Background: The brain vascular system arises from the perineural vascular plexus (PNVP) which sprouts radially into the neuroepithelium and subsequently branches off laterally to form a secondary plexus in the subventricular zone (SVZ), the subventricular vascular plexus (SVP). The process of SVP formation remains to be fully elucidated. We investigated the role of Foxc1 in early stage vascular formation in the ventral telencephalon. Results: The Foxc1 loss of function mutant mouse, Foxc1 ch/ch , showed enlarged telencephalon and hemorrhaging in the ventral telencephalon by embryonic day 11.0. The mutant demonstrated blood vessel dilation and aggregation of endothelial cells in the SVZ after the invasion of endothelial cells through the radial path, which lead to failure of SVP formation. During this early stage of vascular development, Foxc1 was expressed in endothelial cells and pericytes, as well as in cranial mesenchyme surrounding the neural tube. Correspondingly, abnormal deposition pattern of basement membrane proteins around the vessels and increased strong Vegfr2 staining dots were found in the aggregation sites. Conclusions: These observations reveal an essential role for Foxc1 in the early stage of vascular formation in the telencephalon. Developmental Dynamics 244:703-711, 2015. V C 2015 Wiley Periodicals, Inc.
BackgroundHypercholesterolemia is a major risk factor for interstitial lung disease (ILD). Atorvastatin and ezetimibe are antilipemic drugs that have pleiotropic effects. However, their effects on pulmonary fibrosis prevention and the mechanisms underlying hypercholesterolemia have not been fully investigated. This study aimed to evaluate the individual effects of atorvastatin and ezetimibe on lung inflammation and fibrosis in high-cholesterol diet (HCD)-fed rats.Materials and methodsMale Sprague-Dawley rats were divided into four groups — standard diet (S), standard diet + 1% cholesterol (SC), standard diet + 1% cholesterol with 30 mg/kg/day atorvastatin (SCA), and standard diet + 1% cholesterol with 10 mg/kg/day ezetimibe (SCE). At the end of an 8-week dietary schedule, serum lipid parameters and the levels of lung oxidative stress, inflammatory cytokines, and fibrotic mediators were determined.ResultsAtorvastatin and ezetimibe treatment remarkably reduced serum lipid profiles with reversed pulmonary histological alterations, in addition to reducing the levels of lung oxidative stress, inflammation, and fibrosis in hypercholesterolemic rats.ConclusionAtorvastatin and ezetimibe treatment showed a protective effect against hypercholesterolemia-induced pulmonary fibrosis in rats. This information appears potentially useful in the prevention of PF in a hypercholesterolemia model; however, further rigorous investigations are needed to prove their clinical utility on antifibrosis.
Introduction: Many studies have indicated that Forkhead Box C1 (FOXC1) is highly expressed in a various malignant neoplasms and its over expression is associated with tumour development, progression and metastasis. However, the role of FOXC1 in odontogenic lesions remains to be elucidated. Aim: This study aimed to investigate FOXC1 expression in selective Odontogenic Cysts (OC) and Odontogenic Tumours (OT). Materials and Methods: A descriptive study on OC and OT was performed on oral biopsy specimens at Faculty of Dentistry, Naresuan University, Phitsanulok, Thailand, between January 2009 and December 2016. Institute of Cancer Research (ICR) mouse were used as study animal. Immunohistochemical reaction was performed using antibody against FOXC1 in 23 formalin-fixed and paraffin-embedded tissues of eight Ameloblastoma (AM), one Adenomatoid Odontogenic Tumour (AOT), seven Odontogenic Keratocyst (OKC), five Dentigerous Cyst (DC), two Calcifying Odontogenic Cyst (COC) and three mouse embryonic head at Embryonic Day (E)14. The expression level of FOXC1 was evaluated using semi-quantitative analysis. Results: Immunoreactivity of FOXC1 was not detected in the epithelial lining of OKC, DC and COC but it was identified in the epithelial compartment of AM and AOT. Overall, semi-quantitative analysis demonstrated moderate staining of FOXC1 and staining score was 4.13 in AM and 5 in AOT. In addition, FOXC1 was not detected in normal tooth bud of mouse including both enamel organ and condensing ectomesenchyme. Conclusion: Expression of FOXC1 may contribute in tumouriogenesis of OT whereas it is may not be related with normal odontogenesis.
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