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Li C.,Harbin Medical University | Jiang Z.,Fudan University | Liu X.,Bio pharmaceutical Key Laboratory of Heilongjiang Province
Biological Trace Element Research

The possible biochemical mechanism of gallium was studied in this paper. One-day-old hens were fed to up to 68 weeks on a control diet and diets containing gallium. Serum calcium and phosphorus, serum alkaline phosphatase, tartrate resistant acid phosphatase (TRAP), serum osteocalcin, homocysteine, C-terminal crosslinked telopeptides of collagen type I, and bone mineral content were measured, respectively. The beneficial effects of gallium supplementation on improvement of cage layer osteoporosis were attributable mainly to decrease TRAP activity, C-terminal crosslinked telopeptides of collagen type I level, plasma calcium and phosphate concentrations, and increase the mineral content in the bones and osteocalcin level in plasma. © 2009 Humana Press Inc. Source

Liu H.-B.,Harbin Medical University | Yang B.-F.,Harbin Medical University | Dong D.-L.,Harbin Medical University | Dong D.-L.,Bio pharmaceutical Key Laboratory of Heilongjiang Province
Trends in Cardiovascular Medicine

Calcineurin is a cytoplasmic Ca 2+/calmodulin-dependent protein phosphatase that contributes to cardiac hypertrophy. Numerous studies have demonstrated that calcineurin/nuclear factor of activated T cell pathway affects the architecture of the heart under pathologic conditions, and the effects of calcineurin/nuclear factor of activated T cell pathway on cardiac hypertrophy have been well reviewed. Cardiac electrical remodeling is generally accompanied with the cardiac hypertrophy, and alteration of cardiac ion channel activity also leads to the changes of calcineurin activity and cardiac hypertrophy. Many studies have linked calcineurin with changes of a variety of ion channels, but the therapeutic approaches to target calcineurin for correcting cardiac electrical disturbance have not been formulated. Here, we review the recent progress in calcineurin and electrical remodeling in pathologic cardiac hypertrophy. © 2010 Elsevier Inc. Source

Liu Y.,Harbin Medical University | Ma C.,Harbin Medical University | Zhang Q.,Harbin Medical University | Yu L.,Harbin Medical University | And 7 more authors.
International Journal of Biochemistry and Cell Biology

Our laboratory has proved that 15-hydroxyeicosatetraenoic acid, a product of arachidonic acid catalyzed by 15-lipoxygenase (15-LO), plays a pivotal role in hypoxic pulmonary arterial hypertension. However, the mechanisms of how hypoxia regulates 15-LO expression are still unclear. As the formation of endogenous transforming growth factor-beta1 (TGF-β1), implicated in pulmonary arterial hypertension pathogenesis, was promoted by hypoxia, we suspect whether hypoxia-induced the expression of 15-LO is via the TGF-β1 pathway. We found that treatment of pulmonary artery smooth muscle cells with TGF-β1 significantly increased the expression of 15-LO and levels of 15-hydroxyeicosatetraenoic acid, product of 15-LO, which were inhibited by transforming growth factor-beta receptor I (TGFβRI) inhibitor, SD-208 and siRNA targeted to knockdown rat TGFβRI. Moreover, our results showed that TGF-β1 regulated the cell cycle progression and made more cells from the G0/G1 phase to the G2/M + S phase and enhanced the microtubule formation in cell nucleus. Additionally, we found that the 15-LO pathway was involved in TGFβ-1-mediated cell viability, DNA synthesis and the cell cycle progression. Our data provide novel evidence that hypoxia induced 15-LO expression is through TGF-β1, and 15-LO pathway plays a critical role in TGFβRI mediated the proliferation of pulmonary artery smooth muscle cells induced by hypoxia. Thus, new strategies aimed at combined blockade of TGFβRI as well as 15-LO may yield optimal therapeutic benefits. Crown Copyright © 2012 Published by Elsevier Ltd. All rights reserved. Source

Ma J.,Harbin Medical University | Liang S.,Harbin Medical University | Wang Z.,Harbin Medical University | Zhang L.,Harbin Medical University | And 7 more authors.
Journal of Cellular Physiology

15-Hydroxyeicosatetraenoic acid (15-HETE), a product of arachidonic acid (AA) catalyzed by 15-lipoxygenase (15-LO), plays an essential role in hypoxic pulmonary arterial hypertension. We have previously shown that 15-HETE inhibits apoptosis in pulmonary artery smooth muscle cells (PASMCs). To test the hypothesis that such an effect is attributable to the hypoxia-induced pulmonary vascular remodeling (PVR), we performed these studies. We found subtle thickening of proximal media/adventitia of the pulmonary arteries (PA) in rats that had been exposed to hypoxia. This was associated with an up-regulation of the anti-apoptotic Bcl-2 expression and down-regulation of pro-apoptotic caspase-3 and Bax expression in PA homogenates. Nordihydroguaiaretic acid (NDGA), which inhibits the generation of endogenous 15-HETE, reversed all the alterations following hypoxia. In situ hybridization histochemistry and immunocytochemistry showed that the 15-LO-1 mRNA and protein were localized in pulmonary artery endothelial cells (PAECs), while the 15-LO-2 mRNA and protein were localized in both PAECs and PASMCs. Furthermore, the Rho-kinase (ROCK) pathway was activated by both endogenous and exogenous 15-HETE, alleviating the serum deprivation (SD)-induced PASMC apoptosis. Thus, these findings indicate that 15-HETE protects PASMC from apoptosis, contributing to pulmonary vascular medial thickening, and the effect is, at least in part, mediated via the ROCK pathway. © 2009 Wiley-Liss, Inc. Source

Liu F.,Harbin Medical University | Yu Y.,Harbin Medical University | Jin Y.,Harbin Medical University | Fu S.,Harbin Medical University | Fu S.,Bio pharmaceutical Key Laboratory of Heilongjiang Province
Molecular Biology Reports

Understanding the genesis and development of tumors is an essential component in cancer research. It is of interest to discover unknown genes that are responsible for cellular transformation. A cDNA library of a highly metastatic lung adenocarcinoma cell line was constructed. This library was introduced into the NIH3T3 mouse embryonic fibroblast cell line to screen for cDNAs that increase anchorage-independent colony formation in soft agar. The expression of TSG101 in lung cancer cell lines and specimens was confirmed using reverse transcription-polymerase chain reaction. The level of TSG101 protein in transfected A549 cells was determined by western blotting. Cell-cycle distribution was analyzed using a FACStar Plus flow cytometer. One of the candidate cDNAs that increases anchorage-independent colony formation was shown to correspond to the TSG101 cDNA sequence. Levels of TSG101 mRNA were higher in lung cancer cell lines and specimens compared to matched normal lung tissues. Ectopic expression of TSG101 in the A549 lung adenocarcinoma cell line increased the numbers of cells in S phase, suggesting an increased cell proliferation rate. These results indicate that TSG101 may induce the malignant phenotype of cells. © 2009 Springer Science+Business Media B.V. Source

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