title: Differential expression of YAMA/CPP-32 by T lymphocytes in popliteal artery aneurysm.
abstract: BACKGROUND
  We have previously demonstrated that programmed cell death, proteolytic activity, and inflammatory infiltrate in the aneurysmal wall may have a role in the pathogenesis of popliteal artery aneurysms (PAA). This investigation examines the expression of a cell death-promoting molecule, a cysteine protease, YAMA/CPP-32 in a series of PAA specimens.
  
  
  METHODS
  Twenty PAA specimens were obtained from patients undergoing elective surgical repair. Normal controls were popliteal arteries obtained from patients without PAA who were undergoing infrainguinal bypass surgery (n = 8). Standard histochemistry techniques were used to assess inflammatory infiltrates in PAA. Expression of apoptosis-promoting molecule, CPP-32, vascular smooth muscle cells (VSMC), macrophages, and T lymphocytes was detected by immunohistochemistry.
  
  
  RESULTS
  There is a conspicuous disruption and fragmentation of elastic lamellae and increased inflammatory infiltrate in the PAA as compared with normal arteries. As compared with normal popliteal artery tissues, the PAA demonstrated large number of cells immunopositive for CPP-32 (60.45 +/- 4.25% P < 0.05). This study revealed significantly increased expression of CPP-32 in the T-cell population of the PAA as compared with the other cells (P < 0.01). Dual immunolabeling and investigation of serial sections demonstrated that co-expression of CPP-32 was maximum in the CD8+ subset (37 +/- 3.3% of the total CPP-32 immunoreactive cells identified).
  
  
  CONCLUSIONS
  The data emphasize that the inflammatory infiltrate in the PAA walls has a significant role in the pathogenesis of this vascular disorder. Cells expressing death-promoting molecules are present in large numbers and are predominantly T lymphocytes in PAA. In addition to compromising the mechanical integrity of the vessel wall, apoptosis in the inflammatory infiltrate may contribute to the production of cytokines, activation of other signaling molecules such as stress proteins that could eventually favor PAA development.
authors.affiliation: Division of Vascular Surgery, Maimonides Medical Center, Brooklyn, New York 11219, USA.
authors.forename: Theresa
authors.initials: T
authors.lastname: Jacob
authors.forename: Richard
authors.initials: R
authors.lastname: Schutzer
authors.forename: Anil
authors.initials: A
authors.lastname: Hingorani
authors.forename: Enrico
authors.initials: E
authors.lastname: Ascher
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000783:Aneurysm / Q000276:immunology*; D017209:Apoptosis / Q000276:immunology; D053148:Caspase 3; D020169:Caspases / Q000096:biosynthesis*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000276:immunology; D011150:Popliteal Artery; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: C505407:CASP3 protein, human; D053148:Caspase 3; D020169:Caspases