scholarly journals Multiple omental hemangiomas in a Himalayan cat: Incidental finding in a laparotomy

2021 ◽  
pp. 13-13
Author(s):  
Amir Amniattalab ◽  
Amin Rezazadeh
Keyword(s):  
Endothelial Cells ◽  
Complete Blood Count ◽  
Incidental Finding ◽  
Smooth Muscle Actin ◽  
Exploratory Laparotomy ◽  
Lymphocytic Infiltration ◽  
Fusobacterium Necrophorum ◽  
Urine Specific Gravity ◽  
Protein Levels ◽  
The Masses

This report describes the occurrence of omental hemangioma in a five-year-old Himalayan cat. The cat was affected by hemorrhagic gastroenteritis caused by Fusobacterium necrophorum. Also, chronic renal failure (CRF) was demonstrated according to high levels of blood urine nitrogen (BUN), creatinine (Cr), as well as hypoproteinemia and anemia. In this respect, in urinalysis, urine specific gravity (USG) decreased while urea, creatinine and total protein levels increased. Moreover, the complete blood count (CBC) tests showed neutrophilia, monocytosis and lymphopenia. During an exploratory laparotomy, nine masses with a size of 1-5 mm and firm consistency were found to be scattered on the omentum. Histologically, the masses consisted of capillary-cavernous vessels with well-differentiated endothelial cells. No mitotic figures, hemorrhage, or necrosis were found, but there was focal lymphocytic infiltration in the parenchyma of the masses. Immunohistochemically, expression of vimentin and von Willebrand factor (vWF) was found in the endothelial cells, while the immunoreaction to smooth muscle actin (?SMA) was negative. These findings confirmed the diagnosis of hemangioma. To the best of the authors? knowledge, this is the first report of feline omental hemangioma.

scholarly journals Congenital Cutaneous Kaposiform Hemangioendothelioma in a Newborn Calf

2020 ◽  
Vol 43 (2) ◽  
pp. 193-196
Author(s):  
Erkmen Tuğrul Epikmen ◽  
Ahmet Aydogan ◽  
Hamdi Avci ◽  
Sümbül Serap Birincioğlu
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Tumor Cells ◽  
Histopathological Examination ◽  
Smooth Muscle Actin ◽  
Whole Body ◽  
Muscle Actin ◽  
Alpha Smooth Muscle Actin ◽  
Kaposiform Hemangioendothelioma ◽  
The Masses

AbstractA one-day-old female Holstein calf was presented with subcutaneous masses spread over the whole body. Macroscopically, the masses were firm in touch, greyish-white in colour, 0.5-2 cm in diameter range. Histopathological examination confirmed the cutaneous Kaposiform hemangioendothelioma (KHE). Microscopic examination of the tumor revealed sheets of spindled endothelial cells forming vascular slits. Immunohistochemically, the tumor cells and capillaries gave strongly positive reaction for CD31 while vimentin, alpha smooth muscle actin and cytokeratin AE1/AE3 were negative. In this case, macroscopical, detailed histhopathological and immunohistochemical findings of congenital KHE reported firstly in a newborn calf.

High Mobility Group Box Chromosomal Protein-1 Induces Myofibroblast Differentiation and Extracellular Matrix Production via RAGE, p38, JNK and AP-1 Signaling Pathways in Nasal Fibroblasts

2021 ◽  
pp. 194589242199814
Author(s):  
Soo-Hyung Lee ◽  
Jae Hoon Cho ◽  
Joo-Hoo Park ◽  
Jung-Sun Cho ◽  
Heung-Man Lee
Keyword(s):  
Extracellular Matrix ◽  
Chronic Rhinosinusitis ◽  
Smooth Muscle Actin ◽  
High Mobility ◽  
Signal Pathway ◽  
High Mobility Group ◽  
Myofibroblast Differentiation ◽  
Chromosomal Protein ◽  
Protein Levels ◽  
Matrix Production

Background Chronic rhinosinusitis is involved in myofibroblast differentiation and extracellular matrix (ECM) accumulation. High mobility group box chromosomal protein 1 (HMGB-1) is known to stimulate lung fibroblast to produce ECM in lung fibrosis. The aim of this study was to investigate whether HMGB-1 induces myofibroblast differentiation and ECM production in nasal fibroblasts and to identify the signal pathway. Methods Human nasal fibroblasts were cultured. After stimulation with HMGB-1, expressions of α-smooth muscle actin (α-SMA) and fibronectin were determined by real-time PCR and western blot. Total collagen was measured by Sircol assay. To investigate signal pathway, various signal inhibitors and RAGE siRNA were used. Results HMGB-1 increased α-SMA and fibronectin in mRNA and protein levels. It also increased collagen production. RAGE siRNA inhibited HMGB-1-induced α-SMA and fibronectin, and production of collagen. Furthermore, the inhibitors of RAGE downstream molecules such as p38, JNK and AP-1 also blocked the HMGB-1-induced effects. Conclusions HMGB-1 induces myofibroblast differentiation and ECM production in nasal fibroblast, which is mediated by RAGE, p38, JNK and AP-1 signal pathway. These results suggest that HMGB-1 may play an important role in tissue remodeling during chronic rhinosinusitis progression.

