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Production of Type VI Collagen by Human Macrophages: A New Dimension in Macrophage Functional Heterogeneity^{1 ,2}

Michael Schnoor^*, Paul Cullen^*, Julia Lorkowski^*, Katrin Stolle^*, Horst Robenek^*, David Troyer^*, Jürgen Rauterberg^* and Stefan Lorkowski^3,*,

^* Leibniz Institute of Arteriosclerosis Research, Münster, Germany; and Institute of Nutrition, Friedrich Schiller University, Jena, Germany

Macrophages derived from human blood monocytes perform many tasks related to tissue injury and repair. The main effect of macrophages on the extracellular matrix is considered to be destructive in nature, because macrophages secrete metalloproteinases and ingest foreign material as part of the remodeling process that occurs in wound healing and other pathological conditions. However, macrophages also contribute to the extracellular matrix and hence to tissue stabilization both indirectly, by inducing other cells to proliferate and to release matrix components, and directly, by secreting components of the extracellular matrix such as fibronectin and type VIII collagen, as we have recently shown. We now report that monocytes and macrophages express virtually all known collagen and collagen-related mRNAs. Furthermore, macrophages secrete type VI collagen protein abundantly, depending upon their mode of activation, stage of differentiation, and cell density. The primary function of type VI collagen secreted by macrophages appears to be modulation of cell-cell and cell-matrix interactions. We suggest that the production of type VI collagen is a marker for a nondestructive, matrix-conserving macrophage phenotype that could profoundly influence physiological and pathophysiological conditions in vivo.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by grants from the Deutsche Forschungsgemeinschaft (SFB 492 and CU 31/2), the Deutsche Infarktforschungshilfe, and the Karl & Lore Klein-Stiftung. M.S., J.R., K.S., S.L., and P.C. were participants in a project entitled "Macrophage Function and Stability of the Atherosclerotic Plaque" (QLG2-CT-1999-01007) funded by the European Union as part of the Fifth Framework Program.

² This manuscript is dedicated to the memory of our dear colleague, Dr. Beate Brennhausen, who passed away on December 30, 2006.

³ Address correspondence and reprint requests to Dr. Stefan Lorkowski, Institut für Ernährungswissenschaften, Friedrich-Schiller-Universität Jena, Dornburger Strasse 25, 07743 Jena, Germany. E-mail address: stefan.lorkowski{at}uni-muenster.de

⁴ Abbreviations used in this paper: ECM, extracellular matrix; βIG-H3, TGF-β-induced gene H3; COL6A, collagen type VI, -chain; P4HA, prolyl 4-hydroxylase ; SMC, smooth muscle cell; SRP14, 14 M_r(K) signal recognition particle; T6C, type VI collagen.

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