Changes in vascular extracellular matrix accumulation reflect phenotypic differences between the arterial wall of pigeons resistant and susceptible to the development of spontaneous atherosclerosis.
White Carneau pigeons have previously been shown to be genetically susceptible to the development of spontaneous atherogenesis. The severity of development of atheromatous lesions is considerably greater than a more resistant breed of Show Racer pigeons. Analysis of levels of total hydroxyproline and isodesmosine in the thoracic aorta and celiac bifurcation of prelesion, six-week-old White Carneau and Show Racer pigeons, revealed an increased accumulation of total collagen and cross-linked elastin in the White Carneau arterial tissue. Using dot blot hybridization, measurements of steady state levels of several mRNAs in total RNA extracted from pigeon aortic tissue were also determined. While the increased deposition of extracellular matrix proteins was paralleled by a significantly greater recovery of mRNAs coding for pro alpha 1(1) collagen and elastin, in RNA extracted from White Carneau aortal tissue, increased recovery of mRNAs coding for an intracellular protein, gamma-actin were also observed in White Carneau aortal tissue. No differences in steady state levels of mRNAs coding for pro alpha 1(1) collagen and elastin were observed in RNA extracted from pigeon liver, suggesting a tissue specific increase in the mRNAs coding for these connective tissue proteins in aorta. A markedly reduced cell population however, was responsible for this overall increase in biosynthetic activity in White Carneau pigeon aortic tissue. This was demonstrated by a reduced cell count and by the recovery of reduced levels of total DNA in the thoracic aorta and celiac bifurcation of the White Carneau pigeon. The cell population in White Carneau aortic tissue exhibits therefore a markedly different phenotype with respect to a capacity for the biosynthesis of extracellular and intracellular proteins.
Park
H S
HS
Dept. of Surgery, UMDNJ-Robert Wood Johnson Medical School, New Brunswick 08903.
Kniep
A C
AC
Smith
S C
SC
Robie
S M
SM
Smith
E C
EC
Yu
S Y
SY
Mackenzie
J W
JW
Scott
G E
GE
Boyd
C D
CD
D000199:Actins / Q000235:genetics / Q000378:metabolism; D000818:Animals; D001013:Aorta, Thoracic / Q000378:metabolism* / Q000473:pathology; D001161:Arteriosclerosis / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000662:veterinary*; D002445:Celiac Artery / Q000378:metabolism; D003094:Collagen / Q000235:genetics / Q000378:metabolism; D010856:Columbidae; D004247:DNA / Q000378:metabolism; D004549:Elastin / Q000235:genetics / Q000378:metabolism; D016326:Extracellular Matrix Proteins / Q000378:metabolism*; D009693:Nucleic Acid Hybridization; D010641:Phenotype; D012333:RNA, Messenger / Q000378:metabolism
D000199:Actins; D016326:Extracellular Matrix Proteins; D012333:RNA, Messenger; D003094:Collagen; D004247:DNA; D004549:Elastin