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Nina_Wettschureck
Prof. Dr. Nina Wettschureck

Max Planck Institute for Heart and Lung Research
Department of Pharmacology
Ludwigstr. 43
61231 Bad Nauheim
Germany

Phone: +49 (0)6032 705 1214
Fax: +49 (0)6032 705 1204
E-mail: This email address is being protected from spambots. You need JavaScript enabled to view it.


Curriculum Vitae

Since 2012                    Professor for Molecular Pharmacology, University of Frankfurt / Main

Since 2009                    Group Leader, Max-Planck-Institute for Heart and Lung Research Bad Nauheim.

2007                             "Habilitation" for Pharmacology and Toxicology, University of Heidelberg

2000 - 2009                   Postdoctoral Research Fellow, Institute of Pharmacology, University of Heidelberg

1998 – 2000                  Postdoctoral Research Fellow, Institute of Pharmacology, FU Berlin

1996 – 1998                  Dept. of Internal Medicine V, University of Heidelberg

1990 – 1996                  Studies of Medicine, M.D. degree, University of Frankfurt / Main, Germany

 

G-protein signaling group (Wettschureck group)

Group leader: Nina Wettschureck

Postdocs: Denise Tischner, Harmandeep Kaur

PhD students: Jorge Carvalho, Myriam Grimm

Technical assistant: Karin Jäcklein

Our group analyzes basic mechanisms of G-protein signaling in the cardiovascular and immune system. Using various in vitro techniques as well as conditional knockout mice, we identified new functions for the G-protein families G12/13 and Gq/11 in the regulation of immune cells (Herroeder et al., Immunity 2009; Grimm et al., ATVB 2016), endothelial cells (Sivaraj et al., Dev Cell 2013; Sivaraj et al., Cardiovasc Res 2015), endocrine cells (Sassmann et al., J Clin Invest 2010), and cardiomyocytes (Takefuji et al., Circulation 2012; Takefuji et al., J Exp Med 2013). We furthermore showed that the G-protein-coupled receptor HCA2 crucially contributes to the therapeutic effect of dimethyl fumarate in neuroinflammation (Chen et al., J Clin Invest 2014). Other ongoing projects focus on the mechanisms regulating cardiac fibroblast activation (Kaur et al., Circ Res 2016). New projects currently evolve based on single-cell expression analyses in primary murine vascular and immune cells (Kaur et al., Nat Commun 2017; Tischner et al., J Clin Invest Insight 2017). These analyses identified rare cell populations with specific GPCR repertoires; the role of these GPCRs in the regulation smooth muscle differentiation, endothelial activation, or regulation of T cell pathogenicity is currently under investigation.

 Wettschureck group projects illustrated

Graphical overview over the topics addressed by the G-protein signaling group.

 
Selected references

1. Tischner D, Grimm M, Kaur H, Staudenraus D, Carvalho J, Looso M, Günther S, Wanke F, Moos S, Siller N, Breuer J, Schwab N, Zipp F, Waisman A, Kurschus FC, Offermanns S, Wettschureck N (2017): Single-cell profiling reveals GPCR heterogeneity and functional patterning during neuroinflammation. JCI Insight 3;2(15), doi: 10.1172.

2. Kaur H, Carvalho J, Looso M, Singh P, Chennupati R, Preussner J, Günther S, Albarrán-Juárez J, Tischner D, Classen S, Offermanns S, Wettschureck N (2017): Single-cell profiling reveals heterogeneity and functional patterning of GPCR expression in the vascular system. Nat Commun 8:15700; DOI: 10.1038.

3. Kaur H, Takefuji M, Ngai C, Carvalho J, Bayer J, Wietelmann A, Poetsch A, Holper S, Conway SJ, Mollmann H, Looso M, Troidl C, Offermanns S, Wettschureck N (2016): Targeted Ablation of Periostin-Expressing Activated Fibroblasts Prevents Adverse Cardiac Remodeling in Mice. Circ Res. 118:1906-17.

4. Grimm M, Tischner D, Troidl K, Albarran Juarez J, Sivaraj KK, Ferreiros Bouzas N, Geisslinger G, Binder CJ, and Wettschureck N (2016): S1P2/G12/13 Signaling Negatively Regulates Macrophage Activation and Indirectly Shapes the Atheroprotective B1-Cell Population. Arterioscler Thromb Vasc Biol 36:37-48.

5. Sivaraj KK, Li R, Albarran-Juarez J, Wang S, Tischner D, Grimm M, Swiercz JM, Offermanns S, and Wettschureck N (2015): Endothelial Galphaq/11 is required for VEGF-induced vascular permeability and angiogenesis. Cardiovasc Res 108:171-80.

6. Chen H, Assmann JC, Krenz A, Rahman M, Grimm M, Karsten CM, Kohl J, Offermanns S, Wettschureck N*, and Schwaninger M* (2014): Hydroxycarboxylic acid receptor 2 mediates dimethyl fumarate's protective effect in EAE. J Clin Invest 124:2188-92. (*contributed equally)

7. Sivaraj KK, Takefuji M, Schmidt I, Adams RH, Offermanns S, and Wettschureck N (2013): G13 controls angiogenesis through regulation of VEGFR-2 expression. Dev Cell 25:427-34.

8. Takefuji M, Kruger M, Sivaraj KK, Kaibuchi K, Offermanns S, and Wettschureck N (2013): RhoGEF12 controls cardiac remodeling by integrating G protein- and integrin-dependent signaling cascades. J Exp Med 210:665-73.

9. Takefuji M, Wirth A, Lukasova M, Takefuji S, Boettger T, Braun T, Althoff T, Offermanns S, and Wettschureck N (2012): G13-mediated signaling pathway is required for pressure overload-induced cardiac remodeling and heart failure. Circulation 126:1972-82.

10. Sassmann A, Gier B, Grone HJ, Drews G, Offermanns S, and Wettschureck N (2010): The Gq/G11-mediated signaling pathway is critical for autocrine potentiation of insulin secretion in mice. J Clin Invest 120:2184-93.

11. Herroeder S, Reichardt P, Sassmann A, Zimmermann B, Jaeneke D, Hoeckner J, Hollmann MW, Fischer KD, Vogt S, Grosse R, Hogg N, Gunzer M, Offermanns S, Wettschureck N (2009): Guanine nucleotide-binding proteins of the G12 family shape immune functions by controlling CD4+ T cell adhesiveness and motility. Immunity 30:708-20.