Peer-Reviewed Publications

• Lutz SE.#, Smith JR., Kim DH., Olson CVL., Ellefsen K., Bates JM., Gandhi SP., Agalliu D.#, (2017). Caveolin1 Is Required for Th1 Cell Infiltration, but Not Tight Junction Remodeling, at the Blood-Brain Barrier in Autoimmune Neuroinflammation. #Co-corresponding authors. Cell Reports 21 (8):2104–2117.  
• Lim RG., Quan C., Reyes-Ortiz AM., Lutz SE., Kedaigle AJ., Gipson TA., Vatine GD., Stocksdale J., Casale MS., Svendsen CN., Frankel E., Housman DE., Agalliu D., Thompson LM. (2017). Huntington’s Disease iPSC-Derived Brain Microvascular Endothelial Cells Reveal WNT-Mediated Angiogenic and Blood-Brain Barrier Deficits. Cell Reports, 19(7):1365-1377. Protective role for Wnt/beta-catenin pathway in BBB endothelial cells in Huntington’s disease human brains and iPS cells.
• Lengfeld J.*, Lutz SE.*#, Smith JR., Diaconu C., Scott C., Koffman SB., Choi C., Walsh CM., Raine CS., Agalliu I., Agalliu D#. (2017). Endothelial Wnt/β-catenin signaling reduces immune cell infiltration in multiple sclerosis. *Equal contribution co-first-authors. #Co-corresponding authors. Proceedings of the National Academy of Sciences, 114(7): E1168–E1177. We establish a novel protective role for endothelial Wnt/beta-catenin in suppressing adhesion molecule expression and caveolar transcytosis of CD4+ T cells across the blood-brain barrier in human multiple sclerosis and animal models.
• Velasquez S., Malik S., Lutz SE., Scemes E., Eugenin EA.  Pannexin1 channels are required for chemokine-mediated migration of CD4+ T Lymphocytes: Role in Inflammation and Experimental Autoimmune Encephalomyelitis. The opening of Pannexin-1 high conductance plasma membrane channels causes ATP release, purinergic receptor activation, and tissue damage. We now show that CXCL12/SDF1α results in transient opening of Pannexin-1 channels in CD4+ T lymphocytes. The resultant ATP secretion causes focal adhesion kinase phosphorylation, enhanced lymphocyte migration, and autoimmunity in target tissues. Deletion of Pannexin-1 reduces CD4+ T-lymphocyte migration into the spinal cord of mice with EAE. Targeting Pannexin-1 channel activity could provide new therapeutic approaches to limit T-lymphocyte migration in autoimmune disease. Journal of Immunology 2016, 196(10):4338-47.
• Chinnasamy C., Lutz SE., Riascos-Bernal DF., Jeganathan V., Casimiro I., Brosnan CF., Sibinga NE.  Loss of Allograft inflammatory factor-1 ameliorates experimental autoimmune encephalomyelitis by limiting encephalitogenic CD4 T cell expansion.  Molecular Medicine, 2015, 21:233-41.
• Knowland D, Arac A, Sekiguchi KJ, Hsu M, Lutz SE, Perrino J, Steinberg GK, Barres BA, Nimmerjahn A, Agalliu D (2014).  Stepwise Recruitment of Transcellular and Paracellular Pathways Underlies Blood-Brain Barrier Breakdown in Stroke.  Neuron. 2014 May 7;82(3):603-17. We demonstrated that there is an increase in transcellular followed by paracellular barrier permeability after the transient Middle Cerebral Artery Occlusion (tMCAo) model of stroke using functional assays and intravital two-photon microscopy in transgenic mice with green fluorescent tight junction proteins.
• Lutz SE., Gonzalez-Fernandez E., Ventura JCC., Perez-Samartin A., Tarassishin L., Negoro H., Patel NK., Suadicani SO., Lee SC., Matute C., Scemes E. (2013). Contribution of pannexin1 to experimental autoimmune encephalomyelitis.  PLoS ONE 8(6): e66657. Pannexins permit transient passage of cytosolic contents into the extracellular space. We employed an acute spinal cord slice preparation to demonstrate that ATP is released from EAE spinal cords in a Pannexin1-dependent manner. We showed that mice deficient in Pannexin1 channels, or treated with a pharmacologic inhibitor, exhibit delayed onset of EAE and decreased mortality, demyelination and inflammation.  
