The hormonal form of vitamin D, 1alpha,25(OH)(2)-vitaminD(3) [1alpha,25(OH)(2)D(3)], stimulates signal transduction pathways in intestinal cells. To gain insight into the relative importance of the vitamin D receptor (VDR) in the rapid hormone responses, the amounts and localization of the VDR were evaluated in young (3 months) and aged (24 months) rat intestinal cells. Immune-fluorescence and Western blot studies showed that VDR levels are diminished in aged enterocytes. Confocal microscopy assays revealed that the VDR and other immune-reactive proteins have mitochondrial, membrane, cytosol and perinuclear localization. Western blot analysis using specific antibodies detected the 60 and 50 kDa bands expected for the VDR in the cytosol and microsomes and, to a lesser extent, in the nucleus and mitochondria. Low molecular weight immune-reactive proteins were also detected in young enterocytes subcellular fractions. Since changes in hormone receptor levels appear to constitute a common manifestation of the ageing process, we also analyzed 1alpha,25(OH)(2)D(3) binding properties and VDR levels in subcellular fractions from young and aged rats. In competition binding assays, employing [(3)H]-1alpha,25(OH)(2)D(3) and 1alpha,25(OH)(2)D(3), we have detected specific binding in all subcellular fractions, with maximum binding in mitochondrial and nuclear fractions. Both, VDR protein levels and 1alpha,25(OH)(2)D(3) binding, were diminished with ageing. Age-related declines in VDR may have important consequences for correct receptor/effector coupling in the duodenal tissues and may explain age-related declines in the hormonal regulation of signal transduction pathways that we previously reported.
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http://dx.doi.org/10.1007/s10522-007-9118-2 | DOI Listing |
Int J Biol Sci
January 2025
Division of Endocrinology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Dysregulated energy metabolism, particularly lipid metabolism disorders, has been identified as a key factor in the development of diabetic cardiomyopathy (DCM). Sirtuin 2 (SIRT2) is a deacetylase involved in the regulation of metabolism and cellular energy homeostasis, yet its role in the progression of DCM remains unclear. We observed significantly reduced SIRT2 expression in DCM model mice.
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January 2025
Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing 100029, China.
Anthracyclines (ANTs) are widely used in cancer therapy, particularly for lymphoma, sarcoma, breast cancer, and childhood leukemia, and have become the cornerstone of chemotherapy for various malignancies. However, it is associated with fatal and dose-dependent cardiovascular complications, especially cardiotoxicity. Mitochondrial quality control mechanisms, encompassing mitophagy, mitochondrial dynamics, and mitochondrial biogenesis, maintain mitochondrial homeostasis in the cardiovascular system.
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January 2025
Division of Nephrology, Department of Medicine, University of Connecticut School of Medicine, Farmington, CT, USA.
Cisplatin is widely used for the treatment of solid tumors and its antitumor effects are well established. However, a known complication of cisplatin administration is acute kidney injury (AKI). In this study, we examined the role of TEA domain family member 1 (TEAD1) in the pathogenesis of cisplatin-induced AKI.
View Article and Find Full Text PDFSheng Li Xue Bao
December 2024
State Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin 300020, China.
The objective of the present study was to investigate the role and mechanism of bone marrow microenvironmental cells in regulating the mitochondrial mass of leukemia cells, and to uncover the mechanism of leukemia progression at the metabolic level. A mouse model of acute myeloid leukemia (AML) induced by the overexpression of the MLL-AF9 (MA9) fusion protein was established, and the bone marrow cells of AML mice were transplanted into mitochondrial fluorescence reporter mice expressing the Dendra2 protein (mito-Dendra2 mice). The proportion of Dendra2 cells in bone marrow leukemia cells at different stages of AML was quantified by flow cytometry.
View Article and Find Full Text PDFSheng Li Xue Bao
December 2024
Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University; Institute of Advanced Clinical Medicine, Peking University; NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides; Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing 100191, China.
Heart failure is characterized by abnormal β-adrenergic receptor (β-AR) activation and mitochondrial dysfunction. In heart failure, overactivation of β-AR mediates key pathological processes in cardiomyocytes, including oxidative stress, calcium overload and metabolic abnormalities, which subsequently lead to inflammation, myocardial apoptosis and necrosis. Mitochondria are the core organelles for energy metabolism, and also play a vital role in calcium homeostasis, redox balance and signaling transduction.
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