Search for other papers by Majid Almansouri in
Google Scholar
PubMed
Search for other papers by Pooja Patel in
Google Scholar
PubMed
Search for other papers by Janet Chamberlain in
Google Scholar
PubMed
Healthy Lifespan Institute HELSI, University of Sheffield, Medical School, Sheffield, UK
Search for other papers by Sheila Francis in
Google Scholar
PubMed
-1β by caspase-1 ( 9 ). Active IL-1β can then be associated with the NLRP3 inflammasome ( 10 ). Only active IL-1β is released from cells and there is a myriad of mechanisms proposed, mainly in monocytic cells, including through microvesicles
Faculty of Medicine and Health, University of Sydney, Sydney, Australia
Search for other papers by Manisha S Patil in
Google Scholar
PubMed
Faculty of Medicine and Health, University of Sydney, Sydney, Australia
Search for other papers by Siân P Cartland in
Google Scholar
PubMed
Faculty of Medicine and Health, University of Sydney, Sydney, Australia
Search for other papers by Mary M Kavurma in
Google Scholar
PubMed
endothelial cell line, hCMEC/D3 ( 63 ). Instead, in these cells, TRAIL stimulated caspase-1 activity and cell death ( 60 , 63 ). These discrepancies may reflect receptor expression, cell type, origin, or differences in the in vitro angiogenic assay methods
Search for other papers by Sara Sileno in
Google Scholar
PubMed
Search for other papers by Sara Beji in
Google Scholar
PubMed
Search for other papers by Marco D’Agostino in
Google Scholar
PubMed
Search for other papers by Alessandra Carassiti in
Google Scholar
PubMed
Search for other papers by Guido Melillo in
Google Scholar
PubMed
Search for other papers by Alessandra Magenta in
Google Scholar
PubMed
associated with both PASI improvement and local inflammatory response decrease ( 36 ). Interestingly, in MI, miR-135b is downregulated, and its overexpression attenuates pyroptosis, a caspase-1-dependent proinflammatory programmed cell death. Thus, miR-135b