Reduced lung metastasis in endothelial cell-specific transforming growth factor β type II receptor-deficient mice with decreased CD44 expression.

Transforming growth factor β (TGF-β) is abundantly present in the tumor microenvironment, contributing to cancer progression. However, the regulatory mechanism by which TGF-β affects vascular endothelial cells (ECs) in the tumor microenvironment is not well understood. Herein, we generated tamoxifen-inducible TGF-β type II receptor () knockout mice, specifically targeting ECs (TβRII), by crossbreeding TβRII-floxed mice with Pdgfb-icreER mice.

Anatomical study of pterygoid implants: artery and nerve passage through bone dehiscence of the greater palatine canal.

Purpose: Pterygoid implants are an alternative approach to avoid sinus-lifting or other grafting procedures. During pterygoid implant placement, dental surgeons risk damaging the greater palatine canal (GPC). However, they do not have sufficient reasons to avoid GPC injury.

Alteration of Oral and Perioral Soft Tissue in Mice following Incisor Tooth Extraction.

Oral and perioral soft tissues cooperate with other oral and pharyngeal organs to facilitate mastication and swallowing. It is essential for these tissues to maintain their morphology for efficient function. Recently, it was reported that the morphology of oral and perioral soft tissue can be altered by aging or orthodontic treatment.

Endothelial-specific depletion of TGF-β signaling affects lymphatic function.

Background: Transforming growth factor (TGF)-β is a multifunctional cytokine involved in cell differentiation, cell proliferation, and tissue homeostasis. Although TGF-β signaling is essential for maintaining blood vessel functions, little is known about the role of TGF-β in lymphatic homeostasis.

Methods: To delineate the role of TGF-β signaling in lymphatic vessels, TβRII mice were crossed with Prox1-Cre mice to generate TβRII; Prox1-Cre mice.

Transforming growth factor-β signaling enhancement by long-term exposure to hypoxia in a tumor microenvironment composed of Lewis lung carcinoma cells.

Transforming growth factor-β (TGF-β) is a potent growth inhibitor in normal epithelial cells. However, a number of malignant tumors produce excessive amounts of TGF-β, which affects the tumor-associated microenvironment by furthering the progression of tumorigenicity. Although it is known that the tumor-associated microenvironment often becomes hypoxic, how hypoxia influences TGF-β signaling in this microenvironment is unknown.

Smad2/Smad3 in endothelium is indispensable for vascular stability via S1PR1 and N-cadherin expressions.

Transforming growth factor-β (TGF-β) is involved in vascular formation through activin receptor-like kinase (ALK)1 and ALK5. ALK5, which is expressed ubiquitously, phosphorylates Smad2 and Smad3, whereas endothelial cell (EC)-specific ALK1 activates Smad1 and Smad5. Because ALK5 kinase activity is required for ALK1 to transduce TGF-β signaling via Smad1/5 in ECs, ALK5 knockout (KO) mice were not able to give us the precise mechanisms by which TGF-β/ALK5/Smad2/3 signaling is implicated in angiogenesis.