Abstract
15-Lipoxygenase (15-LO) catalyzes the oxygenation of arachidonic acid linoleic acids and has been implicated in the oxidative modification of low-density lipoproteins (LDL). 15-LO mRNA and protein have previously been demonstrated in macrophages of rabbit and human atherosclerotic lesions. The purpose of this study was to investigate whether 15-LO is also present in the accelerated form of coronary artery disease that can complicate cardiac transplantation (TCAD). Immunohistochemical analysis of coronary arteries with TCAD was carried out by using a rabbit polyclonal antibody raised against human recombinant 15-LO and an avidin-biotin-immunoperoxidase system. Normal coronary and pulmonary arteries showed no immunostaining for 15-LO. Two different types of TCAD were observed. One type consisted of concentric intimal proliferation of smooth muscle cells, without lipid or calcium deposits. No immunoreactivity for 15-LO was present in these lesions. The second type of graft arteriosclerosis consisted of complex atheromatous lesions, containing myointimal cells, lipid-laden foam cells, fragmented internal elastic laminae, and calcifications. 15-LO immunostaining of myointimal cells, lipid-laden foam cells, and endothelial cells was consistently present in these atheromatous lesions. The majority of the myointimal and foam cells positive for 15-LO were recognized by antisera to α-smooth muscle actin; the others were identified as macrophages. The results indicate that 15-LO expression is present in endothelial, myointimal, and foam cells in complex atheromatous lesions of TCAD, and suggest that 15-LO may play a role in the pathogenesis of this form of the disease.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 340-348 |
| Number of pages | 9 |
| Journal | Arteriosclerosis, Thrombosis, and Vascular Biology |
| Volume | 15 |
| Issue number | 3 |
| State | Published - 1995 |
| Externally published | Yes |
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Keywords
- 15-lipoxygenase
- coronary artery disease
- graft arteriosclerosis
- lipid oxidation
- transplantation
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
Cite this
Immunohistochemical demonstration of 15-lipoxygenase in transplant coronary artery disease. / Ravalli, S.; Marboe, C. C.; D'Agati, V. D.; Michler, Robert E.; Sigal, E.; Cannon, P. J.
In: Arteriosclerosis, Thrombosis, and Vascular Biology, Vol. 15, No. 3, 1995, p. 340-348.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Immunohistochemical demonstration of 15-lipoxygenase in transplant coronary artery disease
AU - Ravalli, S.
AU - Marboe, C. C.
AU - D'Agati, V. D.
AU - Michler, Robert E.
AU - Sigal, E.
AU - Cannon, P. J.
PY - 1995
Y1 - 1995
N2 - 15-Lipoxygenase (15-LO) catalyzes the oxygenation of arachidonic acid linoleic acids and has been implicated in the oxidative modification of low-density lipoproteins (LDL). 15-LO mRNA and protein have previously been demonstrated in macrophages of rabbit and human atherosclerotic lesions. The purpose of this study was to investigate whether 15-LO is also present in the accelerated form of coronary artery disease that can complicate cardiac transplantation (TCAD). Immunohistochemical analysis of coronary arteries with TCAD was carried out by using a rabbit polyclonal antibody raised against human recombinant 15-LO and an avidin-biotin-immunoperoxidase system. Normal coronary and pulmonary arteries showed no immunostaining for 15-LO. Two different types of TCAD were observed. One type consisted of concentric intimal proliferation of smooth muscle cells, without lipid or calcium deposits. No immunoreactivity for 15-LO was present in these lesions. The second type of graft arteriosclerosis consisted of complex atheromatous lesions, containing myointimal cells, lipid-laden foam cells, fragmented internal elastic laminae, and calcifications. 15-LO immunostaining of myointimal cells, lipid-laden foam cells, and endothelial cells was consistently present in these atheromatous lesions. The majority of the myointimal and foam cells positive for 15-LO were recognized by antisera to α-smooth muscle actin; the others were identified as macrophages. The results indicate that 15-LO expression is present in endothelial, myointimal, and foam cells in complex atheromatous lesions of TCAD, and suggest that 15-LO may play a role in the pathogenesis of this form of the disease.
AB - 15-Lipoxygenase (15-LO) catalyzes the oxygenation of arachidonic acid linoleic acids and has been implicated in the oxidative modification of low-density lipoproteins (LDL). 15-LO mRNA and protein have previously been demonstrated in macrophages of rabbit and human atherosclerotic lesions. The purpose of this study was to investigate whether 15-LO is also present in the accelerated form of coronary artery disease that can complicate cardiac transplantation (TCAD). Immunohistochemical analysis of coronary arteries with TCAD was carried out by using a rabbit polyclonal antibody raised against human recombinant 15-LO and an avidin-biotin-immunoperoxidase system. Normal coronary and pulmonary arteries showed no immunostaining for 15-LO. Two different types of TCAD were observed. One type consisted of concentric intimal proliferation of smooth muscle cells, without lipid or calcium deposits. No immunoreactivity for 15-LO was present in these lesions. The second type of graft arteriosclerosis consisted of complex atheromatous lesions, containing myointimal cells, lipid-laden foam cells, fragmented internal elastic laminae, and calcifications. 15-LO immunostaining of myointimal cells, lipid-laden foam cells, and endothelial cells was consistently present in these atheromatous lesions. The majority of the myointimal and foam cells positive for 15-LO were recognized by antisera to α-smooth muscle actin; the others were identified as macrophages. The results indicate that 15-LO expression is present in endothelial, myointimal, and foam cells in complex atheromatous lesions of TCAD, and suggest that 15-LO may play a role in the pathogenesis of this form of the disease.
KW - 15-lipoxygenase
KW - coronary artery disease
KW - graft arteriosclerosis
KW - lipid oxidation
KW - transplantation
UR - http://www.scopus.com/inward/record.url?scp=0028936955&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0028936955&partnerID=8YFLogxK
M3 - Article
VL - 15
SP - 340
EP - 348
JO - Arteriosclerosis, Thrombosis, and Vascular Biology
JF - Arteriosclerosis, Thrombosis, and Vascular Biology
SN - 1079-5642
IS - 3
ER -