In solid tumors, cancer cells adapt to hypoxic and nutrient deprived environments to support malignant progression. This study examined whether hypoxic and low glucose conditions enhance malignant behaviors more strongly in highly migratory MG63-R10 cells, which are derived from osteosarcoma MG-63 cells, compared to parental MG-63 cells, and further investigated whether lysophosphatidic acid (LPA) receptor signaling regulates this adaptation.

Type 1 diabetes (T1D) is an autoimmune disorder that causes selected destruction of insulin-secreting pancreatic beta cells leading to insulin deficiency, hyperglycemia, and long-term complications. T1D has no cure and is primarily self-managed with blood sugar monitoring and exogenous insulin injections, which do not enable proper metabolic control and decreases patient's and caregivers' quality of life. Beta cell replacement through islet transplantation could cure T1D if current limitations such as the need for chronic systemic immunosuppression to prevent rejection and recurrence of autoimmunity are addressed. A potential new treatment addressing these limitations is based on transplantation of donor islets encapsulated in hydrogels with suitable and stable permselectivity and mechanical properties. Specifically, these hydrogel coatings must be () permeable to nutrients, insulin and glucose, necessary for coated cell viability and functionality, but impermeable to antibodies, to enable immune isolation, and () resistant to degradation, over time.

Rotator cuff injuries are the most common type of tendinopathies affecting up to 10% of young adults and more than 60% of the elderly. Tendons have notoriously limited regenerative capacity which is attributed to their low vascularisation and low cell-to-tissue ratio. That leads to an inefficient repair process resulting in fibrotic scar tissue with poorer mechanical properties. Recent advances in tissue engineering and biofabrication techniques have been anticipated with great hope in the field of regenerative medicine.

Directed cell migration is essential in many biological processes and is driven by a variety of directional cues, including aligned fibrils in the extracellular matrix (ECM), a phenomenon known as contact guidance. How different cells respond to aligned fibrils and how internal regulators like formins and Arp2/3 control contact guidance is unknown.

The periodontal ligament (PDL), which contains osteoblasts, is a unique connective tissue that resists mineralization despite being located between mineralized cementum and alveolar bone. The role of physiological mechanical stress, particularly the cyclic hydrostatic pressure (HP) generated during mastication, in regulating osteogenic potential remains poorly understood. This study aimed to compare the effects of static and cyclic HP on osteogenic differentiation and to elucidate the underlying mechanisms.

Approximately 15% of dilated cardiomyopathy (DCM) cases are associated with Bcl2-associated athanogene 3 (BAG3) gene mutations, which play a crucial role in myofilament organization and contractile behavior. Previous studies have highlighted the role of dynamic mechanical stress in myofibril alignment in human-induced pluripotent stem cell-derived cardiomyocytes (hiPSCCMs). In this study, we employed thermo-responsive shape memory polymers (SMPs) to mimic the dynamic mechanical environment of the extracellular matrix (ECM) and investigated their impact on myofibril assembly in healthy wild-type (WT) and BAG3 knockout (BAG3-/-) hiPSC-CMs.

Articular chondrocytes synthesize and maintain the avascular and aneural articular cartilage. In vivo these cells are surrounded by a 3D pericellular matrix (PCM) containing predominantly collagen VI. The PCM protects chondrocytes and facilitates mechanotransduction. PCM stiffness is critical in transmitting biomechanical signals to chondrocytes. Various culture systems with different hydrogels are used to encapsulate chondrocytes for 3D culture, but many lack either the PCM or the in vivo stiffness of the cartilage matrix. This study aimed at establishing a culture system to investigate (a) if chondrocytes cultured in alginate will develop a PCM and (b) study mechanotransduction via metabolic changes induced in 3D agarose-embedded chondrocytes upon mechanical stimulation.

[This corrects the article DOI: 10.1007/s12195-025-00853-2.].

The gut microbiome interacts with many systems throughout the human body. Microbiome disruption reduces bone tissue mechanics but paradoxically slows osteoarthritis progression. The microbiome also mediates inflammatory and immune responses, including serum cytokines. Towards our long-term goal of studying how the gut microbiome interacts with synovial joint health and disease, we examined how antibiotics-induced changes to microbial taxa abundance associated to serum cytokine levels.

