title: Monocyte chemoattractant protein-1 gene expression in prostatic hyperplasia and prostate adenocarcinoma.
abstract: Human monocyte chemoattractant protein-1 (MCP-1) has been shown to act as a chemokine in the recruitment of monocyte/macrophages during inflammation states. Furthermore, there is increasing evidence that MCP-1 is involved in the recruitment of tumor-associated macrophages. In vivo, one of the major cellular sources of MCP-1 are the smooth muscle cells. As MCP-1 gene expression and/or protein production in these cells is not necessarily correlated with the accumulation of inflammatory cells, there might possibly be additional functions of this cytokine. In the present study, we investigated by use of 35S-labeled antisense RNA probes whether the MCP-1 gene is expressed in tissue specimens of benign prostatic hyperplasia (n = 13) and specimens of prostate carcinoma (n = 8), both of which are characterized by a prominent fibromuscular stroma and inconspicuous inflammatory infiltrates. MCP-1 transcripts were located in stromal smooth muscle cells and, additionally, in basal cells of benign prostatic glands. In prostate carcinoma, the number of MCP-1 mRNA-expressing cells was significantly less than in benign prostatic hyperplasia. MCP-1 transcripts were located in preserved fibromuscular stroma and in basal cells of entrapped non-neoplastic glands but not in carcinomatous cells. Immunohistochemical staining with polyclonal antibodies raised against MCP-1 revealed strong reactivity in the fibromuscular stroma surrounding both benign and malignant glands. MCP-1 gene expression or immunoreactivity for anti-MCP-1 antibodies was not related to the rare, lymphocytic interstitial infiltrates. The results show that 1) in the absence of significant leukocyte accumulation, it is unlikely that MCP-1 exerts chemotactic functions in the prostate and 2) that MCP-1, in contrast to previous findings in a wide variety of other human neoplasms, is not expressed in carcinomatous cells of the prostate.
authors.affiliation: Institute of Pathology, University of Bern, Switzerland.
authors.forename: L
authors.initials: L
authors.lastname: Mazzucchelli
authors.forename: P
authors.initials: P
authors.lastname: Loetscher
authors.forename: A
authors.initials: A
authors.lastname: Kappeler
authors.forename: M
authors.initials: M
authors.lastname: Uguccioni
authors.forename: M
authors.initials: M
authors.lastname: Baggiolini
authors.forename: J A
authors.initials: JA
authors.lastname: Laissue
authors.forename: C
authors.initials: C
authors.lastname: Mueller
mesh_terms: D000230:Adenocarcinoma / Q000235:genetics* / Q000473:pathology; D000328:Adult; D000368:Aged; D002452:Cell Count; D018932:Chemokine CCL2 / Q000096:biosynthesis / Q000235:genetics*; D015870:Gene Expression; D006801:Humans; D006965:Hyperplasia / Q000235:genetics / Q000473:pathology; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D008297:Male; D008875:Middle Aged; D011470:Prostatic Hyperplasia / Q000235:genetics* / Q000473:pathology; D011471:Prostatic Neoplasms / Q000235:genetics* / Q000473:pathology; D015347:RNA Probes; D012333:RNA, Messenger / Q000032:analysis*
chemical_list: D018932:Chemokine CCL2; D015347:RNA Probes; D012333:RNA, Messenger