PMID- 8872602 OWN - NLM STAT- MEDLINE DCOM- 19970116 LR - 20191024 IS - 0730-2312 (Print) IS - 0730-2312 (Linking) VI - 62 IP - 3 DP - 1996 Sep 1 TI - Monocyte chemoattractant protein-1 gene expression in injured pig artery coincides with early appearance of infiltrating monocyte/macrophages. PG - 303-13 AB - Monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8) are potent chemokines which attract circulating monocytes and neutrophils respectively to inflamed tissues. JE/MCP-1 gene expression has been previously studied in rabbit aortae after endothelial denudation and the rapid appearance of this transcript was thought to precede emigration of phagocytes. We now report MCP-1 gene expression following de-endothelialization of iliac arteries in the pig, a species which can develop spontaneous atherosclerosis. Using Northern blot analysis, we demonstrated that MCP-1 mRNA was rapidly induced in pig arteries at 2 h and continued to increase to reach a maximum at 8 h before returning to low levels at 16-24 h after injury. The increase seen for MCP-1 mRNA at 8 h was also observed for IL-8 mRNA but was not apparent for growth-related gene expressions, urokinase-type plasminogen activator (u-PA), and plasminogen activator inhibitor-1 (PAI-1). Since smooth muscle cells, endothelial cells, and phagocytes are all capable of expressing MCP-1, we examined pig arteries for immunostaining using a monoclonal antibody to human MCP-1 (5D3-F7). At 8 h after injury, the predominant cell type staining positive for MCP-1 was the monocyte/macrophage. Staining was also observed in occasional scattered neutrophils, but MCP-1 protein could not be detected in smooth muscle cells or on extracellular matrix within the sensitivity constraints posed by our methodology. Our results are consistent with invading monocyte/macrophages having a major input into the production of this chemokine in the arterial wall following injury. The fact that MCP-1 expression accompanied monocyte/macrophage presence in damaged artery, rather than preceding it, is suggestive that continued MCP-1 expression is required for functions other than chemoattraction. FAU - Wysocki, S J AU - Wysocki SJ AD - University of Western Australia, Department of Surgery, Fremantle Hospital, Australia. FAU - Zheng, M H AU - Zheng MH FAU - Smith, A AU - Smith A FAU - Lamawansa, M D AU - Lamawansa MD FAU - Iacopetta, B J AU - Iacopetta BJ FAU - Robertson, T A AU - Robertson TA FAU - Papadimitriou, J M AU - Papadimitriou JM FAU - House, A K AU - House AK FAU - Norman, P E AU - Norman PE LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - J Cell Biochem JT - Journal of cellular biochemistry JID - 8205768 RN - 0 (Chemokine CCL2) RN - 0 (Interleukin-8) RN - 0 (Plasminogen Activator Inhibitor 1) RN - 0 (RNA, Messenger) RN - EC 3.4.21.73 (Urokinase-Type Plasminogen Activator) SB - IM MH - Animals MH - Arteries/*injuries/*metabolism MH - Catheterization/adverse effects MH - Chemokine CCL2/biosynthesis/*genetics/immunology MH - Endothelium, Vascular/injuries/physiology MH - Gene Expression Regulation MH - Humans MH - Hyperplasia MH - Iliac Artery/injuries/pathology/physiopathology MH - Interleukin-8/genetics MH - Macrophages/*physiology MH - Male MH - Monocytes/*physiology MH - Plasminogen Activator Inhibitor 1/genetics MH - RNA, Messenger/biosynthesis MH - Swine MH - Time Factors MH - Urokinase-Type Plasminogen Activator/genetics EDAT- 1996/09/01 00:00 MHDA- 2000/06/20 09:00 CRDT- 1996/09/01 00:00 PHST- 1996/09/01 00:00 [pubmed] PHST- 2000/06/20 09:00 [medline] PHST- 1996/09/01 00:00 [entrez] AID - 10.1002/(SICI)1097-4644(199609)62:3<303::AID-JCB1>3.0.CO;2-V [pii] AID - 10.1002/(sici)1097-4644(199609)62:3<303::aid-jcb1>3.0.co;2-v [doi] PST - ppublish SO - J Cell Biochem. 1996 Sep 1;62(3):303-13. doi: 10.1002/(sici)1097-4644(199609)62:3<303::aid-jcb1>3.0.co;2-v.