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PLATELET‐DERIVED GROWTH FACTOR B‐CHAIN COMPRISES THE MAJOR PART OF ENHANCED RELEASED MITOGEN FROM AORTIC ENDOTHELIAL CELLS OF STROKE‐PRONE SPONTANEOUSLY HYPERTENSIVE RATS
Author(s) -
Sasahara M.,
Hayase Y.,
Yang X. H.,
Iihara K.,
Amano S.,
Hazama F.
Publication year - 1995
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1995.tb02848.x
Subject(s) - endocrinology , medicine , platelet derived growth factor , vascular smooth muscle , endothelial stem cell , stimulation , spontaneously hypertensive rat , endothelium , platelet , growth factor , platelet derived growth factor receptor , biology , chemistry , blood pressure , in vitro , smooth muscle , biochemistry , receptor
Summary 1. The present study was conducted to analyse the release and production of mitogen in cultured aortic endothelial cells of stroke‐prone spontaneously hypertensive rats (SHRSP), for the further understanding of the role of arterial endothelial cells in the genesis of vascular lesions in hypertension. 2. The cultured aortic endothelial cells derived from SHRSP increased released mitogens were compared with those from control Wistar‐Kyoto rats (WKY) with respect to cultured vascular medial smooth muscle cells and fibroblasts. 3. Biochemical analyses determined that the major part of mitogen released from aortic endothelial cells of both SHRSP and controls was the platelet‐derived growth factor B‐chain. 4. Further northern analyses revealed that the transcripts of PDGF B‐chain were constitutively accumulated three‐ to fourfold in quiescent aortic endothelial cells from SHRSP, compared with those from WKY through passages 2 to 5. 5. However, the half‐lives of the transcripts after actinomy cin D treatment were 1.12 h (s.d. = 0.14, n = 4) and 1.28 h (s.d. = 0.08, n = 3), in SHRSP and in WKY, respectively, showing no significant difference. 6. These suggest that the increased accumulated transcripts of PDGF B‐chain in SHRSP are due to an enhanced trans‐criptional rate. These enhanced release and production of PDGF‐B chain in arterial endothelial cells, which may be induced under chronic hypertensive conditions, is suggested to contribute to the genesis of vascular lesion in hypertension, through the stimulation of vascular smooth muscle cell proliferation and hypertrophy.