scholarly journals Mid-luteal angiogenesis and function in the primate is dependent on vascular endothelial growth factor

2001 ◽  
Vol 168 (3) ◽  
pp. 409-416 ◽  
Author(s):  
SE Dickson ◽  
R Bicknell ◽  
HM Fraser
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Luteal Phase ◽  
Smooth Muscle Actin ◽  
Proliferation Index ◽  
Endothelial Cell Proliferation ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

Vascular endothelial growth factor (VEGF) is essential for the angiogenesis required for the formation of the corpus luteum; however, its role in ongoing luteal angiogenesis and in the maintenance of the established vascular network is unknown. The aim of this study was to determine whether VEGF inhibition could intervene in ongoing luteal angiogenesis using immunoneutralisation of VEGF starting in the mid-luteal phase. In addition, the effects on endothelial cell survival and the recruitment of periendothelial support cells were examined. Treatment with a monoclonal antibody to VEGF, or mouse gamma globulin for control animals, commenced on day 7 after ovulation and continued for 3 days. Bromodeoxyuridine (BrdU), used to label proliferating cells to obtain a proliferation index, was administered one hour before collecting ovaries from control and treated animals. Ovarian sections were stained using antibodies to BrdU, the endothelial cell marker, CD31, the pericyte marker, alpha-smooth muscle actin, and 3' end DNA fragments as a marker for apoptosis. VEGF immunoneutralisation significantly suppressed endothelial cell proliferation and the area occupied by endothelial cells while increasing pericyte coverage and the incidence of endothelial cell apoptosis. Luteal function was markedly compromised by anti-VEGF treatment as judged by a 50% reduction in plasma progesterone concentration. It is concluded that ongoing angiogenesis in the mid-luteal phase is primarily driven by VEGF, and that a proportion of endothelial cells of the mid-luteal phase vasculature are dependent on VEGF support.

Abstract 418: Co-Culture of Endothelial Cells, Smooth Muscle Cells and Monocytes in Collagen Scaffold: A Novel i n vitro Model of Atherosclerosis

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Martin Liu ◽  
Angelos Karagiannis ◽  
Matthew Sis ◽  
Srivatsan Kidambi ◽  
Yiannis Chatzizisis
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Type I Collagen ◽  
Smooth Muscle Actin ◽  
Muscle Cells ◽  
Type I ◽  
Collagen Gels ◽  
Human Coronary Artery

Objectives: To develop and validate a 3D in-vitro model of atherosclerosis that enables direct interaction between various cell types and/or extracellular matrix. Methods and Results: Type I collagen (0.75 mg/mL) was mixed with human artery smooth muscle cells (SMCs; 6x10 5 cells/mL), medium, and water. Human coronary artery endothelial cells (HCAECs; 10 5 /cm 2 ) were plated on top of the collagen gels and activated with oxidized low density lipoprotein cholesterol (LDL-C). Monocytes (THP-1 cells; 10 5 /cm 2 ) were then added on top of the HCAECs. Immunofluorescence showed the expression of VE-cadherin by HCAECs (A, B) and α-smooth muscle actin by SMCs (A). Green-labelled LDL-C particles were accumulated in the subendothelial space, as well as in the cytoplasm of HCAECs and SMCs (C). Activated monocytes were attached to HCAECs and found in the subendothelial area (G-I). Both HCAECs and SMCs released IL-1β, IL-6, IL-8, PDGF-BB, TGF-ß1, and VEGF. Scanning and transmission electron microscopy showed the HCAECs monolayer forming gap junctions and the SMCs (D-F) and transmigrating monocytes within the collagen matrix (G-I). Conclusions: In this work, we presented a novel, easily reproducible and functional in-vitro experimental model of atherosclerosis that has the potential to enable in-vitro sophisticated molecular and drug development studies.

