Epidermal growth factor responsiveness in smooth muscle cells from hypertensive and normotensive rats.

Scott‐Burden, Timothy; Resink, Thérèse J.; Baur, U; Bürgin, Maria; Bühler, Fritz R.

doi:10.1161/01.hyp.13.4.295

Cited by 139 publications

(63 citation statements)

References 41 publications

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“…16 The isolation, phenotypic characterization, and propagation of human VSMCs from either microarterioles associated with omental tissue or from the lower thoracic aorta (both obtained postoperatively) were performed according to previously described procedures. 11 Immunohistochemical characterization of all VSMC isolates (positive for smooth muscle-specific a-actin and negative for factor VIII) was performed on primary cultures as described.…”

Section: Cell Culturementioning

confidence: 99%

“…11 Immunohistochemical characterization of all VSMC isolates (positive for smooth muscle-specific a-actin and negative for factor VIII) was performed on primary cultures as described. 11 ' 16 A single VSMC isolate from each of the different tissues (specified in figure and table legends) was used for the experiments, and each isolate used was between passages 4 and 13. Unless otherwise specified, cultures of VSMCs were rendered quiescent by serum deprivation and maintenance in serum-free medium containing 0.1% (wt/vol) bovine serum albumin for 48 hours before examination of signaling responses to agonists.…”

Section: Cell Culturementioning

confidence: 99%

“…' 16 After removal of the radiolabeled medium and washing of the cell layers, VSMCs were preincubated for 20 minutes at 37°C in serum-free culture medium containing 15 mmol/L LiCl. 1116 Thereafter, agonists were added and incubations were terminated by addition of trichloroacetic acid to a final concentration of 4.6%, and after 30 minutes of gentle shaking at room temperature the trichloroacetic acid concentration was reduced to 1% by addition of water.…”

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confidence: 99%

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Concerted effects of lipoproteins and angiotensin II on signal transduction processes in vascular smooth muscle cells.

Bochkov

Ткачук

Hahn

et al. 1993

Arterioscler Thromb

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Low-density (LDL) and high-density (HDLj) lipoproteins dose-dependently activate phosphoinositide turnover and elevate cytosolic free Ca 2+ concentrations ([Ca 1+ ]|) in cultured vascular smooth muscle cells (VSMCs) from either human (microarterioles and aorta) or rat (aorta) sources. High-performance liquid chromatography analysis of cell extracts revealed comparable spectra of inositol phosphate isomers generated in response to either LDL, HDL,, or angiotensin II (Ang II 10 Epidemiologic studies also show that hypertension is a major risk factor for development of atherosclerosis. 4 Different hypotheses have been proposed to explain the association between the two diseases, with the common etiologic denominators being either disturbances in plasma lipoprotein concentrations and cellular cholesterol homeostasis, 5 intracellular calcium overload, 6 or altered responses to growth factors and vasoregulatory hormones.1 -3 These theories are not mutually exclusive, however, and linkage between the latter two is predictable because growth factors and vasoregulatory hormones are known to mobilize intracellular calcium. The relation between lipoprotein/cholesterol disturbances and the calcium-based or agonist growth factor-based theories is less conspicuous, but it

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Section: Cell Culturementioning

confidence: 99%

Section: Cell Culturementioning

confidence: 99%

mentioning

confidence: 99%

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Concerted effects of lipoproteins and angiotensin II on signal transduction processes in vascular smooth muscle cells.

Bochkov

Ткачук

Hahn

et al. 1993

Arterioscler Thromb

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“…Cellular proliferation has been reported to be stimulated by LDL in combination with serum [6,7] or with growth factors [8,9] and chemically modified LDLs, such as oxLDL and acLDL, induce macrophage growth [10]. Consistently, macrophage derived foam cells, generated by uptake of modified LDL through the scavenger receptor pathway [11], tend to proliferate in atherosclerotic lesions [12,13].…”

Section: Introductionmentioning

confidence: 99%

Stimulation of mitogen activated protein kinase by LDL and oxLDL in human U‐937 macrophage‐like cells

Deigner

Claus

1996

FEBS Letters

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Mitogen activated protein kinase in extracts of U-937 macrophage-like cells was stimulated by LDL and oxLDL. A maximum value (161% of the basal phosphotransferase activity) was obtained after 6 min exposure to oxidized LDL (27 Ixg/ml) using APRTPGGRR peptide substrate. The activatory effect was more pronounced (LDL 181%, oxLDL 201%) when MAPK of stimulated cells was immnnoprecipitated with anti-p42 MArK antibodies and phuspho~ransferuse activity was assayed in immune complexes. Stimulation produced by oxLDL was inhibited by poly I, fucoidan, dextran sulfate and by the MAPKK inhibitor PD 098059 but not by PMA-mediated depletion of PKC or by pre-treatment with chioroquine or with pertussis toxin. These results suggest a direct mitogenic effect of LDL which, in the case of oxLDL, is dependent on scavenger receptor llgation but not on G-protein mediated or PKCdependent signal transduction.

