A 90-kDa surface antigen of immature smooth muscle cells is ICAM-1

Printseva, O. Yu.; Peclo, M. M.; Tjurmin, A. V.; Gown, A. M.

doi:10.1152/ajpheart.1991.261.4.21

Cited by 6 publications

(3 citation statements)

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“…Indeed, knockout mice which are caspase1 deficient and therefore do not generate mature IL‐1β develop normally and the ex vivo response of cells to various apoptotic stimuli is indistinguishable from cells derived from wild‐type animals [12]. In addition, as 7β‐hydroxycholesterol and 7‐ketocholesterol can stimulate IL‐8 production which is chemotactic for T lymphocytes and neutrophils at picomolar and nanomolar concentrations [37], and as IL‐1 can induce both in vitro and in vivo endothelial expression of the adhesion molecules E‐selectin, ICAM‐1 and VCAM‐1 which are involved in the local adhesion and the subendothelial accumulation of T‐cells and monocytes [38, 39], we speculate that these oxysterols could play a critical role in the recruitment of immunocompetent cells in the atherosclerotic plaque. Interestingly, Bcl‐2 overexpression was associated with a lower IL‐1β secretion in U4 cells treated with 7β‐hydroxycholesterol than in U4 cells treated with 7‐ketocholesterol suggesting that the biological effects of oxysterols could be structure dependent as previously supposed by the various potencies of these compounds to induce apoptosis [3, 5]and to inhibit 3‐hydroxy‐3‐methylglutaryl coenzyme A reductase activity [40].…”

Section: Discussionmentioning

confidence: 99%

Induction of apoptosis and of interleukin‐1β secretion by 7β‐hydroxycholesterol and 7‐ketocholesterol: partial inhibition by Bcl‐2 overexpression

et al. 1997

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The oxysterols, 7ß-hydroxycholesterol and 7-ketocholesterol, are involved in the cytotoxicity of oxidized LDL. To elucidate their molecular mechanisms, the human promonocytic leukemia cells U937 and U4 were used. U4 cells overexpressing Bcl-2 were obtained by transfection of U937 cells. 7ß-hydroxycholesterol and 7-ketocholesterol induced nuclear condensation and/or fragmentation, internucleosomal DNA fragmentation, and IL-lß secretion, which were partially inhibited by Bcl-2 overexpression. These findings underline that these oxysterols could constitute major risk factors in atherosclerosis by their cytotoxicity and their ability to induce IL-lß release which might favor the recruitment of immunocompetent cells in the atherosclerotic plaque.

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Section: Discussionmentioning

confidence: 99%

Induction of apoptosis and of interleukin‐1β secretion by 7β‐hydroxycholesterol and 7‐ketocholesterol: partial inhibition by Bcl‐2 overexpression

et al. 1997

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“…With regard to the differentially expressed known genes, the cellular adhesion molecule ICAM-1 has been reported to be induced in in vitro stimulated human SMCs (25), in addition to its induction in endothelial cells. Moreover, ICAM-1 is expressed in neointimal SMCs in the atherosclerotic lesion (26,27). Induction of GM-CSF expression in cultured SMCs has been well documented (4,28), whereas expression in the atherosclerotic vessel wall has only been reported in rabbits (29).…”

Section: Isolation Of Full-length Cdnasmentioning

confidence: 99%

Differential Display Identification of 40 Genes with Altered Expression in Activated Human Smooth Muscle Cells

Vries

Achterberg

Horrevoets

et al. 2000

Journal of Biological Chemistry

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Detailed knowledge on the molecular and cellular mechanisms that control (re)-differentiation of vascular smooth muscle cells (SMCs) is critical to understanding the pathological processes underlying atherogenesis. We identified by differential display/reverse transcriptase-polymerase chain reaction 40 genes with altered expression in cultured SMCs upon stimulation with the conditioned medium of activated macrophages. This set of genes comprises 10 known genes and 30 novel genes, which we call "smags" (for smooth muscle activation-specific genes). To determine the in vivo significance of these (novel) genes in atherogenesis, we performed in situ hybridization experiments on vascular tissue. Specifically, FLICE (Fas-associated death domain-like interleukin-1␤-converting enzyme)-like inhibitory protein (FLIP) is expressed in neointimal SMCs as well as in lesion macrophages and endothelial cells, whereas the expression of the novel genes smag-63, smag-64, and smag-84 is restricted to neointimal SMCs. Characterization of full-length smag-64 cDNA revealed that it encodes a novel protein of 66 amino acids. smag-82 cDNA comprises the complete, unknown, 3-untranslated region of fibroblast growth factor-5. Collectively, our results illustrate the complex changes of SMC gene expression that occur in response to stimulation with cytokines and growth factors secreted by activated macrophages. Moreover, we identified interesting candidate genes that may play a role in the differentiation of SMCs during atherogenesis.

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“…Normal intima of the aorta and femoral artery as well as atherosclerotic plaques contain SMC which similarly to embryonal SMC express cytokeratin-8 and ICAM-1 [8,10,15]. Previously, we showed that SMC lacking h-caldesmon and/or calponin are phenotypicaUy similar to embryonal SMC and are present in the intima of adult human aorta and in uncomplicated atherosclerotic plaques [2,5].…”

Section: Resultsmentioning

confidence: 99%

Smooth muscle cell heterogeneity in intimal thickenings of various genesis and in organized thrombi

1996

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collagen fibers is one of the atherosclerosis markers. Taken together, our observations indicate that experimental HC induces pronounced atherosclerotic changes in pial arteries. Pat., 42, No. 6, 26-33 (1980). 3. K. G. Volkova, Arkh. Biol. Nauk, 33, No. 3-4, 581-602 (1933 Psikhiatr., 87, No. 7, 992-995 (1987). REFERENCES Smooth Muscle Cell Heterogeneity in lntimal Thickenings of Various Genesis and in Organized Thrombi B. V. Shekhonin, E. M. Tararak, and A. E. ZotikovTranslated from Byulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 122, No. 8, pp. 222-227, August, 1996 Original article submitted May 25, 1995 A population of smooth muscle cells heterogeneous by the expression of myosin, h-caldesmon, and calponin is identified by indirect immunofluorescence in the intima of normal aorta and femoral artery, in the subendothelium in atherosclerosis and Takayasu's disease, and in organized thrombi. The similarity of the extracellular matrix in various forms of arteriosclerosis implies that its hyperproduction is a typical response of smooth muscle cells.

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A 90-kDa surface antigen of immature smooth muscle cells is ICAM-1

Cited by 6 publications

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Induction of apoptosis and of interleukin‐1β secretion by 7β‐hydroxycholesterol and 7‐ketocholesterol: partial inhibition by Bcl‐2 overexpression

Induction of apoptosis and of interleukin‐1β secretion by 7β‐hydroxycholesterol and 7‐ketocholesterol: partial inhibition by Bcl‐2 overexpression

Differential Display Identification of 40 Genes with Altered Expression in Activated Human Smooth Muscle Cells

Smooth muscle cell heterogeneity in intimal thickenings of various genesis and in organized thrombi

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