PMID- 25990773 OWN - NLM STAT- PubMed-not-MEDLINE DCOM- 20150521 LR - 20150520 IS - 1054-8807 (Print) IS - 1054-8807 (Linking) VI - 3 IP - 1 DP - 1994 Jan-Mar TI - Persistently increased expression of the transforming growth factor-beta1 gene in human vascular restenosis: Analysis of 62 patients with one or more episode of restenosis. PG - 57-64 LID - 10.1016/1054-8807(94)90008-6 [doi] AB - Transforming growth factor-beta-1 (TGF-beta1) is a multifunctional cytokine with both growth-promoting and growth-inhibiting properties. Moreover, there is abundant evidence that TGF-beta1 is the principal growth factor responsible for regulating proteoglycan synthesis in human blood vessels. To determine the potential contribution of TGF-beta1 to restenosis, the current investigation sought to determine the time course of expression postangioplasty of the TGF-beta1 gene. In situ hybridization was performed on tissue specimens obtained by directional atherectomy from 62 patients who had previously undergone angioplasty of native coronary or peripheral arteries and/or saphenous vein bypass grafts. The time interval between angioplasty and atherectomy was 1 hour to 25 months (M +/- SEM = 5 +/- 4 months) for all 62 patients, 5 +/- 4 months for coronary arterial specimens, 8 +/- 5 months for vein graft specimens, and 7 +/- 3 months for peripheral arterial specimens. TGF-beta1 mRNA expression remained persistently increased independent of the site from or time interval following which the specimen was obtained. For saphenous vein by pass grafts, TGF-beta1 expression was highest in specimens retreived from patients with multiple versus single episodes of restenosis (16 +/- 5 vs. 6 +/- 5 grains/nucleus, p < 0.01). TGF-beta1 expression did not correlate with patient age, sex, or known risk factors for coronary heart disease. The persistently augmented expression of TGF-beta1 observed in the present series of restenosis lesions provides further support for the concept that TGF-beta1 influences growth and development of restenosis plaque. CI - Copyright (c) 1994. Published by Elsevier Inc. FAU - Nikol, S AU - Nikol S AD - Departments of Medicine (Cardiology) and Biomedical Research, St. Elizabeth's Hospital, Tufts University School of Medicine, Boston, Massachusetts, USA. FAU - Weir, L AU - Weir L AD - Departments of Medicine (Cardiology) and Biomedical Research, St. Elizabeth's Hospital, Tufts University School of Medicine, Boston, Massachusetts, USA. FAU - Sullivan, A AU - Sullivan A AD - Departments of Medicine (Cardiology) and Biomedical Research, St. Elizabeth's Hospital, Tufts University School of Medicine, Boston, Massachusetts, USA. FAU - Sharaf, B AU - Sharaf B AD - Rhode Island Hospital, Providence, Rhode Island, USA. FAU - White, C J AU - White CJ AD - Ochsner Medical Institution, New Orleans, Louisiana, USA. FAU - Zemel, G AU - Zemel G AD - Baptist Hospital, Miami, Florida, USA. FAU - Hartzler, G AU - Hartzler G AD - St. Luke's Hospital, Kansas City, Missouri, USA. FAU - Stack, R AU - Stack R AD - Duke University Medical Center, Durham, North Carolina, USA. FAU - Leclerc, G AU - Leclerc G AD - Departments of Medicine (Cardiology) and Biomedical Research, St. Elizabeth's Hospital, Tufts University School of Medicine, Boston, Massachusetts, USA. FAU - Isner, J M AU - Isner JM AD - Departments of Medicine (Cardiology) and Biomedical Research, St. Elizabeth's Hospital, Tufts University School of Medicine, Boston, Massachusetts, USA. LA - eng PT - Journal Article PL - United States TA - Cardiovasc Pathol JT - Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology JID - 9212060 EDAT- 1994/01/01 00:00 MHDA- 1994/01/01 00:01 CRDT- 2015/05/21 06:00 PHST- 1993/06/22 00:00 [received] PHST- 1993/09/28 00:00 [accepted] PHST- 2015/05/21 06:00 [entrez] PHST- 1994/01/01 00:00 [pubmed] PHST- 1994/01/01 00:01 [medline] AID - 1054-8807(94)90008-6 [pii] AID - 10.1016/1054-8807(94)90008-6 [doi] PST - ppublish SO - Cardiovasc Pathol. 1994 Jan-Mar;3(1):57-64. doi: 10.1016/1054-8807(94)90008-6.