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Vanadium Compounds as Pro-Inflammatory Agents: Effects on Cyclooxygenases.

Korbecki J, Baranowska-Bosiacka I, Gutowska I, Chlubek D - Int J Mol Sci (2015)

Bottom Line: We refer mainly to the effects of vanadate (orthovanadate), vanadyl and pervanadate ions; the main focus is placed on their impact on intracellular signaling.We describe the exact mechanism of the effect of vanadium compounds on protein tyrosine phosphatases (PTP), epidermal growth factor receptor (EGFR), PLCγ, Src, mitogen-activated protein kinase (MAPK) cascades, transcription factor NF-κB, the effect on the proteolysis of COX-2 and the activity of cPLA2.For a better understanding of these processes, a lot of space is devoted to the transformation of vanadium compounds within the cell and the molecular influence on the direct targets of the discussed vanadium compounds.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry and Medical Chemistry, Pomeranian Medical University, Powstańców Wlkp. 72 Av., 70-111 Szczecin, Poland. jan.korbecki@onet.eu.

ABSTRACT
This paper discusses how the activity and expression of cyclooxygenases are influenced by vanadium compounds at anticancer concentrations and recorded in inorganic vanadium poisonings. We refer mainly to the effects of vanadate (orthovanadate), vanadyl and pervanadate ions; the main focus is placed on their impact on intracellular signaling. We describe the exact mechanism of the effect of vanadium compounds on protein tyrosine phosphatases (PTP), epidermal growth factor receptor (EGFR), PLCγ, Src, mitogen-activated protein kinase (MAPK) cascades, transcription factor NF-κB, the effect on the proteolysis of COX-2 and the activity of cPLA2. For a better understanding of these processes, a lot of space is devoted to the transformation of vanadium compounds within the cell and the molecular influence on the direct targets of the discussed vanadium compounds.

No MeSH data available.


Related in: MedlinePlus

The mechanism of activation of NF-κB by vanadium compounds. Vanadium compounds at low concentrations activate NF-κB via NIK. This results in the degradation of IκBα and the release of NF-κB. The activation of IKK by vanadium compounds may also involve kinases from the JNK MAPK cascade. At high concentrations vanadium compounds have a different mechanism of NF-KB activation. They inhibit the activity of NIK and cause IκBα phosphorylation at Tyr42, which triggers the release of NF-κB but inhibits the proteolytic degradation of IκBα.
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ijms-16-12648-f005: The mechanism of activation of NF-κB by vanadium compounds. Vanadium compounds at low concentrations activate NF-κB via NIK. This results in the degradation of IκBα and the release of NF-κB. The activation of IKK by vanadium compounds may also involve kinases from the JNK MAPK cascade. At high concentrations vanadium compounds have a different mechanism of NF-KB activation. They inhibit the activity of NIK and cause IκBα phosphorylation at Tyr42, which triggers the release of NF-κB but inhibits the proteolytic degradation of IκBα.

Mentions: The described pathway leads to the activation of NF-κB by vanadium compounds at low concentrations (30 μM) [63,65,90] as well as the activation of NIK responsible for the activation of IKK (Figure 5) [64,65]. Nevertheless, the exact mechanism of NIK activation by vanadium compounds is unclear. This kinase is sensitive to changes in low concentrations of ROS and can be activated by vanadium-generated ROS [64]. It is also possible that vanadate directly activates this kinase reaction by catalyzing the H2O2-induced oxidation of cysteine residues which leads to activation of NIK [40]. Probably this process also inactivates highly ROS-sensitive serine/threonine phosphatases [64]. Another pathway of IKK activation by low concentrations of vanadium compounds are the kinases of JNK MAPK cascades, where IKK activation occurs via mitogen-activated protein kinase/ERK kinase kinase 1 (MEKK1) and SAPK/ERK kinase 1 (SEK1) [63,91].


Vanadium Compounds as Pro-Inflammatory Agents: Effects on Cyclooxygenases.

Korbecki J, Baranowska-Bosiacka I, Gutowska I, Chlubek D - Int J Mol Sci (2015)

The mechanism of activation of NF-κB by vanadium compounds. Vanadium compounds at low concentrations activate NF-κB via NIK. This results in the degradation of IκBα and the release of NF-κB. The activation of IKK by vanadium compounds may also involve kinases from the JNK MAPK cascade. At high concentrations vanadium compounds have a different mechanism of NF-KB activation. They inhibit the activity of NIK and cause IκBα phosphorylation at Tyr42, which triggers the release of NF-κB but inhibits the proteolytic degradation of IκBα.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4490466&req=5

ijms-16-12648-f005: The mechanism of activation of NF-κB by vanadium compounds. Vanadium compounds at low concentrations activate NF-κB via NIK. This results in the degradation of IκBα and the release of NF-κB. The activation of IKK by vanadium compounds may also involve kinases from the JNK MAPK cascade. At high concentrations vanadium compounds have a different mechanism of NF-KB activation. They inhibit the activity of NIK and cause IκBα phosphorylation at Tyr42, which triggers the release of NF-κB but inhibits the proteolytic degradation of IκBα.
Mentions: The described pathway leads to the activation of NF-κB by vanadium compounds at low concentrations (30 μM) [63,65,90] as well as the activation of NIK responsible for the activation of IKK (Figure 5) [64,65]. Nevertheless, the exact mechanism of NIK activation by vanadium compounds is unclear. This kinase is sensitive to changes in low concentrations of ROS and can be activated by vanadium-generated ROS [64]. It is also possible that vanadate directly activates this kinase reaction by catalyzing the H2O2-induced oxidation of cysteine residues which leads to activation of NIK [40]. Probably this process also inactivates highly ROS-sensitive serine/threonine phosphatases [64]. Another pathway of IKK activation by low concentrations of vanadium compounds are the kinases of JNK MAPK cascades, where IKK activation occurs via mitogen-activated protein kinase/ERK kinase kinase 1 (MEKK1) and SAPK/ERK kinase 1 (SEK1) [63,91].

Bottom Line: We refer mainly to the effects of vanadate (orthovanadate), vanadyl and pervanadate ions; the main focus is placed on their impact on intracellular signaling.We describe the exact mechanism of the effect of vanadium compounds on protein tyrosine phosphatases (PTP), epidermal growth factor receptor (EGFR), PLCγ, Src, mitogen-activated protein kinase (MAPK) cascades, transcription factor NF-κB, the effect on the proteolysis of COX-2 and the activity of cPLA2.For a better understanding of these processes, a lot of space is devoted to the transformation of vanadium compounds within the cell and the molecular influence on the direct targets of the discussed vanadium compounds.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry and Medical Chemistry, Pomeranian Medical University, Powstańców Wlkp. 72 Av., 70-111 Szczecin, Poland. jan.korbecki@onet.eu.

ABSTRACT
This paper discusses how the activity and expression of cyclooxygenases are influenced by vanadium compounds at anticancer concentrations and recorded in inorganic vanadium poisonings. We refer mainly to the effects of vanadate (orthovanadate), vanadyl and pervanadate ions; the main focus is placed on their impact on intracellular signaling. We describe the exact mechanism of the effect of vanadium compounds on protein tyrosine phosphatases (PTP), epidermal growth factor receptor (EGFR), PLCγ, Src, mitogen-activated protein kinase (MAPK) cascades, transcription factor NF-κB, the effect on the proteolysis of COX-2 and the activity of cPLA2. For a better understanding of these processes, a lot of space is devoted to the transformation of vanadium compounds within the cell and the molecular influence on the direct targets of the discussed vanadium compounds.

No MeSH data available.


Related in: MedlinePlus