Tin mesoporphyrin (SnMP), a competitive heme oxygenase (HO) inhibitor, also induces HO-1 mRNA and protein expression by a mechanism that is not fully understood. We examined whether the induction by SnMP is mediated by a de-repression of Bach1, a transcription factor that suppresses the HO-1 gene. Incubation of NIH3T3-HO-1-luc cells with SnMP attenuated HO activity with a concomitant increase in HO-1 mRNA and protein and a decrease in Bach1 and HO-2 proteins, which was not due to transcriptional down-regulation, but accelerated protein decay. Similarly, HO-1 protein degradation was increased by SnMP, despite of an elevation in HO-1 transcription. Transfection of Bach1 shRNA in Hepa cells raised basal HO-1 expression significantly, and SnMP treatment further increased HO-1 mRNA. In conclusion, SnMP induces HO-1 expression not only by de-repressing the HO-1 promoter by binding Bach1, but also by accelerating Bach1 degradation.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1805812 | PMC |
| http://dx.doi.org/10.1016/j.bbrc.2007.01.050 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Dietary γ-Aminobutyric Acid Promotes Growth and Immune System Performance and Improves Erythropoiesis and Angiogenesis in Gibel Carp ().
Animals (Basel)
January 2025
Tongwei Agricultural Development Co., Ltd., Key Laboratory of Nutrition and Healthy Culture of Aquatic, Livestock and Poultry, Ministry of Agriculture and Rural Affairs, Healthy Aquaculture Key Laboratory of Sichuan Province, Chengdu 610093, China.
This experiment aimed to investigate the effect of dietary supplementation of γ-aminobutyric acid (GABA) on the growth performance, immune response, and oxygen-transport-related factors of Gibel carp (). An eight-week culturing experiment was designed with five experimental diets, with the actual GABA content being 368 mg/kg (G1, control group), 449 mg/kg (G2), 527 mg/kg (G3), 602 mg/kg (G4), and 675 mg/kg (G5). The results showed that the level of 527 mg/kg (G3) of GABA significantly increased the specific growth rate (SGR), weight gain rate (WGR), and final body weight (FBW) of Gibel carp, while the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), and glucose (GLU) were also increased significantly.
View Article and Find Full Text PDFAntiosteoporosis and Bone Protective Effect of Phyllanthin Against Glucocorticoid-induced Osteoporosis in Rats via Alteration of HO-1/Nrf2 and RANK/RANKL/OPG Pathway.
Dokl Biochem Biophys
January 2025
Department of Orthopaedics, Affiliated Hospital of Hebei University, 071000, Baoding, China.
Unlabelled: Osteoporosis is a condition where bones weaken due to a loss in density and quality, making them fragile and more susceptible to fractures, even from minor stress or injury. In this experimental study, we scrutinized the antiosteoporosis effect of phyllanthin against glycocorticoid (GIOP) induced osteoporosis in rats.
Methods: : SD rats were used in this study and subcutaneous administration of DEX (3 mg/kg) was used for the induction of osteoporosis and rats were treated with phyllanthin and alendronate for 12 weeks.
Chemoprotective Effect of Myrrhone against Diethylnitrosamine and Ferric Nitrile Induced Renal Cancer via Alteration of HO-1/Nrf2 and TRL4/NF-κB Signaling Pathway.
Dokl Biochem Biophys
January 2025
Affiliated Hospital of Hebei University, 071000, Baoding City, Hebei Province, China.
Unlabelled: . Renal cell carcinoma (RCC) is the most prevalent form of kidney cancer and is the primary malignancy affecting the genitourinary system. It represents the majority of kidney cancer cases and is distinguished by its aggressive nature and high mortality rate.
View Article and Find Full Text PDFGossypin Ameliorates Collagen-Induced Arthritic Rats by Inhibiting Angiogenesis, Inflammation and Oxidative Stress.
Basic Clin Pharmacol Toxicol
February 2025
Department of Pharmacology, Venkateshwara College of Pharmacy, Meerut, India.
Background: Rheumatoid arthritis (RA) is a long-term inflammatory autoimmune disease that damages cartilage and synovial membranes while also affecting bones and joints. The aim of the current study was to investigate the antiarthritic effect of gossypin against collagen-induced arthritis (CIA) in rats.
Methods: Intraperitoneal administration of Type II collagen (2 mg/mL) was used to induce arthritis in the rats, followed by oral administration of gossypin (5, 10 and 15 mg/kg) for 28 days.
Methyltransferase-like 3 mediates m6A modification of heme oxygenase 1 mRNA to induce ferroptosis of renal tubular epithelial cells in acute kidney injury.
Free Radic Biol Med
January 2025
Traditional Chinese Medicine Integrated Department of Nephrology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China; Research Institute of Nephrology, Zhengzhou University, Zhengzhou, Henan province, China; Henan Province Research Center for Kidney Disease, Zhengzhou, Henan Province, China; Key Laboratory of Precision Diagnosis and Treatment for Chronic Kidney Disease in Henan Province, Zhengzhou, Henan Province, China; Tianjian Laboratory of Advanced Biomedical Sciences, Academy of Medical Sciences, Zhengzhou University, Zhengzhou, Henan Province, China; Innovation Center of Basic Research for Metabolic-Associated Fatty Liver Disease, Ministry of Education of China, Zhengzhou, Henan Province, China. Electronic address:
Acute kidney injury (AKI) involves a series of syndromes characterized by a rapid increase in creatinine levels. Ferroptosis, as an iron-dependent mode of programmed cell death, reportedly participates in the pathogenesis of AKI. Methyltransferase-like 3 (METTL3)-mediated N6-methyladenosine (m6A) modification has been recently associated with various kidney diseases; however, the mechanism of METTL3 crosstalk with the molecules involved in ferroptosis is not clearly understood.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!