ArticleMolecular and cellular biochemistry2012
Tumor necrosis factor alpha stimulates cathepsin K and V activity via juxtacrine monocyte-endothelial cell signaling and JNK activation.
Article in Molecular and cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- The many roles of cathepsins in restenosis.Heliyon · 2024Article
- Inflammaging, immunosenescence, and cardiovascular aging: insights into long COVID implications.Frontiers in cardiovascular medicine · 2024Review
- Surface-Functionalized Stem Cell-Derived Extracellular Vesicles for Vascular Elastic Matrix Regenerative Repair.Molecular pharmaceutics · 2023Article
- Multiple sites on SARS-CoV-2 spike protein are susceptible to proteolysis by cathepsins B, K, L, S, and V.Protein science : a publication of the Protein Society · 2021Article
- Homocysteine in Neurology: A Possible Contributing Factor to Small Vessel Disease.International journal of molecular sciences · 2021Review
- Sickle Cell Anemia Mediates Carotid Artery Expansive Remodeling That Can Be Prevented by Inhibition of JNK (c-Jun N-Terminal Kinase).Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- Praeruptorin B Mitigates the Metastatic Ability of Human Renal Carcinoma Cells through Targeting CTSC and CTSV Expression.International journal of molecular sciences · 2020Article
- Cysteinyl cathepsins in cardiovascular diseases.Biochimica et biophysica acta. Proteins and proteomics · 2020Review
- Long-Term Cryopreservation and Revival of Tissue-Engineered Skeletal Muscle.Tissue engineering. Part A · 2019Article
- Sequential, but not Concurrent, Incubation of Cathepsin K and L with Type I Collagen Results in Extended Proteolysis.Scientific reports · 2019Article
- l-Homocysteine-induced cathepsin V mediates the vascular endothelial inflammation in hyperhomocysteinaemia.British journal of pharmacology · 2018Article
- Endothelium as a Potential Target for Treatment of Abdominal Aortic Aneurysm.Oxidative medicine and cellular longevity · 2018Review
- Novel in vivo and in vitro techniques to image and model the cerebral vasculature in sickle cell disease.Blood cells, molecules & diseases · 2017Review
- Supraspinatus tendon overuse results in degenerative changes to tendon insertion region and adjacent humeral cartilage in a rat model.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2017Article
- Investigating the Life Expectancy and Proteolytic Degradation of Engineered Skeletal Muscle Biological Machines.Scientific reports · 2017Article
- Cathepsin K-targeted sub-micron particles for regenerative repair of vascular elastic matrix.Acta biomaterialia · 2017Article
- Biomechanical and biochemical regulation of cathepsin K expression in endothelial cells converge at AP-1 and NF-κB.Biological chemistry · 2016Article
- Cathepsin Protease Inhibition Reduces Endometriosis Lesion Establishment.Reproductive sciences (Thousand Oaks, Calif.) · 2016Article
- Review
- Low-Cost Method to Monitor Patient Adherence to HIV Antiretroviral Therapy Using Multiplex Cathepsin Zymography.Molecular biotechnology · 2016Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Inflammation and damage promote monocyte adhesion to endothelium and cardiovascular disease (CVD). Elevated inflammation and increased monocyte-endothelial cell interactions represent the initial stages of vascular remodeling associated with a multitude of CVDs. Cathepsins are proteases produced by both cell types that degrade elastin and collagen in arterial walls, and are upregulated in CVD. We hypothesized that the inflammatory cytokine tumor necrosis factor alpha (TNFα) and monocyte binding would stimulate cathepsins K and V expression and activity in endothelial cells that may be responsible for initiating local proteolysis during CVD. Confluent human aortic endothelial cells were stimulated with TNFα or THP-1 monocyte co-cultures, and multiplex cathepsin zymography was used to detect changes in levels of active cathepsins K, L, S, and V. Direct monocyte-endothelial cell co-cultures stimulated with TNFα generated maximally observed cathepsin K and V activities compared to either cell type alone (n = 3, p < 0.05) by a c-Jun N-terminal kinase (JNK)-dependent manner. Inhibition of JNK with SP6000125 blocked upregulation of cathepsin K activity by 49 % and cathepsin V by 81 % in endothelial cells. Together, these data show that inflammatory cues and monocyte-endothelial cell interactions upregulate cathepsin activity via JNK signaling axis and identify a new mechanism to target toward slowing the earliest stages of tissue remodeling in CVD.
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