High Expression of Cathepsin E is Associated with the Severity of Airflow Limitation in Patients with COPD

Cao, Weijun; Li, Manhui; Li, Jianxiong; Xu, Xin; Ren, Shengxiang; Rajbanshi, Bhavana; Xu, Jin‐Fu

doi:10.3109/15412555.2015.1057273

Cited by 8 publications

(6 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In general, two aspartic acid residues in the active site act as a proton donor and acceptor to catalyze the hydrolysis of the peptide bond in substrates . Among aspartic proteases are cathepsin D and cathepsin E, and presenilins . Despite the relative small number of aspartic proteases compared to other proteases families, they play a key role in several physiopathological processes .…”

Section: Comparative Analysis Of Proteases Distribution Among Distincmentioning

confidence: 99%

Reviewing Mechanistic Peptidomics in Body Fluids Focusing on Proteases

et al. 2018

View full text Add to dashboard Cite

The comprehension of how protease networks sculpt proteomes might help to disclose the functional annotation of the peptidome in health and disease. Envisioning to add new insights on the protease networks involved in the regulation of body fluid peptidomes, the authors apply Proteasix software to predict the proteases involved in the generation of the naturally occurring peptides present in six of the most studied human body fluids. Peptidome data is collected from the databases and from experimental studies. The analysis highlights 132 putative proteases from four families with the predominance of serine proteases and metalloproteases. From these, 49 proteases seem to be common to all fluids and are mostly associated to extracellular matrix organization as well as protein/peptide hormone processing. Data analysis also emphasizes: i) the similarity between plasma and CSF protease profiles; ii) that saliva and tears share proteases involved in the generation of peptides with antimicrobial activity; iii) that urine is the body fluid with the highest number of unique putative proteases, precluding an easy tracing of proteolytic events in this case. Taken together, the analysis emphasizes the intricate modus operandi of proteases, challenged by the interconnected pathways and amplification cascades in which they are involved.

show abstract

Section: Comparative Analysis Of Proteases Distribution Among Distincmentioning

confidence: 99%

Reviewing Mechanistic Peptidomics in Body Fluids Focusing on Proteases

et al. 2018

View full text Add to dashboard Cite

show abstract

“…Among them, nine genes (Gpnmb, Trem2, Clec4d, Slc26a4, Ear6, Cd300lf, Ctsd, Ptgir, and Tacc3) were upregulated in the APM group relative to the DEP group in a dosedependent manner. The top nine genes have important roles in lung inflammation, asthma, COPD, pulmonary fibrosis, and lung cancer [35][36][37][38][39][40][41][42][43] . In this study, we observed common lung inflammation in the DEP and APM groups through histological assessment, and the severity was higher in the APM group relative to the DEP group.…”

Section: Discussionmentioning

confidence: 99%

Establishment of an artificial particulate matter-induced lung disease model through analyzing pathological changes and transcriptomic profiles in mice

Kim

Song

Yuk

et al. 2023

Sci Rep

View full text Add to dashboard Cite

Particulate matter (PM), an environmental risk factor, is linked with health risks such as respiratory diseases. This study aimed to establish an animal model of PM-induced lung injury with artificial PM (APM) and identify the potential of APM for toxicological research. APM was generated from graphite at 600 °C and combined with ethylene. We analyzed diesel exhaust particulate (DEP) and APM compositions and compared toxicity and transcriptomic profiling in lungs according to the exposure. For the animal study, C57BL/6 male mice were intratracheally administered vehicle, DEP, or APM. DEP or APM increased relative lung weight, inflammatory cell numbers, and inflammatory protein levels compared with the vehicle control. Histological assessments showed an increase in particle-pigment alveolar macrophages and slight inflammation in the lungs of DEP and APM mice. In the only APM group, granulomatous inflammation, pulmonary fibrosis, and mucous hyperplasia were observed in the lungs of some individuals. This is the first study to compare pulmonary toxicity between DEP and APM in an animal model. Our results suggest that the APM-treated animal model may contribute to understanding the harmful effects of PM in toxicological studies showing that APM can induce various lung diseases according to different doses of APM.

show abstract

“…Similar to MMPs, CTS activity acts in similar manner to degrade ECM proteins, and thus contribute to COPD pathogenesis [154]. CTSS [155] CTSG [156], and CTSE [157] levels are increased in the serum of COPD patients compared to healthy control patients. Both CTSE and CTSS are negatively correlated with the severity of airflow limitation [155, 157], and CTSS is also negatively related to the severity of emphysema [155].…”

Section: Pp2a Inactivation Creates a Favourable Microenvironment For mentioning

confidence: 99%

Protein phosphatase 2A (PP2A): a key phosphatase in the progression of chronic obstructive pulmonary disease (COPD) to lung cancer

et al. 2019

View full text Add to dashboard Cite

Lung cancer (LC) has the highest relative risk of development as a comorbidity of chronic obstructive pulmonary disease (COPD). The molecular mechanisms that mediate chronic inflammation and lung function impairment in COPD have been identified in LC. This suggests the two diseases are more linked than once thought. Emerging data in relation to a key phosphatase, protein phosphatase 2A (PP2A), and its regulatory role in inflammatory and tumour suppression in both disease settings suggests that it may be critical in the progression of COPD to LC. In this review, we uncover the importance of the functional and active PP2A holoenzyme in the context of both diseases. We describe PP2A inactivation via direct and indirect means and explore the actions of two key PP2A endogenous inhibitors, cancerous inhibitor of PP2A (CIP2A) and inhibitor 2 of PP2A (SET), and the role they play in COPD and LC. We explain how dysregulation of PP2A in COPD creates a favourable inflammatory micro-environment and promotes the initiation and progression of tumour pathogenesis. Finally, we highlight PP2A as a druggable target in the treatment of COPD and LC and demonstrate the potential of PP2A re-activation as a strategy to halt COPD disease progression to LC. Although further studies are required to elucidate if PP2A activity in COPD is a causal link for LC progression, studies focused on the potential of PP2A reactivating agents to reduce the risk of LC formation in COPD patients will be pivotal in improving clinical outcomes for both COPD and LC patients in the future.

show abstract

High Expression of Cathepsin E is Associated with the Severity of Airflow Limitation in Patients with COPD

Abstract: Cat E contributes to the severity of airflow limitation during progression of COPD.

Cited by 8 publications

References 37 publications

Reviewing Mechanistic Peptidomics in Body Fluids Focusing on Proteases

Reviewing Mechanistic Peptidomics in Body Fluids Focusing on Proteases

Establishment of an artificial particulate matter-induced lung disease model through analyzing pathological changes and transcriptomic profiles in mice

Protein phosphatase 2A (PP2A): a key phosphatase in the progression of chronic obstructive pulmonary disease (COPD) to lung cancer

Contact Info

Product

Resources

About