Cagla Eroglu

Cagla Eroglu is a Turkish neuroscientist and Associate Professor of Cell Biology and Neurobiology at Duke University in Durham, North Carolina. Eroglu is also the Director of Graduate Studies in Cell and Molecular Biology at Duke University Medical Center. Eroglu is a leader in the field of glial biology and her lab focuses on exploring the role of glial cells, specifically astrocytes, in synaptic development and connectivity.
Early life and education.
Eroglu was born in Turkey and pursued her Bachelors in Chemical Engineering from 1992 to 1996 at the Middle East Technical University in Ankara, Turkey. After completing her B.Sc., Eroglu pursued a Masters in Molecular Biology at the Bilkent Üniversitesi in Ankara, Turkey in 1996. After completing her Masters in 1998, Eroglu moved to Germany to pursue her graduate studies in Molecular Biology at Ruprecht-Karls-Universität Heidelberg in Germany. Eroglu’s Ph.D. was supported by the European Molecular Biology Laboratory Ph.D. program as she studied under the mentorship of Irmgard Sinning, whose lab moved from EMBL to Heidelberg University in 2000. Eroglu’s Ph.D. was broadly focused in the study of membrane proteins biology. Using Drosophila as a model organism, Eroglu looked at how metabotropic glutamate receptor (mGluRs) affinity is modulated. She found that when mGluRs are associated with cholesterol rich lipid rafts within the membrane, they exist in a high affinity state for glutamate. When mGluRs are not associated with sterol-rich rafts, they exist in a low affinity state for glutamate binding.
After completing her Ph.D. in 2002, Eroglu came to the United States to study under the mentorship of Ben Barres at Stanford University. Eroglu began studying glial cells under Barres’ mentorship. Eroglu, along with her colleagues in the Barres Lab, brought to light the critical and understudied role glial cells play in shaping synapses and neural circuits during development. Eroglu and her team found that an astrocyte derived factor, called Thrombospondin, is important in promoting synaptogenesis in the central nervous system. Eroglu then characterized the receptor to which Thrombospondin binds, called α2δ-1, which happened to also be the receptor to which the drug gabapentin binds. When they over-expressed α2δ-1, they found increases in synaptogenesis and when they blocked the receptor with gabapentin, they found markedly decreased excitatory synapse formation. Her findings showed both the role that astrocyte secreted factors play in specifically excitatory synapse formation, as well as the potential therapeutic mechanism why which gabapentin is able to mediate analgesia and prevent seizures. Another discovery that Eroglu made while in the Barres Lab was the identification and function of hevin and SPARC, two astrocyte-secreted proteins, in the regulation of excitatory synapse development. She found that hevin induces the formation of synapses, while SPARC antagonizes the synaptogenic actions of hevin. Her further further highlighted the critical role astrocytes play in the direct regulation of synapse formation in the central nervous system. Eroglu completed her postdoctoral work in 2008.
Career and research.
In 2008, Eroglu joined the faculty at Duke University as an Associate Professor in the Department of Cell Biology and in the Department of Neuroscience. Eroglu is also a Faculty Network Member of the Duke Institute for Brain Sciences, an Associate of the Duke Initiative for Science and Society, an Affiliate of the Regeneration Next Initiative, as well as a member of the ALICE program within the Duke University School of Medicine.
Eroglu’s lab studies the mechanisms underlying synaptic connectivity in the central nervous system. The lab focuses significantly on the cellular and molecular role astrocytes play in shaping synapse development, function, and plasticity. Their focus on the communication between astrocytes and neurons in the healthy brain is paving the way towards eventually understanding how this communication becomes pathological in disease states and how it can be therapeutically targeted.
Synapse development in Huntington's Disease.
Eroglu and her team sought to understand how synaptic connectivity was altered in models of Huntington’s Disease. They directly probed the role of Huntingtin protein (htt) in synaptic connectivity and they found that when htt was silenced, excitatory synapses in the cortex and striatum formed at a rapid pace and then started to deteriorate shortly after their rapid development. They then knocked-in the disease causing htt mutation and saw similar findings to when they knocked out htt suggesting that proper htt function is necessary for normal cortical and striatal development.
Astrocytes in cortical development.
After discovering hevin, the astrocyte secreted factor implicated in synapse development, in her postdoctoral work, Eroglu continued to explore its role in shaping cortical development in the mouse brain. She found that, when hevin is knocked out, there are reductions in the thalamocortical synapses yet increases in excitatory connections within the cortex. They further found that critical pruning of spines with multiple excitatory contacts fails to take place when hevin is knocked out. These in vivo results emphasize the critical regulatory role played by the astrocytic factor, hevin, in normal cortical development.
Thrombospondin.
Eroglu and a team of researchers were interested in exploring the therapeutic potential of human Umbilical Tissue Derived cells (hUTCs) in synaptogenesis. They found that hUTCs could support neural growth specifically through the release of thrombospondin. A further in depth analysis into the role of thrombospondin and their receptors α2δ-1, which Eroglu discovered in her postdoc, highlighted the critical role signalling between thrombospondin and their receptors have in synaptogenesis. Eroglu then found that specifically inhibiting postsynaptic α2δ-1 (thrombospondin receptors) on neurons leads to decreased synaptogenesis and spine formation. They further show that the regulation of synaptogenesis is dependent on Rac1, suggesting its role in development and pathology.