Intracranial and spinal dural arteriovenous fistulas (DAVFs) are vascular pathologies of the dural membrane with arteriovenous shunts. They are abnormal communications between arteries and veins or dural venous sinuses that sit between the two sheets of the dura mater. The dura propria faces the surface of brain, and the osteal dura faces the bone. The location of the shunt points is not distributed homogeneously on the surface of the dural membrane, but there are certain areas susceptible to DAVFs. The dura mater of the olfactory groove, falx cerebri, inferior sagittal sinus, tentorium cerebelli, and falx cerebelli, and the dura mater at the level of the spinal cord are composed only of dura propria, and these areas are derived from neural crest cells. The dura mater of the cavernous sinus, transverse sinus, sigmoid sinus, and anterior condylar confluence surrounding the hypoglossal canal are composed of both dura propria and osteal dura; this group is derived from mesoderm. Although the cause of this heterogeneity has not yet been determined, there are some specific characteristics and tendencies in terms of the embryological features. The possible reasons for the segmental susceptibility to DAVFs are summarized based on the embryology of the dura mater.
Arteries ; Brain ; Cavernous Sinus ; Central Nervous System Vascular Malformations ; Colon, Sigmoid ; Dura Mater ; Embryology ; Membranes ; Mesoderm ; Neural Crest ; Pathology ; Population Characteristics ; Spinal Cord ; Veins

Endothelium, Vascular ; pathology ; physiopathology ; Epithelial-Mesenchymal Transition ; Humans ; Hypertension, Pulmonary ; physiopathology ; Lung ; blood supply ; pathology ; physiopathology ; Mesoderm ; pathology ; physiopathology

Renal dysplasia is a developmental disorder of the renal parenchyma involving anomalous differentiation. It is characterized by persistent metanephric ducts surrounded by primitive mesenchyme, fetal or immature glomeruli, fetal or immature tubules, interstitial fibrosis, and dysontogenic metaplasia involving tissues such as cartilage. Renal dysplasia has been rarely reported in rats. Here, we observed a small left kidney in a rat used in a short-term repeat toxicity study. The rat showed no clinical signs throughout the study. All parameters, including those reflecting kidney functions, were normal upon hematological examination and urinalysis. Grossly, the kidney was small (5 x 8 mm) and its surface appeared normal. Histological examination revealed that the cortex and medulla were poorly demarcated and contained immature/atrophic glomeruli, immature renal tubules, and mesenchymal cells. The cortex contained immature glomeruli, atrophic glomeruli with cystic dilatation of Bowman's capsular space, and some atypical tubules. Primitive metanephric tubules in the medulla were larger in diameter than normal collecting ducts, lined by a tall columnar epithelium with pale cytoplasm and basal nucleus, and surrounded by loose mesenchymal cells. Occasional tubules contained pale eosinophilic homogenous material in the lumen. Thus, this was diagnosed as a case of renal dysplasia on the basis of histologic features and is the first reported case of renal dysplasia in Sprague Dawley rats.
Animals ; Cartilage ; Cytoplasm ; Dilatation ; Eosinophils ; Epithelium ; Fibrosis ; Kidney ; Mesoderm ; Metaplasia ; Pathology ; Rats* ; Rats, Sprague-Dawley ; Urinalysis

Adult ; Female ; Hemangioma ; pathology ; Humans ; Mesoderm ; pathology ; Placenta ; pathology ; Placenta Diseases ; pathology ; Pregnancy ; Young Adult

Bone Cysts, Aneurysmal ; diagnostic imaging ; pathology ; surgery ; Cartilage Diseases ; diagnostic imaging ; pathology ; surgery ; Female ; Hamartoma ; diagnostic imaging ; pathology ; surgery ; Humans ; Infant ; Mesoderm ; diagnostic imaging ; pathology ; surgery ; Nasal Cavity ; diagnostic imaging ; pathology ; surgery ; Neoplasm Recurrence, Local ; Nose Diseases ; diagnostic imaging ; pathology ; surgery ; Tomography, X-Ray Computed

OBJECTIVETo investigate the relationship between endothelial-to-mesenchymal transition (EndMT) and myocardial fibrosis in acute viral myocarditis (VMC).

