1/30 – Sana Nasim, Boston Children’s Hospital & Harvard Medical School
Biomedical Engineering Seminar
January 30, 2026
11:00 AM - 12:00 PM
Location
BME Seminar in SEO 236
Address
851 S Morgan St, Chicago, IL 60607
Calendar
Download iCal FileSpeaker:
Sana Nasim, PhD
Instructor, Vascular Biology Program
Boston Children's Hospital
Harvard Medical School
Title: Exploring the Mechanisms of Capillary Malformations: Macrophages, Increased Permeability and MAPK Signaling Provide Therapeutic Insights
Abstract: During early embryogenesis, blood vessels are formed through the process of vasculogenesis. Once this primitive network is established, the vessels differentiate into a network of capillaries, veins, arteries, and lymphatics. Most vascular malformations occur as a result of somatic mutations that cause aberrant expression of vascular determinants, leading to alterations in cellular signaling and differentiation. These somatic mutations arise during or after embryonic development and are not inherited as part of the germline DNA. Vascular malformations are defects in the architecture and function of endothelial cells and their surrounding mural cells. They can manifest as simple birthmarks or progress to severe, life-threatening vascular abnormalities.
My research focuses on capillary malformations, a slow-flow vascular abnormality that primarily presents as cutaneous lesions but can also extend to cerebral and ocular regions. In 90% of cases, capillary malformations are associated with a somatic activating mutation in GNAQ (p.R183Q), which is enriched in endothelial cells. Through my work, I have identified key characteristics of GNAQ driven malformation, including increased vascular permeability and molecular factors that compromise the endothelial barrier in mutant cells. These findings highlight potential therapeutic targets for restoring normal capillary architecture. Additionally, I have observed elevated macrophage localization and adhesion in brain lesions, as well as distinct morphological, cellular, and molecular differences between skin and brain capillary malformations. Furthermore, I discovered that mutant endothelial cells fail to align in response to flow and exhibit dysregulated signaling pathways, contributing to the progression of the disease.
In my lab, I aim to develop a multicellular model that incorporates extracellular matrix components, soluble factors, and physical forces. These elements will collectively provide the necessary cues to regulate cellular function, enabling us to investigate the role of cellular interactions and signaling. The multicellular model will also serve as a predictive platform for drug screening in contrast to traditional 2D cell cultures, effectively mimicking tissue responses to drugs and allowing for the evaluation of drug efficacy and toxicity. Furthermore, I plan to adapt this platform to study other vascular entities, with the goal of identifying targeted therapies.
Date posted
Dec 5, 2025
Date updated
Dec 5, 2025