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Ex vivo Demonstration of Functional Deficiencies in Popliteal Lymphatic Vessels From TNF-Transgenic Mice With Inflammatory Arthritis
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Abstract
Background: Recent studies demonstrated lymphangiogenesis and expansion of draining lymph nodes during chronic inflammatory arthritis, and lymphatic dysfunction associated with collapse of draining lymph nodes in rheumatoid arthritis (RA) patients and TNF-transgenic (TNF-Tg) mice experiencing arthritic flare. As the intrinsic differences between lymphatic vessels afferent to healthy, expanding, and collapsed draining lymph nodes are unknown, we characterized the ex vivo behavior of popliteal lymphatic vessels (PLVs) from WT and TNF-Tg mice. We also interrogated the mechanisms of lymphatic dysfunction through inhibition of nitric oxide synthase (NOS). Methods: Popliteal lymph nodes (PLNs) in TNF-Tg mice were phenotyped as Expanding or Collapsed by in vivo ultrasound and age-matched to WT littermate controls. The PLVs were harvested and cannulated for ex vivo functional analysis over a relatively wide range of hydrostatic pressures (0.5–10 cmH 2 O) to quantify the end diastolic diameter (EDD), tone, amplitude (AMP), ejection fraction (EF), contraction frequency (FREQ), and fractional pump flow (FPF) with or without NOS inhibitors Data were analyzed using repeated measures two-way ANOVA with Bonferroni’s post hoc test. Results: Real time videos of the cannulated PLVs demonstrated the predicted phenotypes of robust vs. weak contractions of the WT vs. TNF-Tg PLV, respectively. Quantitative analyses confirmed that TNF-Tg PLVs had significantly decreased AMP, EF, and FPF vs. WT ( p < 0.05). EF and FPF were recovered by NOS inhibition, while the reduction in AMP was NOS independent. No differences in EDD, tone, or FREQ were observed between WT and TNF-Tg PLVs, nor between Expanding vs. Collapsed PLVs. Conclusion: These findings support the concept that chronic inflammatory arthritis leads to NOS dependent and independent draining lymphatic vessel dysfunction that exacerbates disease, and may trigger arthritic flare due to decreased egress of inflammatory cells and soluble factors from affected joints.
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Lymphatic valve dysfunction occurs in animal models of diet-induced obesity and TNFα overexpression.
“lymphatic valve dysfunction in animal models of diet-induced obesity and tumor necrosis factor alpha (TNFα) overexpression (58)”
From Transport and Immune Functions of the Lymphatic System. (2025) · cites this paper as [58]
The Discussion reports impaired popliteal lymphatic vessel contractions in TNF-transgenic mice with inflammatory arthritis. That supports lymphatic dysfunction in the TNF-overexpression model, but it does not establish valve dysfunction. Our copy also provides no finding about a diet-induced obesity model (searched: valve dysfunction, diet-induced obesity). (LLM, conf=0.82)
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Metadata
- Authors
- Scallan, J. P., Bouta, E. M., Rahimi, H., Kenney, H. M., Ritchlin, C. T., Davis, M. J., & Schwarz, E. M.
- Affiliations
- University of South Florida (US)
- University of Rochester Medicine (US)
- University of Missouri (US)
- Corresponding author
- Schwarz, Edward M.
- ORCID
- Venue
- Frontiers in Physiology
- Publisher
- Frontiers Media SA
- Published
- 2021-09-27
- Volume
- 12
- Pages
- 745096-745096
- ISSN
- 1664-042X (ISSN-L)
- PMC
- PMC8503619
- OpenAlex
- W3204420259
- Cited by
- 22
- References
- 45
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 3 · 2023: 6 · 2022: 7 · 2021: 1
- FWCI
- 1.55
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Physiology (publishedVersion, cc-by)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institute of General Medical Sciences (T32 GM007356)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (T32 AR076950, R01 AR069000, R01 AR056702, P30 AR069655)
- National Heart, Lung, and Blood Institute (R01 HL12256, R01 HL120867, R01 HL142905)
- Topics
- Health Sciences › Medicine › Oncology › Lymphatic System and Diseases
- Health Sciences › Medicine › Surgery › Lymphatic Disorders and Treatments
- Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
- Keywords
- lymphatic dysfunction, TNF transgenic mice, inflammatory arthritis, rheumatoid arthritis, lymphangiogenesis, nitric oxide synthase, ejection fraction, lymphatic vessel contraction
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