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Research interests

Corry-Anke Brandsma, born in Leeuwarden in 1980, completed her master in Medical Biology at the RUG, Groningen in 2003. She was appointed as a PhD student from 2003-2007 on a joined project of the departments of Pathology and Pulmonary diseases of the UMCG on the inflammatory response in COPD. From 2007-2014 she worked as a post-doc on several research projects funded by the Dutch Lung Foundation. In 2011 she received international research fellowships from the European Respiratory Society and the Dutch Lung Foundation to work in the lab of Prof. J.C. Hogg in Vancouver (Canada). In 2014 she was appointed as staff member by the department of Pathology of the UMCG.

During her first post-doc, she focused on the role of adaptive immunity and B lymphocytes in COPD and demonstrated the presence of a smoke-induced specific immune response, which differed between COPD patients and healthy controls. After that, she steered her research focus to the role of accelerated lung aging and abnormal tissue repair in COPD, which is currently her main research focus. Using primary lung cells and lung tissue from well-characterized COPD patients and non-COPD control subjects she tries to unravel the molecular mechanisms underlying accelerated lung aging and abnormal tissue repair in COPD. For this, she uses a “multi-omics” approach combining information on changes in the genome (DNA), transcriptome (RNA, miRNA) and the proteome (protein) to identify causal molecular networks in COPD.  


3D Culture of human lung fibroblasts decreases proliferative and increases extracellular matrix remodeling genes

A bronchial gene signature specific for severe COPD that is retained in the nose

Age-associated differences in the human lung extracellular matrix

A proteomics approach to identify COPD-related changes in lung fibroblasts

Cellular Senescence Is Associated With Extracellular Matrix Dysregulation in COPD

Collagen type XIV is proportionally lower in the lung tissue of patients with IPF

IL-1β Induces a Proinflammatory Fibroblast Microenvironment that Impairs Lung Progenitors' Function

IL-33 Expression Is Lower in Current Smokers at Both Transcriptomic and Protein Level

Smoking increases expression of the SARS-CoV-2 spike protein-binding long ACE2 isoform in bronchial epithelium

Smoking induces shifts in cellular composition and transcriptome within the bronchial mucus barrier

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Is COPD een verzamelnaam voor verschillende ziekten?

Interview Longwijzer