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Role of heat shock protein 70 in induction of stress fiber formation in rat arterial endothelial cells in response to stretch stress.

Luo SS, Sugimoto K, Fujii S, Takemasa T, Fu SB, Yamashita K - Acta Histochem Cytochem (2007)

Bottom Line: In contrast, treatment with quercetin, an HSP 70 inhibitor, inhibited both upregulation of endothelial HSP 70 and formation of SFs in response to tensile stress.In addition, treatment of stretched ECs with cytochalasin D, which disrupts SF formation, did not adversely affect stretch-induced upregulation of endothelial HSP 70.Our data suggest that endothelial HSP 70 plays an important role in inducing SF formation in response to tensile stress.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Anatomy, Nippon Medical School, Tokyo 113-8602, Japan.

ABSTRACT
We investigated the mechanism by which endothelial cells (ECs) resist various forms of physical stress using an experimental system consisting of rat arterial EC sheets. Formation of actin stress fibers (SFs) and expression of endothelial heat-shock stress proteins (HSPs) in response to mechanical stretch stress were assessed by immunofluorescence microscopy. Stretch stimulation increased expression of HSPs 25 and 70, but not that of HSP 90. Treatment with SB203580, a p38 MAP kinase inhibitor that acts upstream of the HSP 25 activation cascade, or with geldanamycin, an inhibitor of HSP 90, had no effect on the SF formation response to mechanical stretch stress. In contrast, treatment with quercetin, an HSP 70 inhibitor, inhibited both upregulation of endothelial HSP 70 and formation of SFs in response to tensile stress. In addition, treatment of stretched ECs with cytochalasin D, which disrupts SF formation, did not adversely affect stretch-induced upregulation of endothelial HSP 70. Our data suggest that endothelial HSP 70 plays an important role in inducing SF formation in response to tensile stress.

No MeSH data available.


Related in: MedlinePlus

Rhodamine-phalloidin staining in non-stretch-stressed (A) and stretch-stressed (B) ECs from the common iliac artery of rat. The ECs formed many long SFs (arrows) in response to application of mechanical stretch stress at 30% amplitude for 1 hr. Images A and B are shown at the same magnification; bar=20 µm.
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Figure 1: Rhodamine-phalloidin staining in non-stretch-stressed (A) and stretch-stressed (B) ECs from the common iliac artery of rat. The ECs formed many long SFs (arrows) in response to application of mechanical stretch stress at 30% amplitude for 1 hr. Images A and B are shown at the same magnification; bar=20 µm.

Mentions: Under non-stretch-stress conditions, fewer than 25% of the ECs in all the straight portions of the rat arteries examined were SF positive (Figs. 1 and 2). In the middle parts of the abdominal aorta and common iliac artery, formation of long SFs in response to stretch stress applied at more than ~20% amplitude was clearly evident (data for 30% amplitude shown in Figs. 1 and 2; other amplitude data not shown). Most of SFs were aligned parallel to the direction of stretching (Fig. 1). In contrast, in the proximal part of the thoracic aorta and the common carotid artery, stretching induced only a slight increase in SFs under the same conditions (Fig. 2). For the remainder of this report, all of the data for stretch-stressed ECs were from arterial segments subjected to application of mechanical stretch stress for 30% amplitude for 1 hr.


Role of heat shock protein 70 in induction of stress fiber formation in rat arterial endothelial cells in response to stretch stress.

Luo SS, Sugimoto K, Fujii S, Takemasa T, Fu SB, Yamashita K - Acta Histochem Cytochem (2007)

Rhodamine-phalloidin staining in non-stretch-stressed (A) and stretch-stressed (B) ECs from the common iliac artery of rat. The ECs formed many long SFs (arrows) in response to application of mechanical stretch stress at 30% amplitude for 1 hr. Images A and B are shown at the same magnification; bar=20 µm.
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC1828078&req=5

Figure 1: Rhodamine-phalloidin staining in non-stretch-stressed (A) and stretch-stressed (B) ECs from the common iliac artery of rat. The ECs formed many long SFs (arrows) in response to application of mechanical stretch stress at 30% amplitude for 1 hr. Images A and B are shown at the same magnification; bar=20 µm.
Mentions: Under non-stretch-stress conditions, fewer than 25% of the ECs in all the straight portions of the rat arteries examined were SF positive (Figs. 1 and 2). In the middle parts of the abdominal aorta and common iliac artery, formation of long SFs in response to stretch stress applied at more than ~20% amplitude was clearly evident (data for 30% amplitude shown in Figs. 1 and 2; other amplitude data not shown). Most of SFs were aligned parallel to the direction of stretching (Fig. 1). In contrast, in the proximal part of the thoracic aorta and the common carotid artery, stretching induced only a slight increase in SFs under the same conditions (Fig. 2). For the remainder of this report, all of the data for stretch-stressed ECs were from arterial segments subjected to application of mechanical stretch stress for 30% amplitude for 1 hr.

Bottom Line: In contrast, treatment with quercetin, an HSP 70 inhibitor, inhibited both upregulation of endothelial HSP 70 and formation of SFs in response to tensile stress.In addition, treatment of stretched ECs with cytochalasin D, which disrupts SF formation, did not adversely affect stretch-induced upregulation of endothelial HSP 70.Our data suggest that endothelial HSP 70 plays an important role in inducing SF formation in response to tensile stress.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Anatomy, Nippon Medical School, Tokyo 113-8602, Japan.

ABSTRACT
We investigated the mechanism by which endothelial cells (ECs) resist various forms of physical stress using an experimental system consisting of rat arterial EC sheets. Formation of actin stress fibers (SFs) and expression of endothelial heat-shock stress proteins (HSPs) in response to mechanical stretch stress were assessed by immunofluorescence microscopy. Stretch stimulation increased expression of HSPs 25 and 70, but not that of HSP 90. Treatment with SB203580, a p38 MAP kinase inhibitor that acts upstream of the HSP 25 activation cascade, or with geldanamycin, an inhibitor of HSP 90, had no effect on the SF formation response to mechanical stretch stress. In contrast, treatment with quercetin, an HSP 70 inhibitor, inhibited both upregulation of endothelial HSP 70 and formation of SFs in response to tensile stress. In addition, treatment of stretched ECs with cytochalasin D, which disrupts SF formation, did not adversely affect stretch-induced upregulation of endothelial HSP 70. Our data suggest that endothelial HSP 70 plays an important role in inducing SF formation in response to tensile stress.

No MeSH data available.


Related in: MedlinePlus