Title Lanthanum chloride suppresses hydrogen peroxide-enhanced calcification in rat calcifying vascular cells
Authors Shi, Yu
Gou, Bao-Di
Shi, Yan-Ling
Zhang, Tian-Lan
Wang, Kui
Affiliation Peking Univ, Dept Biol Chem, Sch Pharmaceut Sci, Beijing 100191, Peoples R China.
Capital Med Univ, Dept Biol Chem, Sch Pharmaceut Sci, Beijing 100069, Peoples R China.
Peking Univ, Dept Biol Chem, Sch Pharmaceut Sci, 38 Xueyuan Rd, Beijing 100191, Peoples R China.
Keywords Lanthanum
Hydrogen peroxide
Calcifying vascular cells
Calcification
MAPK signaling
SMOOTH-MUSCLE-CELLS
PROTEIN-KINASE-C
OXIDATIVE STRESS
ARTERIAL CALCIFICATION
EXTRACELLULAR CALCIUM
TYROSINE KINASE
ACINAR-CELLS
IN-VITRO
MECHANISMS
APOPTOSIS
Issue Date 2009
Publisher biometals
Citation BIOMETALS.2009,22,(2),317-327.
Abstract Lanthanum chloride (LaCl(3)) has been shown to retard the progression of established atherosclerotic lesions in animal models, and used as a calcium channel blocker in various cellular experiments. In this study, we assessed the role of lanthanum chloride (LaCl(3)) in H(2)O(2)-enhanced calcification in rat calcifying vascular cells (CVCs) and examined the involvement of MAPK signaling pathways. H(2)O(2) induced growth inhibition of CVCs, as well as increases in intracellular levels of calcium and reactive oxygen species, ALP activity, apoptosis and calcium deposition. These effects of H(2)O(2) were suppressed by pretreatment of the cells with 1 mu M of LaCl(3) for 2 h. In addition, H(2)O(2) activated the phosphorylation of ERK1/2, JNK and p38 MAPK, but only the last two were associated with the ALP activity. Our findings demonstrate that H(2)O(2)-enhanced osteoblastic differentiation and apoptosis are responsible for the increased calcification in rat CVCs, and LaCl(3) can counteract these effects by suppressing the activation of JNK (JNK2, but not JNK1) and p38 MAPK signaling pathway.
URI http://hdl.handle.net/20.500.11897/156878
ISSN 0966-0844
DOI 10.1007/s10534-008-9168-1
Indexed SCI(E)
PubMed
Appears in Collections: 药学院

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