METHODSTwenty-eight Balb/c mice were randomized into 3 groups: control group (n=8), VMC group(n=10) and intervention group(n=10). Mice in VMC and intervention groups were injected intraperitoneally(i.p) with single dose of coxsackievirus B3, mice in control group were injected with equal amount of viral-free vehicle. In the following day, mice in control and VMC groups were injected i.p with 0.1 ml of saline and intervention group with 0.1 ml of recombinant human bone morphogenetic protein 7(rh-BMP7) at a concentration of 300 μg/kg. The mice hearts were harvested after 7 d, cardiac collagen volume fraction (CVF) was calculated on picrosirius red-stained sections. mRNA and protein expression of TGF-β1, CD31, VE-cadherin, fibroblast special protein 1 (FSP-1) and α-smooth muscle actin (α-SMA) and collagen 1α1 in myocardiac tissues were detected by real-time RT-PCR and Western blot analysis, respectively.

RESULTSCompared to controls, overt fibrosis was presented in necrotic area of myocardium in VMC group. Meanwhile, marked increase of TGF-β1 expression accompanied with EndMT characterized by loss of endothelial phenotype (decreased expression of CD31 and VE-cadherin), gain of mesenchymal proteins (overexpression of FSP-1 and α-SMA) and increased synthesis of collagen was also demonstrated. Both EndMT and cardiac fibrosis were simultaneously reversed by TGF-β1 inhibition.

CONCLUSIONEndMT is involved in cardiac fibrosis in acute viral myocarditis, TGF-β1 might be a main mediator.

Acute Disease ; Animals ; Antigens, CD ; metabolism ; Cadherins ; metabolism ; Collagen ; metabolism ; Coxsackievirus Infections ; metabolism ; pathology ; Disease Models, Animal ; Endothelium ; pathology ; Fibrosis ; Male ; Mesoderm ; pathology ; Mice ; Mice, Inbred BALB C ; Myocarditis ; metabolism ; pathology ; virology ; Myocardium ; metabolism ; pathology ; Transforming Growth Factor beta1 ; metabolism

OBJECTIVE: To explore the expression and distribution of vimentin in different types of chronic rhinosinusitis and its significance. METHOD: There were four groups including control (10 samples), Eos CRSwNP (10 samples), non-Eos CRSwNP (12 samples) and CRSsNP (10 samples). The expression of vimentin in chronic rhinosinusitis were detected by immunohistochemistry technique. The double-immunofluorescence was used to detect the positive staining of both vimentin and E-cadherin, both of which were the marker of epithelial cells. RESULT: The positive staining of vimentin were observed both in epithelium and lamina propria. The expression of vimentin were found in myofibroblast, endothelium and other mesenchymal cells. The vimentin positive cells in epithelium were epithelial cells but not mesenchymal cells, as they also expressed E-cadherin. CONCLUSION The vimentin positive staining cells distribute in lamina propria and epithelium of both normal nasal mucosa and chronic rhinosinusitis. The positive staining epithelial cells may generate from epithelial-mesenchymal transition. So the vimentin may play an important role in the development of chronic rhinosinusitis.
Adult ; Antigens, CD ; Cadherins ; metabolism ; Chronic Disease ; Epithelial Cells ; metabolism ; Female ; Humans ; Male ; Mesoderm ; cytology ; metabolism ; Middle Aged ; Nasal Mucosa ; metabolism ; Sinusitis ; metabolism ; pathology ; Vimentin ; metabolism ; Young Adult

BACKGROUND AND OBJECTIVEIt has been proven that epithelial-mesenchymal transition (EMT) not only correlated with embryonic development but also could promote tumor invasion and metastasis. Transforming growth factor beta-1 (TGF-beta1) has been identified as the main inducer of tumor EMT. The aim of this study was to investigate the effects of TGF-beta1 on EMT and PI3K/AKT signaling pathway in lung adencarcinoma PC9 cells.