The role of matrix metalloproteinase activity in the maturation of human capillary endothelial cells in vitro

1999 ◽  
Vol 112 (10) ◽  
pp. 1599-1609 ◽  
Author(s):  
B.M. Kraling ◽  
D.G. Wiederschain ◽  
T. Boehm ◽  
M. Rehn ◽  
J.B. Mulliken ◽  
...  
Keyword(s):  
Cell Culture ◽  
Cell Proliferation ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Endothelial Cell Proliferation ◽  
Protein Levels ◽  
Matrix Deposition ◽  
Capillary Endothelial Cells ◽  
Vessel Maturation

Vessel maturation during angiogenesis (the formation of new blood vessels) is characterized by the deposition of new basement membrane and the downregulation of endothelial cell proliferation in the new vessels. Matrix remodeling plays a crucial, but still poorly understood role, in angiogenesis regulation. We present here a novel assay system with which to study the maturation of human capillary endothelial cells in vitro. When human dermal microvascular endothelial cells (HDMEC) were cultured in the presence of dibutyryl cAMP (Bt2) and hydrocortisone (HC), the deposition of a fibrous lattice of matrix molecules consisting of collagens type IV, type XVIII, laminin and thrombospondin was induced. In basal medium (without Bt2 and HC), HDMEC released active matrix metalloproteinases (MMPs) into the culture medium. However, MMP protein levels were significantly reduced by treatment with Bt2 and HC, while protein levels and activity of endogenous tissue inhibitor of MMPs (TIMP) increased. This shift in the proteolytic balance and matrix deposition was inhibited by the specific protein kinase A inhibitors RpcAMP and KT5720 or by substituting analogues without reported glucocorticoid activity for HC. The addition of MMP inhibitors human recombinant TIMP-1 or 1,10-phenanthroline to cultures under basal conditions induced matrix deposition in a dose-dependent manner, which was not observed with the serine protease inhibitor epsilon-amino-n-caproic acid (ACA). The deposited basement membrane-type of matrix reproducibly suppressed HDMEC proliferation and increased HDMEC adhesion to the substratum. These processes of matrix deposition and downregulation of endothelial cell proliferation, hallmarks of differentiating new capillaries in the end of angiogenesis, were recapitulated in our cell culture system by decreasing the matrix-degrading activity. These data suggest that our cell culture assay provides a simple and feasible model system for the study of capillary endothelial cell differentiation and vessel maturation in vitro.

Abstract 531: Tie-2/Cre--Mediated Conditional Deletion of Lipid Phosphate Phosphatase-3 Reveals Its Role in Endothelial Cell Apoptosis

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Ishita Chatterjee ◽  
Kishore K Wary
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Genome Wide Association Study ◽  
Vascular Endothelial Cell ◽  
Protein Levels ◽  
Conditional Deletion ◽  
Transmission Electron ◽  
Increased Risk

Rationale: A recent genome-wide association study (GWAS) has linked a frequently occurring variation in the LPP3 (also known as PPAP2b) loci to increased risk of coronary heart disease (CAD). However, the in vivo function of LPP3 in vascular endothelial cell is incompletely understood. Goal: To address the endothelial cell (EC) specific function of Lpp3 in mice. Results: Tie-2/Cre mediated Lpp3 deletion did not affect normal vasculogenesis in early embryonic development, in contrast, in late embryonic stages it led to impaired angiogenesis associated with hemorrhage, edema and late embryonic lethal phenotype. Immunohistochemical staining followed by microscopic analyses of mutant embryos revealed reduced fibronectin and VE-cadherin expression throughout different vascular bed, and increased apoptosis in CD31+ vascular structures. Transmission electron microscopy (TEM) showed the presence of apoptotic endothelial cells and disruption of adherens junctions in mutant embryos. LPP3-knockdown in vitro showed an increase in p53 and p21 protein levels, with concomitant decrease in cell proliferation. LPP3-knockdown also decreased transendothelial electrical resistance (TER), interestingly re-expression of ß-catenin cDNA into LPP3-depleted endothelial cells partially restored the effect of loss of LPP3. Conclusion: These results suggest the ability of LPP3 to regulate survival and apoptotic activities of endothelial cells during patho/physiological angiogenesis.

scholarly journals Anti-Inflammatory and Anti-Apoptotic Effects of Stybenpropol A on Human Umbilical Vein Endothelial Cells

2019 ◽  
Vol 20 (21) ◽  
pp. 5383 ◽  
Author(s):  
Li Zhang ◽  
Feifei Wang ◽  
Qing Zhang ◽  
Qiuming Liang ◽  
Shumei Wang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Umbilical Vein ◽  
Caspase 9 ◽  
Protein Levels ◽  
Tnf Α ◽  
Umbilical Vein Endothelial Cells ◽  
Cell Adhesion Molecule 1

