The Effect of Cadmium on Cytosolic Free Calcium, Protein Kinase C, and Collagen Synthesis in Rat Osteosarcoma (ROS 17/2.8) Cells

Long, Gregory J.

doi:10.1006/taap.1996.8060

Cited by 48 publications

(24 citation statements)

References 41 publications

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“…Cadmium was previously reported to increase the intracellular cAMP level (Cook et al, 1985;Kumar and Bhattacharya, 2000) and was also demonstrated to bind to the CRE and promote transcriptional activity of stress genes in HepG2 cells (Tchounwou et al, 2001). Additionally, earlier reports suggested that cadmium can directly activate PKC (Long, 1997), and recent studies have dem- The total amount of transfected DNA was kept constant using empty vector. After 40 hr of transfection, the cells were incubated with increasing doses of CdCl 2 (5, 10, 20, 30 μM) for an additional 8 hr.…”

Section: Discussionmentioning

confidence: 99%

Cadmium up-regulates transcription of the steroidogenic acute regulatory protein (StAR) gene through phosphorylated CREB rather than SF-1 in K28 cells

Park

Gomes

et al. 2015

J. Toxicol. Sci.

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-Cadmium is a widely used heavy metal in industry and affects the male reproductive system of animals, including humans, as a result of occupational and environmental exposures. However, the molecular mechanism underlying its effect on steroidogenesis in gonads remains unclear. In this study, we demonstrated that exposure of K28 mouse testicular Leydig tumor cells to cadmium led to a significant increase in the mRNA level, promoter activity and protein level of the steroidogenic acute regulatory protein (StAR), an essential factor for steroid biosynthesis. It has been well documented that StAR gene transcription is regulated by multiple transcription factors, including cAMP-responsive element binding protein (CREB) family members and SF-1. Cadmium treatment caused an increase in CREB phosphorylation but did not alter the CREB protein level in the nucleus. EMSA studies revealed that cadmiuminduced phosphorylated CREB formed specific complexes with the proximal region of the StAR gene promoter. Furthermore, co-transfection with a CREB expression plasmid significantly increased cadmium-induced StAR promoter activity. However, the nuclear level and the affinity of SF-1 protein for the StAR proximal promoter were dramatically decreased upon exposure to cadmium. Taken together, these results suggest that cadmium up-regulates StAR gene expression through phosphorylated CREB rather than through SF-1 in mouse testicular Leydig cells.

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Section: Discussionmentioning

confidence: 99%

Cadmium up-regulates transcription of the steroidogenic acute regulatory protein (StAR) gene through phosphorylated CREB rather than SF-1 in K28 cells

Park

Gomes

et al. 2015

J. Toxicol. Sci.

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“…It is unclear whether cadmium can activate protein kinase C in vascular endothelial cells or not. However, in other cell types including NRK-49F cells, 28) mouse 3T3/10T1/2 fibroblasts, 29) rat osteosarcoma (ROS 17/2.8) cells 30) and PC12 cells, 31) it has been suggested that cadmium can activate protein kinase C, although it is also possible that the metal may directly inhibit the kinase. 32) We postulate that endothelial protein kinase C can be activated by cadmium and then mediates the induction of PAI-1 synthesis in the cells.…”

Section: Discussionmentioning

confidence: 99%

Induction of Plasminogen Activator Inhibitor Type 1 Synthesis by Cadmium in Human Vascular Endothelial Cells in Culture.

Yamamoto

Kaji

2002

JOURNAL OF HEALTH SCIENCE

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Cadmium is a unique heavy metal that stimulates the secretion of plasminogen activator inhibitor type 1 (PAI-1) from vascular endothelial cells. However, it has been incompletely understood whether cadmium stimulation of PAI-1 secretion actually results in a reduction of endothelial fibrinolytic activity and whether the stimulation results from an induction of endothelial PAI-1 synthesis. To address these questions, human umbilical vein endothelial cells were cultured with cadmium chloride in the presence or absence of actinomycin D, H-7 or HA1004. The activity of tissue type and urokinase type plasminogen activators (t-PA and u-PA, respectively) in the conditioned medium was analyzed by fibrin zymography and mRNAs coding t-PA, u-PA and PAI-1 were determined by quantitative reverse transcription-polymerase chain reaction. Results of the experiments indicate that cadmium reduces the activity of both t-PA and u-PA in vascular endothelial cells through induction of PAI-1 synthesis which is mediated by protein kinase C activation. Since the PAI-1 induction by cadmium was observed in neither human vascular smooth muscle cells nor human fibroblasts, it was suggested that vascular endothelial cells are a particular cell type of which PAI-1 synthesis is stimulated by cadmium.

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“…Protein kinase C is well-established as a key regulator of endothelial cell-cell adhesion, cytoskeletal organization and microvascular permeability, and activation of protein kinase C is usually associated with a loss of endothelial cell-cell adhesion and an increase in microvascular permeability (Aird, 2004;Defouw and Defouw, 2001;Harrington et al, 2003;Yuan, 2002). While we know of no studies specifically examining the role of protein kinase C in mediating the effects of Cd on endothelial permeability, there is a great deal of evidence in the literature showing that relatively low levels of Cd can activate protein kinase C in a variety of cell types both in vitro (Long, 1997;Matsuoka and Call, 1995) and in vivo (Bagchi et al, 1997;Beyersmann et al, 1994;Romare and Lundholm, 1999). In addition, Cd can also activate several related or parallel MAP kinase signaling pathways (Ding and Templeton, 2000;Hirano et al, 2005;Lag et al, 2005;Lui et al, 2003) that have also been implicated as regulators of endothelial permeability (Birukova et al, 2005;Bogatcheva et al, 2003;Borbiev et al, 2004;Lui et al, 2003;Yuan, 2002).…”

Section: Effects Of CD On Ve-cadherin and Other Cell Adhesion Moleculesmentioning

confidence: 98%

The vascular endothelium as a target of cadmium toxicity

2006

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The Effect of Cadmium on Cytosolic Free Calcium, Protein Kinase C, and Collagen Synthesis in Rat Osteosarcoma (ROS 17/2.8) Cells

Cited by 48 publications

References 41 publications

Cadmium up-regulates transcription of the steroidogenic acute regulatory protein (StAR) gene through phosphorylated CREB rather than SF-1 in K28 cells

Cadmium up-regulates transcription of the steroidogenic acute regulatory protein (StAR) gene through phosphorylated CREB rather than SF-1 in K28 cells

Induction of Plasminogen Activator Inhibitor Type 1 Synthesis by Cadmium in Human Vascular Endothelial Cells in Culture.

The vascular endothelium as a target of cadmium toxicity

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