Exposure to C26 colon adenocarcinoma cells induced segment-specific functional and mechanical alterations in the descending thoracic aorta alongside a 16.1% body weight reduction in female mice.
Does injection with C26 colon adenocarcinoma cells alter vascular reactivity and passive mechanical properties of the descending thoracic aorta in adult female CD2F1 mice?
Tumor exposure induces segment-specific functional and mechanical alterations in the descending thoracic aorta of female mice, suggesting tumors directly influence vascular structure independent of cachexia or therapy.
Background: Cancer survivors exhibit an increased risk of cardiovascular disease (CVD) that cannot be fully explained by traditional risk factors or cardiotoxic therapies. Emerging evidence suggests that tumors may exert direct systemic effects on the vasculature via inflammatory and circulating factors. However, most preclinical studies focus on vascular dysfunction in the context of cachexia or anticancer therapies, leaving the independent effects of tumor presence on vascular structure and function poorly understood. We hypothesized that exposure to C26 adenocarcinoma cells would alter vascular reactivity and passive mechanical properties of the descending thoracic aorta in female mice, contributing to increased cardiovascular risk independent of cachexia or therapy. Methods: Adult female CD2F1 mice were injected with C26 colon adenocarcinoma cells (n = 4) or vehicle (n = 5). After four weeks, descending thoracic aortae were isolated and divided into proximal (S1) and distal (S4) segments for myography. Vascular reactivity was assessed using potassium (K + , 60 mM), phenylephrine (PE, 0.01–100 µM), and acetylcholine (ACh, 0.01–100 µM). Structural properties were evaluated via lumen diameter and passive length–tension relationships under Ca 2 + -free conditions. Data were analyzed using Student’s t-test and nonlinear regression. Results: Tumor exposed (TE) mice exhibited modest body weight reductions (16.1%). Distal aortic segments from TE mice exhibited greater K+-induced constriction compared to controls, while proximal segments were unchanged. PE-induced contractions were enhanced in TE mice, with the greatest effect observed in S1 segments. ACh-induced relaxation was increased at lower concentrations in S1 segments from TE mice, with no differences in S4 segments. Passive length–tension analysis revealed greater force development in S1 segments from TE mice, while lumen diameter did not differ between groups. Conclusions: Tumor exposure induces segment-specific functional and mechanical alterations in the descending thoracic aorta of female mice, independent of cachexia or therapeutic intervention. These findings suggest that tumors themselves may directly influence vascular structure and systemic physiology, contributing to early vascular dysfunction and increased cardiovascular risk. Further studies across tumor types and vascular beds are warranted to define the mechanisms underlying tumor-associated vascular dysfunction. Funding: Biochemistry Start-Up Funds (MS), Biomedical Sciences Program (KR, SJ, DME), and Biomedical Sciences Start-Up Funds (DME). This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
Rosito et al. (Fri,) conducted a other in Tumor exposure (n=9). C26 colon adenocarcinoma cells vs. Vehicle was evaluated on Vascular reactivity and passive mechanical properties of the descending thoracic aorta. Exposure to C26 colon adenocarcinoma cells induced segment-specific functional and mechanical alterations in the descending thoracic aorta alongside a 16.1% body weight reduction in female mice.
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