• Negoro H, Lutz SE, Liou LS, Kanematsu A, Ogawa O, Scemes E, Suadicani SO. (2013). Pannexin 1 involvement in bladder dysfunction in a multiple sclerosis model.  Scientific Reports 3 Article 2152. doi: 10.1038/srep02152. A common clinical issue for MS patients is urinary incontinence. The MOG EAE model reproduces neurogenic bladder dysfunction, which was ameliorated in Pannexin1-/- mice due to decreased interleukin-1β production.
• Lutz SE, Raine CS, Brosnan CF (2012).  Loss of astrocyte connexins 43 and 30 does not significantly alter susceptibility or severity of acute experimental autoimmune encephalomyelitis in mice. Journal of Neuroimmunology 245(1-2):8-14.
• Santiago MF, Veliskova J, Patel NK, Lutz SE, Caille D, Charollais A, Meda P, Scemes E (2011). Targeting Pannexin1 improves seizure outcome.  PLoS ONE 6(9): e25178.
• Lutz SE, Zhao Y, Gulinello M, Lee S, Raine CS, Brosnan CF (2009).  Deletion of astrocyte connexin 43 and 30 leads to a dysmyelinating phenotype and hippocampal CA1 vacuolation.  Journal of Neuroscience 29(24):7743-52. We showed that in the absence of astrocyte gap junctions, oligodendrocytes make less myelin, fail to wrap axons, and undergo apoptosis.  Astrocytes become hypertrophic and vacuolated.  These mice exhibit behavioral abnormalities. This work supports the critical importance of the astrocyte-oligodendrocyte pan-glial syncytium for white and gray matter ultrastructural and functional integrity.
• Omari KM, Lutz SE, Santambrogio L, Lira SA, Raine CS (2009).  Neuroprotection and remyelination in experimental autoimmune encephalomyelitis (EAE) mice inducibly over-expressing CXCL1.  American Journal of Pathology 174: 164-176.
• Buch S, Khurdayan VK, Lutz SE, Knapp PE, El-Hage N, Hauser KF (2007).  Glial-restricted precursors: Patterns of expression of opioid receptors and relationship to HIV-1 Tat and morphine susceptibility in vitro.  Neuroscience 146(4):1546-54.
• Zhao Y, Rivieccio MA, Lutz S, Scemes E, Brosnan CF (2006).  The TLR3 ligand polyI: C downregulates connexin 43 expression and function in astrocytes by a mechanism involving the NF-kappaB and PI3 kinase pathways. Glia 54(8):775-85.
• Singh IN, El-Hage N, Campbell ME, Lutz SE, Knapp PE, Nath A, Hauser KF (2005).  Differential involvement of p38 and JNK MAP kinases in HIV-1 Tat and gp120-induced apoptosis and neurite degeneration in striatal neurons.  Neuroscience 135(3):781-90.
• Khurdayan VK, Buch S, El-Hage N, Lutz SE, Goebel SM, Singh IN, Knapp PE, Turchan-Cholewo J, Nath A, Hauser KF (2004).  Preferential vulnerability of astroglia and glial precursors to combined opioid and HIV-1 Tat exposure in vitro.  European Journal of Neuroscience 19:3171-3182.
• Singh IN, Goody RJ, Dean C, Ahmad NM, Lutz SE, Knapp PE, Nath A, Hauser KF (2004).  Apoptotic death of striatal neurons induced by HIV-1 Tat and gp120: differential involvement of caspase-3 and endonuclease G.  Journal of Neurovirology 10:141-151.

Reviews, Book chapters, and Commentaries:

• Lutz SE and Tenner A.  C1q as a unique player in angiogenesis with therapeutic implication in wound healing.  This is a “News and Views” on an article by Bossi et al., Proc Natl Acad Sci USA. 2014; 111:4209-4214.  Published in Focus On Complement, the Newsletter of the International Complement Society, Issue 34, June 1 2014.
• Lutz SE*, Lengfeld J*, Agalliu D.  Stem cell-based therapies for multiple sclerosis: recent advances in animal models and human clinical trials.  Regen Med. 2014 Mar;9(2):129-32
• Lutz SE, Raine CS, Brosnan CF.  Astrocyte involvement in the acquired demyelinating diseases.  In “Astrocytes: Wiring the Brain,” Book editors: E. Scemes and D.C. Spray.  Pages 283-310. Boca Raton: CRC Press. 2012