PLATELET‐DERIVED GROWTH FACTOR B‐CHAIN COMPRISES THE MAJOR PART OF ENHANCED RELEASED MITOGEN FROM AORTIC ENDOTHELIAL CELLS OF STROKE‐PRONE SPONTANEOUSLY HYPERTENSIVE RATS

M. Sasahara, Y. Hayase, X. H. Yang, K. Iihara, S. Amano, F. Hazama

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)S123-S125
JournalClinical and Experimental Pharmacology and Physiology
Volume22
DOIs
Publication statusPublished - Nov 1995
Externally publishedYes

Fingerprint

Inbred SHR Rats
Mitogens
Intercellular Signaling Peptides and Proteins
Endothelial Cells
Vascular Smooth Muscle
Smooth Muscle Myocytes
Blood Vessels
Proto-Oncogene Proteins c-sis
Hypertension
Hypertrophy
Fibroblasts
Cell Proliferation

All Science Journal Classification (ASJC) codes

  • Physiology
  • Pharmacology
  • Physiology (medical)

Cite this

@article{9b5cfac8378c4b91ba2acf4b876b1876,
title = "PLATELET‐DERIVED GROWTH FACTOR B‐CHAIN COMPRISES THE MAJOR PART OF ENHANCED RELEASED MITOGEN FROM AORTIC ENDOTHELIAL CELLS OF STROKE‐PRONE SPONTANEOUSLY HYPERTENSIVE RATS",
abstract = "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.",
author = "M. Sasahara and Y. Hayase and Yang, {X. H.} and K. Iihara and S. Amano and F. Hazama",
year = "1995",
month = "11",
doi = "10.1111/j.1440-1681.1995.tb02848.x",
language = "English",
volume = "22",
pages = "S123--S125",
journal = "Clinical and Experimental Pharmacology and Physiology",
issn = "0305-1870",
publisher = "Wiley-Blackwell",

}

TY - JOUR

T1 - PLATELET‐DERIVED GROWTH FACTOR B‐CHAIN COMPRISES THE MAJOR PART OF ENHANCED RELEASED MITOGEN FROM AORTIC ENDOTHELIAL CELLS OF STROKE‐PRONE SPONTANEOUSLY HYPERTENSIVE RATS

AU - Sasahara, M.

AU - Hayase, Y.

AU - Yang, X. H.

AU - Iihara, K.

AU - Amano, S.

AU - Hazama, F.

PY - 1995/11

Y1 - 1995/11

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0029588576&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029588576&partnerID=8YFLogxK

U2 - 10.1111/j.1440-1681.1995.tb02848.x

DO - 10.1111/j.1440-1681.1995.tb02848.x

M3 - Article

C2 - 9072322

AN - SCOPUS:0029588576

VL - 22

SP - S123-S125

JO - Clinical and Experimental Pharmacology and Physiology

JF - Clinical and Experimental Pharmacology and Physiology

SN - 0305-1870

ER -