The aim of this study was to investigate the involvement of androgen, mainly testosterone, in the expression of renal senescence marker protein-30 (SMP30) in male rats. We found that the renal SMP30 expression was up-regulated by endogenous testosterone stimulation during puberty. Interestingly, androgen-deficient orchidectomized (ORX) rats exhibited lower SMP30 mRNA and protein expression in the kidney, and that was restored by testosterone propionate (TP) replacement. Abrogation of androgen receptor (AR) activity by co-treatment with flutamide abolished testosterone-induced SMP30 expression in the kidney as well as in the NRK52E cells. However, SMP30 expression was unaltered in the liver of ORX rats. We also showed a positive correlation between renal SMP30 expression and plasma testosterone level during the aging process. TP-induced SMP30 expression in ovariectomized (OVX) rats was observed and was an evidence to explain the gender difference of SMP30 levels. Immunofluorescence assay showed that renal SMP30 was specifically expressed in the proximal tubular segments of the kidney. The urinary Ca(2+) level was increased in both ORX and male aging rats. Taken together, our results indicate a novel role of testosterone in regulating SMP30 expression specifically in the kidney to contribute to urinary calcium absorption.
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http://dx.doi.org/10.1038/srep32085 | DOI Listing |
Curr Eye Res
December 2024
Department of Ophthalmology, First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Purpose: Oxidative stress, ultraviolet radiation, and calcium imbalance are key components in the onset and advancement of cataract, which continue to be the leading cause of blindness globally. An important newly discovered aging maker, Senescence marker protein 30 (SMP30) regulates calcium and participates in mitigating oxidative stress damage. Here, we examined the beneficial role of SMP30 in protecting against ultraviolet radiation type B (UVR-B)-induced cataract in rats.
View Article and Find Full Text PDFJ Neuropathol Exp Neurol
January 2025
Neurovascular Center, Changhai Hospital, Naval Medical University, Shanghai, China.
Ischemic stroke is a major cause of global death and permanent disability. Major consequences of ischemic stroke include neuronal mitochondrial dysfunction. We investigated the effects of senescence marker protein 30 (SMP30) on mitochondria-mediated apoptosis and histone deacetylase 4 (HDAC4)/postsynaptic density-95 (PSD-95) signaling in stroke models in vivo and in vitro.
View Article and Find Full Text PDFFront Biosci (Landmark Ed)
June 2024
Department of Biochemistry and Molecular Biology, School of Pre-clinical Medicine, Guangxi Medical University, 530021 Nanning, Guangxi, China.
Background: The senescence marker protein 30 (SMP30) is a calcium-binding protein whose expression decreases with age, and is closely associated with hepatocellular carcinoma (HCC) development. The primary goal of this study was to examine the mechanistic effect of SMP30 on HCC migration and invasion.
Methods: Bioinformatic and immunohistochemical approaches were used to examine the expression of SMP30 in HCC tissues and its relationship to patient survival.
J Nutr Sci Vitaminol (Tokyo)
January 2024
Department of Nutritional Science and Food Safety, Faculty of Applied Bioscience, Tokyo University of Agriculture.
Senescence marker protein-30 (SMP30) is a senescence marker molecule that exhibits lactonase activity in the ascorbic acid (AsA) biosynthesis pathway, except in primate mammals, including humans. Although numerous studies have shown that hepatic AsA deficiency causes acute-phase responses, details of the relationship between SMP30 expression and acute-phase responses in AsA-deficient conditions remain to be elucidated. Here, we investigated the effects of AsA deficiency on the relationship between SMP30 and acute liver injury in osteogenic disorder Shionogi (ODS) rats, which have a hereditary defect in AsA biosynthesis.
View Article and Find Full Text PDFIn Vivo
December 2023
Kyungpook National University, College of Veterinary Medicine, Department of Veterinary Pathology, Daegu, Republic of Korea;
Background/aim: Chronic kidney disease (CKD) is one of the most common causes of mortality in wild non-domestic felidae. The molecular mechanism regulating renal fibrosis in nephropathy is not fully understood especially in the felidae. This study aimed to elucidate senescence marker protein 30 (SMP30) expression patterns and its relationship with epithelial-mesenchymal transition (EMT) by immunostaining in two necropsied Siberian tigers (Panthera tigris altaica) with CKD.
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