Michael Matise, PhD

Dr. Matise is an Associate Professor in the Department of Neuroscience and Cell Biology, current organizer of the Rutgers-Central NJ Brain Bee, and former Co-director of the Neuroscience SURP at Rutgers. He received a PhD in Neuroscience in 1994 from the University of Pittsburgh under Dr. Cynthia Lance-Jones where his work focused on defining a "critical period" for motoneuron muscle-target specification using classical embryological approaches in chick embryos, and postdoctoral training in Developmental Genetics at the Skirball Institute/NYU Medical School with Dr. Alexandra Joyner, where he used gene targeting and transgenic mice to establish the central role of Gli proteins in mediating the transcriptional response to morphogenic Sonic Hedgehog signaling in the embryonic spinal cord. He established his own lab in the Department of Neuroscience & Cell Biology in 2000 where his work continues to make important contributions to understanding the role of Shh signaling in both the healthy and injured or diseased CNS.

Research Interests

**Dr. Matise is not currently accepting PhD students in his lab.**

Pubmed link to Dr. Matise's publications.

The coordinated symphony of interactions that take place between cells in the CNS are crucial for its development, function, and ability to adapt and respond to injury and disease. Research in my laboratory focuses on understanding the molecular mechanisms governing these interactions, with particular interest in the role of the Sonic hedgehog (Shh) signaling pathway.

While our past work has contributed to a better understanding of the role of the Shh pathway in CNS development, we have recently shifted our focus to examine its role in the adult CNS. The overall goal of this work is to elucidate the molecular and signaling mechanisms employed by cells within the CNS to maintain homeostasis and responds to injury or disease. Our current studies employ cutting edge molecular genetic, surgical, pharmacological, histological and transcriptomic approaches in mice.

We are interested in uncovering the role of Shh signaling in adult astrocytes. These important support cells play a central role in the process of reactive gliosis, which helps protect the CNS from damage and disease by restoring tissue homeostasis but can itself create problems if it becomes chronic. Chronic reactive gliosis is associated with the development of various neurological disorders including AD, MS and ALS. Thus, understanding the mechanisms that trigger this process in the CNS has direct clinical significance. Despite this, our current knowledge of the specific roles that different glial cell types and signaling pathways play in reactive gliosis is incomplete.

The two primary cell types in the CNS that mediate reactive gliosis are astrocytes and microglia. Astrocytes in particular are known to play various and important roles in response to CNS inflammation and insult, including helping to repair tissue damage by forming a “glial scar” and restoring the BBB. Notably, recent molecular genetic evidence indicates that astrocytes respond in a specific way to different inducing stimuli. However, one major outstanding question that remains is whether distinct subsets of astrocytes exist in the CNS that play specific roles in response to different inducements.

It has previously been shown that a subset of protoplasmic astrocytes in the CNS maintain responsiveness to Sonic Hedgehog (Shh) signaling into adulthood. These cells can be identified by their unique expression of Gli1, a target gene of the Shh pathway that is only turned on in cells when the pathway is turned on by ligand binding to the Ptch1 receptor, or by de-repression. Gli1+ cells populate the gray matter regions of the deep cortical layers, parts of the striatum, the hypothalamus, the thalamus, brainstem and spinal cord, among other regions. Notably, we have found that Gli1+ astrocytes mount a novel response to diverse types of brain injuries, placing them in a central role in this process. Our observations indicate that Gli1+ cells possess a unique molecular and functional identity that distinguishes them from all other glial cell types in the CNS.