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Speaker: Dr. Kalpana Mandal
Terasaki Institute for Biomedical Innovation
Title: "Mechanotransduction and Biochemical Signaling in
Biopolymer-Based Adhesive Materials: Insights into
Cellular Dynamics and Applications".
Day and Date: Thursday, July 17, 2025
Time: 11.00 am.
Venue: Room no. 350, Chemistry Department
Second floor, Annex
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Hosted by Prof. Amber Jain
Abstract The rapidly advancing field of biopolymers and adhesive
materials is transforming both biomedical engineering and industrial
technology. This transformation lies in the dynamic interplay between
an understanding of cellular behavior and development of the
materials that emulate these dynamic interactions. This approach
addresses critical biomedical needs like smart wound healing and
high-performance sealants, while also expanding industrial
applications in packaging, marine engineering, and advanced electronics.
Traditional biopolymers like hyaluronic acid (HA) and GelMA
(both are extracellular matrix (ECM) proteins) remain
invaluable for applications in tissue engineering and drug delivery due
to their biocompatibility and tunable properties. Central to this
progress lies in understanding cellular mechanotransduction. In our
recent research we investigated the role of upregulated HA in
hepatocellular carcinoma (HCC). Results show that the HCC cells can
organize their cytoskeleton and move effectively on ultra-soft HA
substrates (300 Pa), much as they do on much stiffer ones prepared with
polyacrylamide (PAA) substrate (>30 kPa), when provided with essential
biochemical signals such as HA and integrin ligands.
However, the traction force generated on HA substrate is much lower than
the stiff PAA substrate. This demonstrates that chemical signals can
compensate for mechanical tension in cytoskeletal signaling, a process
dependent on polyphosphoinositide turnover and Akt pathway activation.
Our research further explores the distinct response of normal hepatocytes
and HCC cells to mechanical properties of biopolymers such as elasticity
and viscoelasticity. Unlike normal cells, Huh7 HCC cells spread faster
and wider on viscoelastic substrates and exhibit enhanced motility and
protrusions. Our model suggests that the stress relaxation time scales of
viscoelastic substrates regulate cellular dynamics, indicating differing
binding-unbinding rates of adhesion proteins in HCC cells compared to
normal hepatocytes. This difference might explain varying cell
spreading and motility in metastatic tissues.