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Biology subjects

Nikmaneshi, M.

Publications and source records attributed to Nikmaneshi, M..

3 recordsLinked to original sources

Immortalized smooth muscle cells enhance in vitro vasculogenesis

De novo vessel formation (vasculogenesis) in vitro is a key step in tissue engineering to preserve tissue viability for long-term assays and testing therapeutic agents. However, in vitro vasculogenesis is often unreliable due to differences in vascular-supporting cells, including endothelial cells and stromal cells such as smooth muscle cells (SMCs) and fibroblasts. Here, we developed a robust co-culture system of HUVECs and SMCs to generate stable vascular networks capable of maintaining tissue viability over extended periods. Given that SMC plasticity is a major limitation in supporting endothelial network formation, we systematically evaluated the effects of passage number, confluency, and freezing on primary SMC function. To overcome this limitation, we generated immortalized supportive SMCs, which preserved their vasculogenic gene program and functional capacity even at high passage. In addition, we identified and validated key genes associated with endothelial support, including CD248, C3, and FBLN1, all essential for vasculogenesis. Immortalized SMCs consistently maintained expression of these genes and supported robust vessel formation under variable culture conditions. Collectively, this study demonstrates that immortalized SMCs provide a stable, reproducible platform for endothelial-SMC co-cultures, enabling long-term vascularized tumor models suitable for functional studies and therapeutic screening.

developmental biology↗

A Hybrid Multiscale Model for Predicting CAR-T Therapy Outcomes in SolidTumors

T cell distribution within tumors ("tumor hotness") critically determines immunotherapy success. However, despite numerous strategies to enhance intratumoral T cell accumulation--such as multi-target CAR-Ts and combinatorial approaches--limited mechanistic understanding of T cell-microenvironment interactions has constrained progress. To address this, we developed a physiological mechanistic model of the 3D tumor microenvironment (TME) to evaluate CAR-T performance under environmental fluctuations and different infusion strategies. The model integrates key vascular (rolling, adhesion, endothelial suppression) and interstitial (ECM density, metabolic competition, chemokine sensitivity) barriers. Our simulations reveal that collagen density and metabolic competition dominate CAR-T efficacy. Enhancing vascular adhesion improves infiltration but remains limited by collagen and metabolism. Endothelial suppression markedly reduces tumor hotness, while its alleviation enhances response. Systemic infusion yields higher tumor hotness than intratumoral delivery, but combined routes or reduced collagen restore efficacy even in dense tumors. This mechanistic framework enables rational optimization of CAR-T strategies. Significance StatementThe success of immunotherapies such as CAR-T cells depends on their ability to infiltrate and persist within solid tumors, yet the mechanisms that govern this process remain poorly understood. Using a mechanistic 3D model of the tumor microenvironment, we quantitatively dissected how vascular and interstitial barriers--including endothelial suppression, collagen density, metabolic competition, and chemokine cues--shape CAR-T distribution ("tumor hotness"). Our results reveal that stromal and metabolic constraints, rather than vascular adhesion alone, dominate CAR-T efficacy. This framework bridges molecular, cellular, and tissue-scale mechanisms, providing a quantitative foundation for optimizing CAR-T design and delivery strategies to overcome resistance in solid tumors.

immunology↗

Optimizing Cancer Vaccinations Using a Physiologically Based Pharmacokinetic (PBPK) Model

Antigen-based tumor vaccines rely on adjuvants to stimulate local inflammation, recruit antigen-presenting cells (APCs), and enhance immune activation. However, the complex interplay between antigen transport, lymphatic drainage, and immune cell dynamics across organs remains poorly understood, limiting the rational design of vaccination strategies. Here, we present a multiscale compartmental Physiologically Based Pharmacokinetic (PBPK) model of antigen vaccination that integrates systemic circulation, lymphatic connectivity, and immune cell activation at the whole-body level. The model incorporates arterial, venous, and lymphatic flows, organ-specific interstitium and lymph node (LN) networks, and a superficial skin network. The model reproduces spatiotemporal distributions of antigen and suppressive factors, APC activation, and nT priming across activation sites, including LNs and spleen. Our results show that the sensitivity of vaccination-induced immunity is highly related to antigen and suppressive factor production by the tumor, and that early-stage vaccination, enhances immunity. Since the model is able to identify optimal vaccination administration over the course of tumor growth for each patient with certain levels of antigen and immune suppressive factors, it can serve as the foundation for digital twins of patients to help inform anti-cancer vaccination strategies. TeaserA PBPK model links body-wide immune transport to optimize cancer vaccine design and delivery.

systems biology↗