ADAM-17 Activity and Its Relation to ACE2: Implications for Severe COVID-19
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Published on: November 5, 2021
Jiangming Sun1, Andreas Edsfeldt1,2,3, Joel Svensson4
1Cardiovascular Research-Translational Studies, Department of Clinical Sciences Malmö, Lund University, 205 02 Malmö, Sweden.
Abstract:
There is a lack of studies aiming to assess cellular a disintegrin and metalloproteinase-17 (ADAM-17) activity in COVID-19 patients and the eventual associations with the shedding of membrane-bound angiotensin-converting enzyme 2 (mACE2). In addition, studies that investigate the relationship between ACE2 and ADAM-17 gene expressions in organs infected by SARS-CoV-2 are lacking. We used data from the Massachusetts general hospital COVID-19 study (306 COVID-19 patients and 78 symptomatic controls) to investigate the association between plasma levels of 33 different ADAM-17 substrates and COVID-19 severity and mortality. As a surrogate of cellular ADAM-17 activity, an ADAM-17 substrate score was calculated. The associations between soluble ACE2 (sACE2) and the ADAM-17 substrate score, renin, key inflammatory markers, and lung injury markers were investigated. Furthermore, we used data from the Genotype-Tissue Expression (GTEx) database to evaluate ADAM-17 and ACE2 gene expressions by age and sex in ages between 20-80 years. We found that increased ADAM-17 activity, as estimated by the ADAM-17 substrates score, was associated with COVID-19 severity (p = 0.001). ADAM-17 activity was also associated with increased mortality but did not reach statistical significance (p = 0.06). Soluble ACE2 showed the strongest positive correlation with the ADAM-17 substrate score, follow by renin, interleukin-6, and lung injury biomarkers. The ratio of ADAM-17 to ACE2 gene expression was highest in the lung. This study indicates that increased ADAM-17 activity is associated with severe COVID-19. Our findings also indicate that there may a bidirectional relationship between membrane-bound ACE2 shedding via increased ADAM-17 activity, dysregulated renin-angiotensin system (RAS) and immune signaling. Additionally, differences in ACE2 and ADAM-17 gene expressions between different tissues may be of importance in explaining why the lung is the organ most severely affected by COVID-19, but this requires further evaluation in prospective studies.
Insights
Increased a disintegrin and metalloproteinase-17 (ADAM-17) activity is linked to severe COVID-19 and may affect angiotensin-converting enzyme 2 (ACE2) shedding. This suggests a connection between ADAM-17, ACE2, and COVID-19 severity.
Area of Science:
- Biochemistry and Molecular Biology
- Immunology
- Virology
Background:
- Limited research exists on a disintegrin and metalloproteinase-17 (ADAM-17) activity in COVID-19 patients.
- The association between ADAM-17 activity and the shedding of membrane-bound angiotensin-converting enzyme 2 (mACE2) in COVID-19 is understudied.
- The relationship between ADAM-17 and ACE2 gene expression in SARS-CoV-2 infected organs requires investigation.
Purpose of the Study:
- To assess cellular ADAM-17 activity in COVID-19 patients and its association with disease severity and mortality.
- To investigate the relationship between ADAM-17 activity, soluble ACE2 (sACE2) levels, renin, inflammatory markers, and lung injury.
- To evaluate ADAM-17 and ACE2 gene expression patterns by age and sex in different tissues.
Main Methods:
- Utilized data from the Massachusetts General Hospital COVID-19 study (306 COVID-19 patients, 78 controls).
- Calculated an ADAM-17 substrate score as a surrogate for cellular ADAM-17 activity.
- Analyzed associations between the ADAM-17 substrate score, COVID-19 severity/mortality, sACE2, renin, inflammatory markers, and lung injury markers.
- Examined ADAM-17 and ACE2 gene expression using the Genotype-Tissue Expression (GTEx) database.
Main Results:
- Increased ADAM-17 activity was significantly associated with COVID-19 severity (p = 0.001).
- ADAM-17 activity showed a trend towards association with increased mortality (p = 0.06).
- Soluble ACE2 exhibited the strongest positive correlation with the ADAM-17 substrate score, followed by renin, IL-6, and lung injury biomarkers.
- The ADAM-17 to ACE2 gene expression ratio was highest in the lung.
Conclusions:
- Elevated ADAM-17 activity is associated with severe COVID-19.
- Findings suggest a potential bidirectional relationship between mACE2 shedding (via ADAM-17), dysregulated renin-angiotensin system (RAS), and immune signaling in COVID-19.
- Tissue-specific differences in ACE2 and ADAM-17 gene expression may contribute to the lung's susceptibility to SARS-CoV-2 infection.
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