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“…EGF is a smooth-muscle mitogen that has been implicated previously in hypertensive vascular remodeling. 20 We have shown that the expression of the EGF receptor (EGFR) mRNA is aldosterone sensitive, in vivo it is reduced by spironolactone, and in vitro it can be increased by aldoste- …”

Section: Discussionmentioning

confidence: 99%

Mineralocorticoid Receptor Activation Causes Cerebral Vessel Remodeling and Exacerbates the Damage Caused by Cerebral Ischemia

2006

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Abstract-Mineralocorticoid receptor antagonists protect against ischemic cerebrovascular disease; this appears to be caused by changes in cerebral vessel structure that would promote blood flow. Therefore, we hypothesized that mineralocorticoid receptor activation with deoxycorticosterone acetate would cause deleterious remodeling of the cerebral vasculature and exacerbate the damage caused by cerebral ischemia. Six-week-old male Wistar rats were treated with deoxycorticosterone acetate (200 mg/kg) for 6 weeks. At 12 weeks of age, the deoxycorticosterone acetate-treated rats had elevated systolic blood pressure compared with age-matched controls (157Ϯ5.9 versus 124Ϯ3.1 mm Hg deoxycorticosterone acetate versus control; PϽ0.05). The area of ischemic damage resulting from middle cerebral artery occlusion was greater in the deoxycorticosterone acetate-treated rats than control (63.5Ϯ3.72 versus 46.6Ϯ5.52% of the hemisphere infarcted, deoxycorticosterone acetate versus control; PϽ0.05). Middle cerebral artery structure was assessed using a pressurized arteriograph under calcium-free conditions. Over a range of intralumenal pressures, the lumen and ODs of the middle cerebral arteries were smaller in the deoxycorticosterone acetate-treated rats than the control rats (PϽ0.05). There was also an increase in the wall thickness and wall:lumen ratio in the vessels from deoxycorticosterone acetate-treated rats (PϽ0.05). The vessels from the deoxycorticosterone acetate-treated rats were stiffer than those from control rats as evidenced by a leftward shift in the stress/strain curve. These novel data suggest that mineralocorticoid receptor activation without salt loading and nephrectomy is sufficient to elicit deleterious effects on the cerebral vasculature that lead to inward hypertrophic remodeling and an increase in the ischemic damage in the event of a stroke. Key Words: mineralocorticoids Ⅲ cerebral ischemia Ⅲ remodeling Ⅲ cerebral arteries Ⅲ aldosterone S troke, in particular, ischemic stroke, is a leading cause of death and disability in the Western world. Yet, the factors that increase an individual's risk of having a stroke or exacerbate the damage caused by a stroke are still not completely understood. Studies using stroke-prone spontaneously hypertensive rats (SHRSPs) suggest that cerebral vascular structure plays an important role in the pathogenesis of cerebral ischemia. SHRSPs have larger cerebral infarcts when ischemia is induced by middle cerebral artery (MCA) occlusion than their normotensive counterparts, the Wistar Kyoto rats. 1,2 This difference appears to be because of remodeling of the cerebral vessels that results in the vessels having a smaller lumen diameter and an impaired ability to dilate in response to ischemia. [3][4][5] It is becoming increasingly clear that aldosterone is involved in the pathophysiology of cardiovascular disease. 6 We have shown previously that chronic treatment of SHRSPs with spironolactone, the aldosterone antagonist, reduces the ischemic cerebral infarct size after MCA occlus...

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Epidermal growth factor responsiveness in smooth muscle cells from hypertensive and normotensive rats.

Cited by 139 publications

References 41 publications

Concerted effects of lipoproteins and angiotensin II on signal transduction processes in vascular smooth muscle cells.

Concerted effects of lipoproteins and angiotensin II on signal transduction processes in vascular smooth muscle cells.

Stimulation of mitogen activated protein kinase by LDL and oxLDL in human U‐937 macrophage‐like cells

Mineralocorticoid Receptor Activation Causes Cerebral Vessel Remodeling and Exacerbates the Damage Caused by Cerebral Ischemia

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