Prox1 EMSA Kit Prospero homeobox protein 1
- Known as:
- Prox1 EMSA Kit Prospero homeobox protein 1
- Catalog number:
- GS-0056
- Product Quantity:
- 30
- Category:
- -
- Supplier:
- Signosis 2011
- Gene target:
- Prox1 EMSA Kit Prospero homeobox protein 1
Related genes to: Prox1 EMSA Kit Prospero homeobox protein 1
- Gene:
- PROX1 NIH gene
- Name:
- prospero homeobox 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1q32.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-05-18
- Date modifiied:
- 2016-10-05
Related products to: Prox1 EMSA Kit Prospero homeobox protein 1
Related articles to: Prox1 EMSA Kit Prospero homeobox protein 1
- Lymphatic vessels play essential roles in maintaining fluid homeostasis and responding to inflammatory and tissue environmental changes. During these biological processes, lymphatic endothelial cells (LECs) lining lymphatic vessels adapt to external stimuli in various organs and alter their characteristics. While organ-specific molecular and functional heterogeneity has been well-characterized in blood vascular endothelial cells, the extent and functional significance of such heterogeneity in LECs remain poorly understood. In this study, we established LECs derived from the heart and lung tissues of Prox1-GFP mice for comparative analyses. Both cell types retained lymphatic endothelial marker expression and exhibited tube-forming capacity in two- and three-dimensional culture systems, indicating the preservation of functional LEC phenotypes. Transcriptomic analysis revealed that LEC gene expression profiles were primarily segregated according to the organ of origin, indicating that LECs possess stable organ-specific transcriptional states. Notably, cardiac-derived LECs displayed enrichment of proliferation-related pathways, including MYC signaling, as well as inflammatory pathways such as TNF-α-NFκB and IL2-STAT5 signaling, indicating a transcriptional state primed for enhanced responsiveness to external stimuli. Furthermore, cardiac-derived LECs exhibited increased susceptibility to TGF-β-induced endothelial-to-mesenchymal transition (EndoMT) compared with pulmonary-derived LECs, reflecting enhanced cellular plasticity. These findings demonstrate that organ-specific transcriptional states regulate stimulus responsiveness, thereby defining cellular plasticity in LECs. - Source: PubMed
Publication date: 2026/07/20
Tsuyama YujiTakahashi KazukiKobayashi MihoBenzemam Suzuki LucasAkagi HarukaYokozawa MikiImafuku TadashiHashimoto ShinichiMatsunaga YukikoItoh FumikoHarada HiroyukiHong Young-KwonWatabe Tetsuro - Previous studies predominantly associated lymphatics with skeletal disease and bone loss. However, building on our work, bone lymphatics are emerging as a paradigm-shifting component of the skeletal microenvironment, illustrating their role as positive regulators of bone mass and repair. Here, we present a comprehensive analysis integrating spatial transcriptomics, single-cell RNA sequencing, and imaging across murine and human bones. Spatial transcriptomics identifies Prox1 endothelial cells embedded within bone. Reanalysis of multiple scRNA-seq datasets confirms Prox1 lymphatic endothelial cells (LECs) in bones, despite their underrepresentation in soft-tissue endothelial cell atlases. Periosteum is an insufficient source for bone lymphatics because it contains only sparse LECs. Our analyses further demonstrate that certain mouse models lack the sensitivity required to detect bone lymphatics and highlight the importance of high-resolution imaging. Collectively, convergent multimodal evidence substantiates LECs as an integral functional component of the skeletal microenvironment. This Matters Arising Response paper addresses the Meng et al. (2026) Matters Arising paper, published concurrently in this issue. - Source: PubMed
Yang YangZhang YuhengShi YixinJain SanyamJoseph Jessy DSingh AmitChen JunyuRamasamy Saravana KKusumbe Anjali P - A recent study reported the existence of lymphatic vessels in normal bone and suggested their involvement in bone regeneration after injury. However, this conclusion was based on approaches that do not allow unequivocal identification of the spatial localization of lymphatic endothelial cells (LECs). Here, we employed a Prox1-based genetic tool and a dual-recombinase-mediated LEC-specific labeling system to trace lymphatic vessels with high specificity. We found that LECs are present in the connective tissues, including the periosteum surrounding the bone. However, they do not reside within the bone itself, nor do they penetrate the periosteum to facilitate bone regeneration after injury. By contrast, hyperplastic LECs on the bone surface breach the periosteum and invade bone tissue in mouse models of generalized lymphatic anomaly and Gorham-Stout disease. These data demonstrate that lymphatic vessels are absent from bone during homeostasis and regeneration after injury but invade bone during disease. This Matters Arising paper is in response to Biswas et al. (2023), published in Cell. See also the response by Yang et al. (2026), published in this issue. - Source: PubMed
Meng XinfengLiu KuoTang MuxueWeng WendongZhang ZhenqianHuang XiuzhenHe ZhenHan XimengSun RuilinShen RulingMa XinPetrova Tatiana VMäkinen TaijaDellinger Michael TKruse KaiAdams Ralf HZhou Bin - - Source: PubMed
Mubeen ManahilAhmed Syeda NehaRizwan HaniaBansari KaranSaleem Hassan - Deep vein thrombosis (DVT) is a major cause of morbidity and mortality in critically ill patients. DVT clots typically form in the sinus of the deep venous valves and are strongly associated with immobility and reduced venous flow. Physical activity alters venous blood flow, generating frequent periods of recirculatory flow and oscillatory shear stress (OSS) at venous valves. Endothelial sensing of OSS stimulates expression of a potent antithrombotic endothelial phenotype within the valve sinus, but the phenotype may be lost during prolonged immobility. To test whether restoring OSS-signaling in immobile subjects could prevent thrombosis, we applied rapid cycling compression devices (RCDs) unilaterally to brain-dead organ donors (BDOD), a clinically relevant translational model of critical illness. In healthy subjects, vascular ultrasound showed that RCDs recapitulate valve sinus recirculatory flow comparable to muscular activity. Additionally, in BDOD subjects, we found that RCD treatment caused significantly more valve sinus recirculatory flow compared to currently used sequential compression devices (SCDs). In BDOD, prolonged RCD therapy increased expression of OSS-regulated genes (FoxC2, Prox1) and suppressed adhesion molecules (P-selectin, CCL2). Further, RCD treatment reduced DVT and microthrombus formation in BDOD subjects compared to standard anticoagulation alone. Randomized comparisons with SCDs revealed no systemic biomarker differences, indicating that RCD effects were localized to valve endothelium. These results extend our previous findings by identifying endothelial shear-dependent signaling in response to OSS as a critical mediator of DVT molecular pathology and establishing targeted hemodynamic modulation as a potential strategy in a novel model of human critical illness. - Source: PubMed
Publication date: 2026/08/18
Bandla SravanthiMontoya Rush Matthew NicholasGhosh SarbaniSuresh SreeLakshmyJain AbhishekPuri VarunWelsh John DKahn Mark LMarklin GaryLeonard Jennifer MNiziolek Grace MartinTurnbull Isaiah RHoofnagle Mark Houston