TRAIL expression in vascular smooth muscle

被引:64
作者
Gochuico, BR
Zhang, J
Ma, BY
Marshak-Rothstein, A
Fine, A
机构
[1] Boston Univ, Sch Med, Pulm Ctr R3, Boston, MA 02118 USA
[2] Boston Univ, Sch Med, Dept Microbiol, Boston, MA 02118 USA
关键词
apoptosis; smooth muscle cell; endothelial cell; tumor necrosis factor-related apoptosis-inducing ligand;
D O I
10.1152/ajplung.2000.278.5.L1045
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
TRAIL is a cell-associated tumor necrosis factor-related apoptosis-inducing ligand originally identified in immune cells. The ligand has the capacity to induce apoptosis after binding to cell surface receptors. To examine TRAIL expression in murine vascular tissue, we employed in situ hybridization and immunohistochemistry. In these studies, we found that TRAIL mRNA and protein were specifically localized throughout the medial smooth muscle cell layer of the pulmonary artery. Notably, a similar pattern of expression was observed in the mouse aorta. Consistent with these findings, we found that cultures of primary human aorta and pulmonary artery smooth muscle cells express abundant TRAIL mRNA and protein. We also found that these cells and endothelial cells undergo cell lysis in response to exogenous addition of TRAIL. Last, we confirmed that TRAIL specifically activated a death program by confirming poly(ADP ribose) polymerase cleavage. Overall, we believe that these findings are relevant to understanding the factors that regulate cell turnover in the vessel wall.
引用
收藏
页码:L1045 / L1050
页数:6
相关论文
共 33 条
[1]   TARGETED MUTATION IN THE FAS GENE CAUSES HYPERPLASIA IN PERIPHERAL LYMPHOID ORGANS AND LIVER [J].
ADACHI, M ;
SUEMATSU, S ;
KONDO, T ;
OGASAWARA, J ;
TANAKA, T ;
YOSHIDA, N ;
NAGATA, S .
NATURE GENETICS, 1995, 11 (03) :294-300
[2]   A ROLE FOR CD95 LIGAND IN PREVENTING GRAFT-REJECTION [J].
BELLGRAU, D ;
GOLD, D ;
SELAWRY, H ;
MOORE, J ;
FRANZUSOFF, A ;
DUKE, RC .
NATURE, 1995, 377 (6550) :630-632
[3]  
BERK JL, 1991, J BIOL CHEM, V266, P3192
[4]  
BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3
[5]   The cell biology of atherosclerosis - new developments [J].
Campbell, JH ;
Campbell, GR .
AUSTRALIAN AND NEW ZEALAND JOURNAL OF MEDICINE, 1997, 27 (04) :497-500
[6]   Emerging roles for cysteine proteases in human biology [J].
Chapman, HA ;
Riese, RJ ;
Shi, GP .
ANNUAL REVIEW OF PHYSIOLOGY, 1997, 59 :63-88
[7]   Cloning and characterization of TRAIL-R3, a novel member of the emerging TRAIL receptor family [J].
DegliEsposti, MA ;
Smolak, PJ ;
Walczak, H ;
Waugh, J ;
Huang, CP ;
DuBose, RF ;
Goodwin, RG ;
Smith, CA .
JOURNAL OF EXPERIMENTAL MEDICINE, 1997, 186 (07) :1165-1170
[8]   Fas expression in pulmonary alveolar type II cells [J].
Fine, A ;
Anderson, NL ;
Rothstein, TL ;
Williams, MC ;
Gochuico, BR .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 1997, 273 (01) :L64-L71
[9]   Apoptosis of vascular smooth muscle cells induced by in vitro stimulation with interferon-gamma, tumor necrosis factor-alpha, and interleukin-1 beta [J].
Geng, YJ ;
Wu, Q ;
Muszynski, M ;
Hansson, GK ;
Libby, P .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1996, 16 (01) :19-27
[10]   Airway epithelial Fas ligand expression: potential role in modulating bronchial inflammation [J].
Gochuico, BR ;
Miranda, KM ;
Hessel, EM ;
De Bie, JJ ;
Van Oosterhout, AJM ;
Cruikshank, WW ;
Fine, A .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 1998, 274 (03) :L444-L449