Trauma and sensory systems: Biological mechanisms involving the skin and the 17q21 gene cluster.

Abstract

Childhood trauma experience increases risk for neuropsychiatric and neurodevelopmental disorders, including posttraumatic stress disorder (PTSD), autism spectrum disorders (ASDs), and attention deficit/hyperactivity disorder (ADHD). While the biological mechanisms connecting adverse experiences with later disease presentation are not clear, the concept of Gene x Environment x Development (GxExD) interactions has significant implications for improving our understanding of these diseases. We recently utilized this approach in a study where we found that women exposed to interpersonal violence trauma (the E) uniquely during adolescence (the D), but not childhood or adulthood, had novel protein biomarkers (the G) associated with a sensory cell system in the skin, Merkel cells. Merkel cell mechanosensory signaling is important in gentle and social touch, inflammation-induced pain, and the skin's neuroendocrine stress response. Further, keratinocyte-derived Merkel cell final maturation occurs during the identified vulnerable period of adolescence. Interestingly, many of the genes identified in our study belong to a known 17q21 gene cluster, suggesting an identifiable location in the genome permanently altered by adolescent trauma. These results form a potential functional link between mechanosensory Merkel cells and the pathology and sensory symptomatology in PTSD. Future research directions could identify specific mechanisms involved in tactile alterations following trauma in hopes of revealing additional biomarkers and potentially leading to novel tactile-involved therapies (e.g., massage, electroacupuncture, or focused ultrasound).