Faculty Speakers
Johnson V. John
Assistant Professor and Principal Investigator at Terasaki Institute for Biomedical Innovation (TIBI)
Dr. Johnson V. John is an Assistant Professor and Principal Investigator at the Terasaki Institute for Biomedical Innovation (TIBI). His research focuses on the design and development of advanced biomaterials and nanotechnology-based platforms for applications in regenerative medicine, drug delivery, and tissue engineering. Dr. John’s work integrates materials science, bioengineering, and translational approaches to develop innovative therapeutic solutions aimed at improving patient outcomes. He leads a multidisciplinary research group dedicated to advancing next-generation biomedical technologies from bench to clinical application.
Title of the Talk
Building Healing from the Bottom Up: Modular Biomaterials in Regenerative Medicine
Affiliation
Terasaki Institute for Biomedical Innovation, 21100 Erwin St, Woodland Hills, CA 91367
Abstract
Traditional scaffold technologies in regenerative medicine have largely relied on bulk materials such as nanofibrous membranes and hydrogels. While effective in certain contexts, these static and homogeneous systems often fail to adapt to the dynamic and heterogeneous microenvironments of injured tissues. Over the past decade, growing efforts have focused on the development of modular biomaterials, which introduce a fundamentally different design philosophy for tissue repair. Rather than forming uniform bulk matrices, modular scaffolds assemble healing environments from microscale building blocks that are injectable, customizable, and inherently microporous. This modularity enables enhanced nutrient and oxygen transport, dynamic cell–material interactions, and the integration of multifunctional therapeutic elements, including growth-factor sequestration, immunomodulatory cues, and mechanically responsive features. Importantly, properties such as porosity, shape, mechanics, and bioactivity can be independently programmed to match specific wound microenvironments. Early successes with microgel-based fillers and microporous matrices highlight a clear shift away from static, one-size-fits-all dressings toward dynamic, adaptive, and modular therapeutics. This talk will place modular biomaterials within the broader trajectory of scaffold evolution and discuss how they are poised not only to accelerate healing outcomes but also to redefine regenerative strategies across diverse tissue types.
Khaja Shameem Mohammed Abdul
Postdoctoral Fellow in the Cardiovascular Signaling Laboratory at Huntington Medical Research Institutes (HMRI)
Dr. Khaja Shameem Mohammed Abdul is a Postdoctoral Fellow in the Cardiovascular Signaling Laboratory at the Huntington Medical Research Institutes (HMRI) in Pasadena, California. He earned his PhD from the University of Ruhuna, Sri Lanka, where he was recognized with two prestigious awards: the Vice Chancellor’s Fellowship from University of Ruhuna and the President’s Research Scholarship from the Ministry of Higher Education.
During 2018-2020, he was a post-doctoral fellow at Guangdong University of Technology, China. Where he discovered cardioprotective effects of a novel drug molecule JC105 which was later patented by the lab. Since 2021, Dr. Khaja Shameem joined HMRI as a post-doctoral fellow, where he investigates the role of protein phosphatases PHLPP1 and PHLPP2 in myocardial aging and injury. His work has been published in multiple peer-reviewed journals, including Journal of Molecular and Cellular Cardiology, International Journal of Cardiology, Journal of Cellular and Molecular Medicine and Biochimica et Biophysica Acta-Molecular Cell Research.
Dr. Mohammed Abdul’s long‑term career goal is to become an independent scientist advancing the field of cardiovascular research. Dr. Mohammed Abdul also contributes to the scientific community as an Editorial Board Fellow for Current Opinion in Physiology and as an Editorial Board Member for The Open Cardiovascular Medicine Journal. Beyond his laboratory work, he has served as a Social Media Ambassador for the American Heart Association and as a communications Committee member for the Society for South Asian Heart Research.
Title of the Talk
PHLPP1: The Missing Link in Nicotine Induced Cardiac Damage
Abstract
Nicotine exposure is known to cause oxidative stress and mitochondrial dysfunction in the heart, yet the molecular mechanisms linking nicotine to cardiomyocyte injury remain unclear. Our work identifies Pleckstrin Homology Domain Leucine-Rich Repeat Protein Phosphatase 1 (PHLPP1) as a key mediator of nicotine induced cardiac damage. We found that nicotine significantly elevates PHLPP1 expression in the adolescent rodent heart and in cardiomyocytes, coinciding with increased NOX4 levels, reactive oxygen species production, and apoptosis. Mechanistic studies revealed that nicotine activates the ERK–4E BP1 signaling axis to promote PHLPP1 protein synthesis, and inhibiting ERK or translation effectively blocks this response. Importantly, PHLPP1 was necessary and sufficient for nicotine induced mitochondrial dysfunction. Together, these findings uncover a novel pathway through which nicotine drives cardiomyocyte injury and highlight PHLPP1 as a potential therapeutic target in tobacco and e cigarette related cardiac injury.