title: Transcriptional profiling in coronary artery disease: indications for novel markers of coronary collateralization.
abstract: BACKGROUND
  The development of collateral circulation plays an important role in protecting tissues from ischemic damage, and its stimulation has emerged as one of principal approaches to therapeutic angiogenesis. Clinical observations have documented substantial differences in the extent of collateralization among patients with coronary artery disease (CAD), with some individuals demonstrating marked abundance and others showing nearly complete absence of these vessels. Recent studies have suggested that circulating monocytes play a major role in collateral growth. The present study was undertaken to determine transcriptional profiles of circulating monocytes in CAD patients with different extents of collateral growth.
  
  
  RESULTS
  Monocyte transcriptomes from CAD patients with and without collateral vessels were obtained by use of high-throughput expression profiling. Using a newly developed redundancy-based data mining method, we have identified a set of molecular markers characteristic of a "noncollateralgenic" phenotype. Moreover, we show that these transcriptional abnormalities are independent of the severity of CAD or any other known clinical parameter thought to affect collateral development and correlated with protein expression levels in monocytes and plasma.
  
  
  CONCLUSIONS
  Monocyte transcription profiling identifies sets of patients with extensive versus poorly developed collateral circulation. Thus, genetic factors may heavily influence coronary collateral vessel growth in CAD and affect prognosis and response to therapeutic interventions.
authors.affiliation: Angiogenesis Research Center, Dartmouth Medical School, Hanover, NH 03755, USA.
authors.forename: Thomas W
authors.initials: TW
authors.lastname: Chittenden
authors.forename: Jonathan A
authors.initials: JA
authors.lastname: Sherman
authors.forename: Fei
authors.initials: F
authors.lastname: Xiong
authors.forename: Amy E
authors.initials: AE
authors.lastname: Hall
authors.forename: Anthony A
authors.initials: AA
authors.lastname: Lanahan
authors.forename: Jennifer M
authors.initials: JM
authors.lastname: Taylor
authors.forename: Hangjun
authors.initials: H
authors.lastname: Duan
authors.forename: Justin D
authors.initials: JD
authors.lastname: Pearlman
authors.forename: Jason H
authors.initials: JH
authors.lastname: Moore
authors.forename: Stephen M
authors.initials: SM
authors.lastname: Schwartz
authors.forename: Michael
authors.initials: M
authors.lastname: Simons
mesh_terms: D000368:Aged; D015415:Biomarkers; D015153:Blotting, Western; D003097:Collateral Circulation / Q000235:genetics*; D015897:Comorbidity; D017023:Coronary Angiography; D003327:Coronary Disease / Q000000981:diagnostic imaging / Q000235:genetics / Q000503:physiopathology*; D005260:Female; D020869:Gene Expression Profiling; D006801:Humans; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism*; D005810:Multigene Family; D025341:Principal Component Analysis; D018075:RNA, Complementary / Q000235:genetics; D012307:Risk Factors; D014158:Transcription, Genetic
chemical_list: D015415:Biomarkers; D018075:RNA, Complementary