記述言語：英語   掲載種別：研究論文（学術雑誌）  

Spatial transcriptomics maps whole-transcriptome profiles directly onto tissue sections, correlating between cellular neighborhoods and gene expression and how these activities drive health and disease. Although the approach has transformed oncology, neuroscience, immunology, developmental sciences, and many fields, it has been less widely used in vascular biology, even though vascular disease remains a leading cause of death worldwide. Two obstacles stand out: arteries and veins offer little flat surface for sectioning, and diseased specimens, often atherosclerotic, thrombosed, plaque-laden, or calcified, require harsh treatments such as decalcification that jeopardize morphology and RNA integrity. Yet these same vessels, with their concentric intima, media, and adventitia layered structures, are ideal for spatial analysis because each layer hosts distinct cell types and gene programs that interact across the wall. Few detailed protocols address how to prepare vascular tissues for spatial transcriptomics. This shortage limits researchers' ability to exploit the technique's full potential. To bridge the gap, we present a step-by-step workflow optimized for human tibial arteries with advanced lesions. The protocol covers tissue handling, fixation, and proper decalcification that preserve structure and RNA quality, followed by histological staining to grade calcification severity. We also describe the construction of tissue microarray (TMA) to curb batch effects and region of interest (ROI) selection strategies on the NanoString GeoMx Digital Spatial Profiler (DSP). By lowering technical barriers, this protocol enables vascular researchers to generate reliable spatial transcriptomic data and study layer-specific transcriptional activities in healthy and diseased vessels. We anticipate that it will accelerate the discovery of mechanisms underlying calcification, inflammation, intimal atherosclerosis, and other vascular pathologies and foster broader adoption of spatial transcriptomics in vascular biology.

DOI： 10.3791/69159

PubMed

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Japan experiences more than 1000 perceptible earthquakes annually, including major events such as the 2011 Great East Japan Earthquake and the 1995 Great Hanshin-Awaji Earthquake. These events lead to a documented increase in cardiovascular events, particularly venous thromboembolism (VTE), including pulmonary embolism and deep vein thrombosis (DVT). Disaster-associated VTE is influenced by Virchow's triad: hemodynamic stasis, hypercoagulability, and endothelial injury. The incidence of DVT after earthquakes ranges from 10% to 30%, often developing 1 to 2 weeks post disaster. Early interventions in evacuation shelters to prevent venous stasis and hypercoagulability are critical. Left untreated, DVT can progress to pulmonary embolism, which may be fatal; however, most cases are preventable through timely intervention and improved shelter environments. Various organizations, including the Disaster Medical Assistance Team, the Japan Medical Association Team, and local institutions, contribute to disaster medical responses. In 2016, the Disaster Countermeasure Committee was established by the Japanese Society of Phlebology to lead VTE prevention efforts, including DVT screening, compression stocking distribution, public awareness campaigns, and promoting cardboard beds to enhance shelter conditions. In preparation for future large-scale disasters, it is vital to share evidence-based knowledge with health care professionals and the public to decrease the burden of disaster-associated VTE.

DOI： 10.1016/j.jvsv.2025.102312

PubMed

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

BACKGROUND: Vascular smooth muscle cells (VSMCs) are the primary component of the medial layer of the vessel wall, where they maintain structural integrity and regulate vascular tone. Their dysfunction contributes to vascular diseases such as aortic aneurysms and atherosclerosis. Although VSMCs isolated from thoracic and abdominal aortic regions are widely used in experimental studies, their functional differences have not been systematically compared. METHODS: In this study, we examined functional and phenotypic differences between VSMCs isolated from the descending thoracic (Th-SMCs) and abdominal aortas of male C57BL/6J mice under controlled in vitro conditions. RESULTS: Both cell types maintained high α-smooth muscle actin expression across passages, supporting smooth muscle lineage identity. Functionally, Th-SMCs demonstrated significantly greater migratory and proliferative capacities compared with abdominal SMCs. Under sublethal oxidative stress, Th-SMCs exhibited higher relative viability, accompanied by higher basal expression of antioxidant-related transcripts, including Nrf2, Catalase, and Sod1. CONCLUSIONS: These findings highlight intrinsic differences between region-specific VSMCs and underscore the importance of considering anatomical origin for in vitro models. Incorporating region-specific VSMCs may enhance experimental relevance and contribute to a better understanding of the mechanisms underlying regional vascular diseases. CLINICAL RELEVANCE: Vascular smooth muscle cells (VSMCs) play a key role in the development of vascular diseases. This study demonstrates that VSMCs isolated from the descending thoracic and abdominal aortic regions exhibit distinct functional behaviors under in vitro conditions. These region-specific differences highlight the importance of carefully selecting and reporting the anatomical origin of VSMCs in experimental studies, which may improve the physiological relevance and interpretability of vascular research models.

DOI： 10.1016/j.jvssci.2026.100411

PubMed

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

UNLABELLED: <p>Introduction: Abdominal aortic aneurysm (AAA) is a multifactorial disease with limited identification of contributing genetic factors. p27kip, also known as CDKN1B, is a cell cycle inhibitor that regulates vascular smooth muscle cells (VSMCs) and macrophages (Mϕ). The role of p27 in AAA development was assessed by AAA induction in p27 knockout (p27-/-) and wild-type (WT) mice. METHODS: AAAs were induced in male and female p27-/- and WT mice via topical elastase with oral administration of 3-aminopropionitrile fumarate salt. Aortic diameter was measured with ultrasound. VSMCs and macrophages were quantified by immunohistochemistry. Oxidative stress genes were analyzed using polymerase chain reaction. In vitro cell proliferation, migration, and oxidative stress assay were performed on VSMCs isolated from abdominal aortas. RESULTS: p27-/- mice developed significantly larger AAA diameter than WT mice with reduced VSMCs and increased macrophages. M1ϕ were significantly elevated in p27-/- mice, while M2ϕ were more abundant in WT mice. p27-/- mice had lower expression of the antioxidant gene, Nrf2. In vitro experiments demonstrated increased proliferation and migration in p27-/- cells with increased oxidative stress sensitivity. CONCLUSION: Knockout of p27 accelerated aneurysm growth with increased macrophage infiltration, VSMC loss, and decreased antioxidant factors, highlighting a potential role for p27 in AAA progression. </p>.

DOI： 10.1159/000547829

PubMed

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掲載種別：研究論文（学術雑誌）   出版者・発行元：Japan Society of Phlebology  

DOI： 10.7134/phlebol.25-05

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記述言語：日本語   出版者・発行元：血管外科症例検討会  

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担当区分：筆頭著者   記述言語：日本語   掲載種別：記事・総説・解説・論説等（学術雑誌）  

DOI： 10.2491/jjsth.33.661

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開催年月日： 2026年2月

記述言語：英語   会議種別：口頭発表（一般）  

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開催年月日： 2025年10月

記述言語：日本語   会議種別：口頭発表（招待・特別）  

添付ファイル： JCAA2025抄録_提出版.docx

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開催年月日： 2025年2月

記述言語：英語   会議種別：口頭発表（一般）  

添付ファイル： MON_1411_KAMADA.pptx

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開催年月日： 2024年5月

記述言語：英語   会議種別：ポスター発表  

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開催年月日： 2023年6月

記述言語：英語   会議種別：口頭発表（一般）  

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