Abstract
The current studies were performed to determine whether vascular smooth muscle cells produce stress-induced proteins when subjected to experimental hypertension. Two-dimensional gel electrophoresis was used to analyze labeled proteins in cultured cells in response to either heat shock or arsenite treatment. The major heat shock proteins (HSPs) induced had molecular masses of 70, 90, and 100 kDa. Arsenite treatment produced a similar response with the additional induction of a 30-kDa protein. In vitro translations of total RNA from heat-shocked cells, and RNA blot hybridization using HSP 70 cDNA suggested that HSP 70 induction was transcriptionally regulated. Treatment of cells with norepinephrine or angiotensin II induced cellular hypertrophy without eliciting HSPs. In vitro translation of aortic RNA from rats rendered hypertensive by administration of deoxycorticosterone and a high salt intake also did not reveal HSP induction. The absence of HSP induction using an in vivo model of hypertension suggests that those proteins may not be required to mediate the vascular response to experimental hypertension.
| Original language | English |
|---|---|
| Journal | American Journal of Physiology - Heart and Circulatory Physiology |
| Volume | 258 |
| Issue number | 6 27-6 |
| Publication status | Published - 1990 |
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Keywords
- heart
- heat shock proteins
- hypertension
- vasculature
ASJC Scopus subject areas
- Physiology
Cite this
Stress-induced proteins in aortic smooth muscle cells and aorta of hypertensive rats. / Kohane, D. S.; Sarzani, R.; Schwartz, J. H.; Chobanian, A. V.; Brecher, P.
In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 258, No. 6 27-6, 1990.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Stress-induced proteins in aortic smooth muscle cells and aorta of hypertensive rats
AU - Kohane, D. S.
AU - Sarzani, R.
AU - Schwartz, J. H.
AU - Chobanian, A. V.
AU - Brecher, P.
PY - 1990
Y1 - 1990
N2 - The current studies were performed to determine whether vascular smooth muscle cells produce stress-induced proteins when subjected to experimental hypertension. Two-dimensional gel electrophoresis was used to analyze labeled proteins in cultured cells in response to either heat shock or arsenite treatment. The major heat shock proteins (HSPs) induced had molecular masses of 70, 90, and 100 kDa. Arsenite treatment produced a similar response with the additional induction of a 30-kDa protein. In vitro translations of total RNA from heat-shocked cells, and RNA blot hybridization using HSP 70 cDNA suggested that HSP 70 induction was transcriptionally regulated. Treatment of cells with norepinephrine or angiotensin II induced cellular hypertrophy without eliciting HSPs. In vitro translation of aortic RNA from rats rendered hypertensive by administration of deoxycorticosterone and a high salt intake also did not reveal HSP induction. The absence of HSP induction using an in vivo model of hypertension suggests that those proteins may not be required to mediate the vascular response to experimental hypertension.
AB - The current studies were performed to determine whether vascular smooth muscle cells produce stress-induced proteins when subjected to experimental hypertension. Two-dimensional gel electrophoresis was used to analyze labeled proteins in cultured cells in response to either heat shock or arsenite treatment. The major heat shock proteins (HSPs) induced had molecular masses of 70, 90, and 100 kDa. Arsenite treatment produced a similar response with the additional induction of a 30-kDa protein. In vitro translations of total RNA from heat-shocked cells, and RNA blot hybridization using HSP 70 cDNA suggested that HSP 70 induction was transcriptionally regulated. Treatment of cells with norepinephrine or angiotensin II induced cellular hypertrophy without eliciting HSPs. In vitro translation of aortic RNA from rats rendered hypertensive by administration of deoxycorticosterone and a high salt intake also did not reveal HSP induction. The absence of HSP induction using an in vivo model of hypertension suggests that those proteins may not be required to mediate the vascular response to experimental hypertension.
KW - heart
KW - heat shock proteins
KW - hypertension
KW - vasculature
UR - http://www.scopus.com/inward/record.url?scp=0025324129&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0025324129&partnerID=8YFLogxK
M3 - Article
C2 - 1694409
AN - SCOPUS:0025324129
VL - 258
JO - American Journal of Physiology
JF - American Journal of Physiology
SN - 0363-6119
IS - 6 27-6
ER -