METHODSCultured PC9 cells were treated with different concentrations of TGF-beta1 for 48 h. The morphological changes were observed under phase-contrast microscopy; EMT relative marker protein changes were assessed by Western blot and immunoflurescence staining. In addition, the expression of AKT and P-AKT were also measured by Western blot.

RESULTSThe data showed that TGF-beta1 could induce PC9 morphological alteration from epithelial to mesenchymal and upregulate the expression of mesenchymal maker protein Fibronectin. Obviously, the expression of P-AKT was downregulated by TGF-beta1 treatment for 48 h.

CONCLUSIONTGF-beta1 might induce EMT of PC9 cells, accompanied by the changes of PI3K/AKT signaling pathway.

Adenocarcinoma ; metabolism ; pathology ; Blotting, Western ; Cell Differentiation ; drug effects ; Cell Line, Tumor ; Epithelial Cells ; pathology ; Fibronectins ; metabolism ; Humans ; Lung Neoplasms ; metabolism ; pathology ; Mesoderm ; metabolism ; pathology ; Microscopy, Phase-Contrast ; Proto-Oncogene Proteins c-akt ; metabolism ; Signal Transduction ; drug effects ; Transforming Growth Factor beta1 ; pharmacology

OBJECTIVETo investigate the effect of salvianolic-acid B (SA-B) on epithelia-mesenchymal transition in human renal proximal tubular cells (HK2), induced by transforming growth factor beta1 (TGF-beta1).

METHODEpithelia-mesenchymal transition (EMT) was induced with TGF-beta1 in HK2 cultured in vitro. Different concentrations (2, 5, 10, 20 microg x L(-1)) and stimulant periods (12, 24, 48 h) were tried to find the perfect condition for EMT. At the same time bone morphogenetic protein-7 (BMP-7, positive control) and the SA-B intervention were given to observe their effect on EMT. Western blot and immunofluorescent microscopy were used to analyze the expression of E-cadherin and alpha-smooth muscle actin (alpha-SMA) in HK2.

RESULTBMP-7 significantly inhibited the down-regulation of E-cadherin and the up-regulation of alpha-SMA induced by TGF-beta1 (P < 0.05), and SA-B significantly inhibited the up-regulation of alpha-SMA expression induced by TGF-beta1 (P < 0.05), but not the down-regulation of E-cadherin induced by TGF-beta1.

CONCLUSIONSA-B and BMP-7 can inhibit TGF-beta1-induced EMT in HK2. Their common role is to inhibit the up-regulation of alpha-SMA, and the effect of SA-B on the regulation of E-cadherin needs further study to be confirmed.

Benzofurans ; pharmacology ; Bone Morphogenetic Protein 7 ; pharmacology ; Cadherins ; metabolism ; Cell Differentiation ; drug effects ; Cell Line ; Epithelial Cells ; pathology ; Humans ; Mesoderm ; pathology ; Transforming Growth Factor beta1 ; pharmacology

The epithelial-mesenchymal transition (EMT) plays physiologic roles in the embryogenesis, wound healing, and tissue regeneration. In terms of pathological direction, it causes organ fibrosis, cancer development, progression, metastasis, and chemoresistance. Recently, the underlying mechanism of EMT and many kinds of EMT regulators have been identified. Pharmaceutical treatment strategies which target EMT pathway could be applied for the prevention of tissue fibrosis and cancer progression. In the field of gastroenterology, profuse evidences have been collected about the critical roles of EMT in cancers of the gastrointestinal tract, liver, and pancreas and hepatic fibrosis. However, EMT varies widely among cancer types, and much remains to be identified about the main regulators of EMT in a specific disease. In this review, we present recent research results regarding the roles of EMT in cancers and organic fibrosis, especially in the area of gastroenterology.
Biological Markers/analysis ; Cell Transformation, Neoplastic ; *Epithelial-Mesenchymal Transition ; Epithelium/pathology ; Gastrointestinal Neoplasms/etiology/*pathology ; Humans ; Mesoderm/pathology ; Neoplasm Metastasis ; Neoplastic Stem Cells/pathology