Norbert Weissmann is Professor for Molecular Mechanisms of Emphysema, Hypoxia and Lung Aging at the Department of Internal Medicine, Justus Liebig University (JLU) Giessen, Germany. He studied biology and obtained his PhD at JLU Giessen in 1994. After a postdoctoral training at JLU, he habilitated in 2002.
Norbert is spokesperson of the German Research Foundation (DFG)-funded Collaborative Research Center (CRC) 1213 “Pulmonary Hypertension and Cor Pulmonale”. He is head or member of several JLU boards, including the senate and two PhD boards. Moreover, he is council member of the Faculty of Medicine at JLU. Norbert is area leader and steering committee member of the Cardio-Pulmonary Institute. He is editorial board member of the American Journal of Respiratory and Critical Care Medicine and Associate Editor of the American Journal of Respiratory Cell and Molecular Biology.
The Weissmann lab focuses on pulmonary oxygen sensing and signaling, including pulmonary hypertension (PH). Moreover, mechanisms of chronic obstructive pulmonary disease (COPD) and ageing are part of his research.
The group´s work substantially contributed to progress in the above fields by - among others - the following selected publications:
Oxygen sensing and signaling, including PH:
- SPARC, a Novel Regulator of Vascular Cell Function in Pulmonary Hypertension (Circulation 145:916-933, 2022. doi: 1161/CIRCULATIONAHA.121057001)
- Bypassing mitochondrial complex III using alternative oxidase inhibits acute pulmonary oxygen sensing (Sci Adv 6:eaba0694, 2020. doi: 10.1126/sciadv.aba0694)
- Mitochondrial complex IV Subunit 4 isoform 2 is essential for acute pulmonary oxygen sensing (Circ Res 121:424-438, 2017. doi: 10.1161/CIRCRESAHA.116.310482)
- Pro-proliferative and inflammatory signaling converge on FoxO1 transcription factor in pulmonary hypertension (Nat Med 20:1289-1300, 2014. doi: 10.1038/nm.3695)
- Activation of TRPC6 channels is essential for lung ischaemia-reperfusion induced oedema in mice (Nature Commun 3:649, 2012. doi: 10.1038/ncomms1660)
- PAR-2 inhibition reverses experimental pulmonary hypertension (Circ Res 110:1179-1191, 2012. doi: 10.1161/CIRCRESAHA.111.257568)
- Fhl-1, a new key protein in pulmonary hypertension (Circulation 118:1183-1194, 2008. doi: 10.1161/CIRCULATIONAHA.107.761916)
- Classical transient receptor potential channel 6 (TRPC6) is essential for hypoxic pulmonary vasoconstriction and alveolar gas exchange (Proc Natl Acad Sci. U.S.A. 103:19093-19098, 2006. doi: 10.1073/pnas.0606728103)
Mechanisms of COPD and aging
- CEACAM6 as a Novel Therapeutic Target to Boost HO-1—mediated Antioxidant Defense in COPD (Am J Respir Crit Care Med 207:1576-1590, 2023)
- Fibroblast growth factor 10 reverses cigarette smoke- and elastase-induced emphysema and pulmonary hypertension in mice (Eur Respir J doi: 10.1183/13993003.01606-2022)
- Nicotine promotes e-cigarette vapour-induced lung inflammation and structural alterations (Eur Respir J 61:2200951, doi: 10.1183/13993003.00951-2022)
- Myeloid-cell-specific deletion of inducible nitric oxide synthase protects against smoke-induced pulmonary hypertension in mice (Eur Respir J 59:2101153, 2022. doi: 10.1183/13993003.01153-2021)
- Amelioration of elastase-induced lung emphysema and reversal of pulmonary hypertension by pharmacological iNOS inhibition in mice (Br J Pharmacol 178:152-171, 2021. doi: 10.1111/bph.15057)
- NADPH oxidase subunit NOXO1 is a target for emphysema treatment in COPD (Nat Metab 2:532-546, 2020. doi: 10.1038/s42255-020-0215-8)
- Inducible NOS inhibition reverses tobacco-smoke-induced emphysema and pulmonary hypertension in mice (Cell 147:293-305, 2011. doi: 10.1016/j.cell.2011.08.035)
Further/ongoing projects deal with:
- Identifying molecular targets for reversing PH/COPD(-PH)
- Deciphering the role of reactive oxygen species and protein nitration in PH/COPD (-PH)
- Role of macrophages in COPD-PH pathogenesis and its reversal
- Unraveling the pulmonary cell type/intracellular structure essential for oxygen sensing
- The role of novel transcription factors in vascular cell dysfunction and PH pathogenesis
The Weissmann lab offers:
Disease modeling and phenotyping
- Tobacco smoke-induced COPD/COPD-PH
- chronic hypoxia-induced PH
- e-cigarette-induced COPD
Key technologies:
- Hemodynamics
- Echocardiography
- Lung function testing
- AAV approaches of gene silencing/overexpression
Ex vivo models of human diseases
- Precision cut lung slices (PCLS)
In vitro cell culture
- Primary cell isolation (SMC, EC, FB, macrophages, AT2, pericytes)
- Organoids
- in vitro exposure system (hypoxia, tobacco smoke/e-cigarette smoke)
Electrophysiology
- Electrophysiology (patch clamp, 2 electrode voltage clamp, Raman spectroscopy)
- Myograph
Molecular Biology
- General molecular biology techniques
- Automated capillary-based Western blot analysis (Jess)
- Laser microdissection (LMD)
Imaging
- Histological staining (paraffin/cryo; IHC/IF)
- EVOS Fluorescent Cell Imaging System
- Incucyte
- Confocal microscopy
- Calcium imaging
State-of-the-art methods
- Electron spin resonance (ESR) for measurement/detection of reactive oxygen species (ROS)
Contact
Prof. Dr. Norbert Weißmann
Justus-Liebig University Giessen
ECCPS Building
Aulweg 130
35392 Giessen
Tel: +49 (0) 641 99 42414
Fax: +49 (0) 641 99 42419
Email: Norbert.Weissmann@innere.med.uni-giessen.de
