Research Group Regulatory Mechanisms of Inflammation, Institute of Medical Biochemistry, Centre for Molecular Biology of Inflammation, University of Münster, 48149 Münster, Germany
Peynaz Candan
Research Group Regulatory Mechanisms of Inflammation, Institute of Medical Biochemistry, Centre for Molecular Biology of Inflammation, University of Münster, 48149 Münster, Germany
Nadia Korthals
Research Group Regulatory Mechanisms of Inflammation, Institute of Medical Biochemistry, Centre for Molecular Biology of Inflammation, University of Münster, 48149 Münster, Germany
Christoph Wenzel
Institut für Pharmakologie, Universitätsmedizin Greifswald, 17489 Greifswald, Germany
Hannah Ihle
Institute of Forensic Medicine, University Hospital Jena, 07747 Jena, Germany
Department of General, Visceral, Thoracic and Vascular Surgery, Greifswald University Medical Center, 17475 Greifswald, Germany
Michael Schöfbänker
Institute of Virology (IVM), Center for Molecular Biology of Inflammation (ZMBE), University Hospital Münster, University of Münster, 48149 Münster, Germany
Institute of Forensic Medicine, University Hospital Jena, 07747 Jena, Germany
Stefan Oswald
Institut für Pharmakologie und Toxikologie, Universitätsmedizin Rostock, 18057 Rostock, Germany
Stephan Ludwig
Institute of Virology (IVM), Center for Molecular Biology of Inflammation (ZMBE), University Hospital Münster, University of Münster, 48149 Münster, Germany
Ursula Rescher
Research Group Regulatory Mechanisms of Inflammation, Institute of Medical Biochemistry, Centre for Molecular Biology of Inflammation, University of Münster, 48149 Münster, Germany
In late 2019, the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) as the causative agent of coronavirus disease 2019 (COVID-19) emerged in China and spread rapidly around the world, causing an ongoing pandemic of global concern. COVID-19 proceeds with moderate symptoms in most patients, whereas others experience serious respiratory illness that requires intensive care treatment and may end in death. The severity of COVID-19 is linked to several risk factors including male sex, comorbidities, and advanced age. Apart from respiratory complications, further impairments by COVID-19 affecting other tissues of the human body are observed. In this respect, the human kidney is one of the most frequently affected extrapulmonary organs and acute kidney injury (AKI) is known as a direct or indirect complication of SARS-CoV-2 infection. The aim of this work was to investigate the importance of the protein angiotensin-converting enzyme 2 (ACE2) for a possible cell entry of SARS-CoV-2 into human kidney cells. First, the expression of the cellular receptor ACE2 was demonstrated to be decisive for viral SARS-CoV-2 cell entry in human AB8 podocytes, whereas the presence of the transmembrane protease serine 2 (TMPRSS2) was dispensable. Moreover, the ACE2 protein amount was well detectable by mass spectrometry analysis in human kidneys, while TMPRSS2 could be detected only in a few samples. Additionally, a negative correlation of the ACE2 protein abundance to male sex and elderly aged females in human kidney tissues was demonstrated in this work. Last, the possibility of a direct infection of kidney tubular renal structures by SARS-CoV-2 was demonstrated.