The global rise of obesity has contributed to an increase in the incidence of endometrial cancer, the most common gynecologic malignancy. This obesity-driven increase, alongside limited therapeutic options, presents a growing public health concern. Our previous research indicated that adipose stem cells (ASCs), shed from fat depots, infiltrate the endometrium via the circulation in endometrial cancer patients with obesity. Furthermore, ASCs elicited the malignant transformation of endometrial epithelial cells (EECs) and fostered an oncogenic microenvironment driven by the plasminogen activator inhibitor 1 (PAI-1).

Adipose tissues have long been recognized for their diverse endocrine functions that serve to regulate tissue homeostasis. Although adipose depot-specific secretory profiles can differentially regulate fibroblast fate and fibrotic tissue remodeling, systematic investigation of how adipose depots of varying phenotypes influence fibroblast mechanobiology remains lacking.

Despite the success of immune checkpoint inhibitors (ICIs) that target immunosuppressive interactions, treatment resistance remains a major clinical challenge. The tumor microenvironment is comprised of tumor, immune, and stromal cell types that communicate through secreted and cell surface proteins. This can be represented by a weighted, directed network where pairs of cell types communicate via multiple ligand-receptor interactions with varying strengths. Identifying interaction network motifs that are linked with outcome or evolve pre- to post-ICI presents a rational framework to identify combination therapeutic targets.

In this study, we investigate the plasticity of tumor-associated macrophages, which originate from circulating monocytes and are associated with poor cancer prognosis. The differentiation of monocytes into macrophages is a dynamic and spatiotemporal process, as is the resulting macrophages' polarization. However, traditional methods for measuring polarization, such as qPCR and flow cytometry, provide only static information about polarization. To supplement these methods, we present a novel bioluminescent method that allows for time-resolved measurement of NFκB activation in macrophages while in co-culture with cancer cells. By using a monocyte cell line whose NFκB responsive element is labeled with firefly luciferase, we obtain a quantitative and temporal characterization of macrophage polarization in response to tumor-derived signals.

Sex differences in cellular biology significantly influence cell responses in culture. Yet, the sex-specific effects of culture reagents such as fetal bovine serum (FBS) remain understudied. Increased adoption of cell-based models such as microphysiological systems (MPS) as replacements for animal models demands a greater understanding sex-specific responses to common media formulations. This study examined the effects of FBS and hormone-free charcoal-stripped serum (CSS) on male (XY) and female (XX) cells in 2D and 3D MPS culture models to demonstrate profound sex-specificity in bioassays and inform the development of future sex-specific cell culture protocols and methods.

Stem cell-derived models offer traceable cell sources for studying tissue development and disease mechanisms. However, many such models have inherently immature or fetal-like phenotypes, limiting their relevance for mechanistic studies of specialized adult tissues. Clinical observations suggest a potential link between epithelial cells and their transit-amplifying progenitors in disease onset and viral tropism, but experimental validation is needed. This study aimed to develop mature visceral epithelial cells (podocytes) from human induced pluripotent stem (iPS) cells using a developmental approach and model severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in a vascularized microfluidic kidney-on-a-chip platform exhibiting in vivo-like tissue structure and function.

[This corrects the article DOI: 10.1007/s12195-025-00860-3.].

In muscle tissues, anisotropic cell alignment is essential for optimal muscle fiber development and function. Biomaterials for muscle tissue engineering must guide cellular alignment while supporting cell proliferation and myogenic differentiation.

Triple negative breast cancer (TNBC) has significantly worse outcomes compared to other subtypes. Strains in the tumor microenvironment (TME) generated by cancer-associated fibroblasts (CAFs) can regulate TNBC progression. Recent studies suggest that expression of VEGFR-2 on TNBC is linked to decreased survival, while our prior studies show strains activate VEGFR-2 to drive angiogenesis. We hypothesized that VEGFR-2 on TNBC can be mechanically activated to alter migration and proliferation.

Mitochondrial dysfunction contributes to endothelial injury in vascular diseases and interventions. While mitochondrial transplantation offers a promising therapeutic strategy, current approaches lack target specificity, efficient uptake, and long-term retention. This study presents a surface-engineering approach to enhance mitochondria delivery to the vascular endothelium as a step toward novel endothelial repair strategies.