999; 146(2): 517 - 529. [Abstract] [Full Text] [PDF]

				P. M. YAO, H. LEMJABBAR, M. P. D'ORTHO, B. MAITRE, P. GOSSETT, B. WALLAERT, and C. LAFUMA Balance between MMP-9 and TIMP-1 Expressed by Human Bronchial Epithelial Cells: Relevance to Asthma Ann. N.Y. Acad. Sci., June 30, 1999; 878(1): 512 - 514. [Full Text] [PDF]

				J.-H. Calvet, E. Planus, P. Rouet, S. Pezet, M. Levame, C. Lafuma, A. Harf, and M.-P. D'Ortho Matrix metalloproteinase gelatinases in sulfur mustard-induced acute airway injury in guinea pigs Am J Physiol Lung Cell Mol Physiol, May 1, 1999; 276(5): L754 - L762. [Abstract] [Full Text] [PDF]