Here, we aimed to investigate the expression of chromobox homolog 8 (CBX8) in nucleus pulposus (NP) cells from rat intervertebral disc (IVD) and its function in DNA damage and repair. NP cells were isolated from healthy rat IVD for immunohistochemistry staining. Small interfering RNA (siRNA) of CBX8 was applied for gene silencing, and reverse transcriptase-polymerase chain reaction (RT-PCR) was performed to determine mRNA levels of CBX8, type II collagen, and proteoglycans. Cell proliferation and cell cycle were evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, colony-forming assay, and flow cytometry. Hydrogen peroxide (H2O2) was added to simulate DNA oxidative damage, and expression of CBX8 was examined using RT-PCR and Western blot. After five passages, mRNA levels of type II collagen and proteoglycans decreased but that of CBX8 increased. When CBX8 was silenced by siRNA, the expressions of CBX8, type II collagen and proteoglycans declined, and the cell growth was inhibited. Besides, cell cycle was slowed down as most cells were arrest in G0/G1 phase. Furthermore, CBX8 expression went up responding to DNA oxidative damage caused by H2O2. The data indicated that CBX8 plays important roles in cell proliferation and DNA damage. Cell proliferation and cell cycle were stimulated by CBX8, which may be associated with INK4A-ARF pathway. Moreover, CBX8 plays a role in DNA damage which made it a potential gene therapy target for treatment of disc degeneration.
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http://dx.doi.org/10.1007/s11626-013-9596-2 | DOI Listing |
Cancer Cell Int
December 2024
Department of Applied Chemistry, Graduate Institute of Biomedicine and Biomedical Technology, National Chi Nan University, Puli, Taiwan.
Introduction: Chronic alcohol consumption and tobacco usage are major risk factors for esophageal squamous cell carcinoma (ESCC). Excessive tobacco and alcohol consumption lead to oxidative stress and the generation of reactive carbonyl species (RCS) which induce DNA damage and cell apoptosis. This phenomenon contributes to cell damage and carcinogenesis in various organs including ESCC.
View Article and Find Full Text PDFHum Exp Toxicol
December 2024
Department of neurology, Hubei Provincial Hospital of Traditional Chinese Medicine, Wuhan, China. Hubei Sizhen Laboratory, Affiliated Hospital of Hubei University of Chinese Medicine, Wuhan, China.
Introduction: The incidence of cerebral ischemia-reperfusion injury (I/R) is complex which seriously threatens the life safety of patients. Neither its prevention nor its treatment has been successful so far. Proteins that bind to DNA and belong to the C2/H2 zinc finger family are known as Krüppel-like factors (KLFs).
View Article and Find Full Text PDFCell Prolif
December 2024
Department of Orthodontics, Faculty of Medicine, Justus Liebig University, Giessen, Germany.
Cellular mechanotransduction is a complex physiological process that integrates alterations in the external environment with cellular behaviours. In recent years, the role of the nucleus in mechanotransduction has gathered increased attention. Our research investigated the involvement of lamin A/C, a component of the nuclear envelope, in the mechanotransduction of macrophages under compressive force.
View Article and Find Full Text PDFJ Dairy Sci
December 2024
North Dakota State University, Fargo, ND, USA.
Recent evidence suggests that environmental factors experienced by sires can be transmitted through the ejaculate (seminal plasma + sperm) into the female reproductive tract, influencing fertilization, embryo development, and postnatal offspring outcomes. This concept is termed paternal programming. In rodents, sire nutrition was shown to directly alter offspring outcomes through sperm epigenetic signatures, DNA damage/oxidative stress, cytokine profiles, and/or the seminal microbiome.
View Article and Find Full Text PDFToxicol Appl Pharmacol
December 2024
College of Medicine, Graduate School, Kyung Hee University, 02447, Republic of Korea; Division of Cardiology, Department of Internal Medicine, Kyung-Hee University Hospital, Kyung Hee University, 02447, Republic of Korea. Electronic address:
In the current study, we dosed Didecyldimethylammonium chloride (DDAC) in mice by pharyngeal aspiration for 28 days or 90 days (weekly) and tried to elucidate the relationship between lamellar body formation and the lesions. When exposed for 28 days (0, 5, 10, 50, and 100 μg/head), all the mice in the 50 and 100 μg/head groups died since Day 2 after the third dosing (Day 16 after the first dosing). Edema, necrosis of bronchiolar and alveolar epithelium, and fibrinous exudate were observed in the lungs of all the dead mice, and chronic inflammatory lesions were observed in the lung tissues of alive mice.
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