Inflammation is a key mediator in the progression of atherosclerosis (AS). Benzoinum, a resin secreted from the bark of Styrax tonkinensis, has been widely used as a form of traditional Chinese medicine in clinical settings to enhance cardiovascular function, but the active components of the resin responsible for those pharmaceutical effects remain unclear. To better clarify these components, a new phenylpropane derivative termed stybenpropol A was isolated from benzoinum and characterized via comprehensive spectra a nalysis. We further assessed how this phenylpropane derivative affected treatment of human umbilical vein endothelial cells (HUVECs) with tumor necrosis factor-α (TNF-α). Our results revealed that stybenpropol A reduced soluble intercellular cell adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), interleukin-8 (IL-8), and interleukin-1β (IL-1β) expression by ELISA, inhibited apoptosis, and accelerated nitric oxide (NO) release in TNF-α-treated HUVECs. We further found that stybenpropol A decreased VCAM-1, ICAM-1, Bax, and caspase-9 protein levels, and increased the protein levels of Bcl-2, IKK-β, and IκB-α. This study identified a new, natural phenylpropane derivative of benzoinum, and is the first to reveal its cytoprotective effects in the context of TNF-α-treated HUVECs via regulation of the NF-κB and caspase-9 signaling pathways.

A Step Forward Toward the Understanding of the Long-Term Pathogenesis of Double Capsule Formation in Macrotextured Implants: A Prospective Histological Analysis

2018 ◽  
Vol 39 (11) ◽  
pp. 1191-1199 ◽  
Author(s):  
Caroline A Glicksman ◽  
Michel A Danino ◽  
Johnny I Efanov ◽  
Arij El Khatib ◽  
Monica Nelea
Keyword(s):  
Smooth Muscle ◽  
Histological Analysis ◽  
Incidental Finding ◽  
Smooth Muscle Actin ◽  
Muscle Actin ◽  
Alpha Smooth Muscle Actin ◽  
Level Of Evidence ◽  
Staining Techniques ◽  
Hematoxylin And Eosin ◽  
Mechanical Shearing

Abstract Background Although increasingly reported in the literature, most plastic surgeons cannot define the etiology of double capsules. Often an incidental finding at implant exchange, double capsules are frequently associated with macrotextured devices. Several mechanisms have been proposed, including at the forefront that shearing causes a delamination of the periprosthetic capsule into a double capsule. Objectives This study was designed to confirm the hypothesis that mechanical forces are involved in formation of double capsules by histological analysis. Methods A prospective analysis of consecutive implants with double capsules removed over 2 years was performed. Data collected at the time of surgery included Baker classification, reason for explant, implant manufacturer and style, and any presence of a seroma associated with the capsule. Specimens were sent for analysis by histology utilizing hematoxylin and eosin and alpha-smooth muscle actin staining techniques. Results Eight double capsules were collected for specimen analysis. All capsules demonstrated evidence of granulation tissue, alpha-smooth muscle actin positive myofibroblasts, and folds with embedded texture. Fibrosis surrounded weak areas with presence of layering and splitting, creating a potential space that is prone to separation. Tears and folds from granulomatous reaction are also present within the outer layer of the double capsule, which can only be explained by a mechanical shearing force as a pathogenic mechanism. Conclusions Understanding the pathogenesis of double capsules may allow plastic surgeons to refine their indications for macrotextured implants while providing guidance to patients on avoidance of activities that produce shear-forces. The findings support the hypothesis that shearing forces delaminate the capsule into 2 separate distinct capsules. Level of Evidence: 5

scholarly journals Shiga Toxin 2 Reduces Complement Inhibitor CD59 Expression on Human Renal Tubular Epithelial and Glomerular Endothelial Cells

2013 ◽  
Vol 81 (8) ◽  
pp. 2678-2685 ◽  
Author(s):  
Silvia Ehrlenbach ◽  
Alejandra Rosales ◽  
Wilfried Posch ◽  
Doris Wilflingseder ◽  
Martin Hermann ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Surface ◽  
Shiga Toxin ◽  
Human Kidney ◽  
Enzyme Linked Immunosorbent Assay ◽  
Content Type ◽  
Protein Levels ◽  
Glomerular Endothelial Cells ◽  
Shiga Toxin 2 ◽  
Renal Tubular

ABSTRACTInfections with enterohemorrhagicEscherichia coli(EHEC) are a primary cause of hemolytic-uremic syndrome (HUS). Recently, Shiga toxin 2 (Stx2), the major virulence factor of EHEC, was reported to interact with complement, implying that the latter is involved in the pathogenesis of EHEC-induced HUS. The aim of the present study was to investigate the effect of Stx2 on the expression of membrane-bound complement regulators CD46, CD55, and CD59 on proximal tubular epithelial (HK-2) and glomerular endothelial (GEnC) cells derived from human kidney cells that are involved in HUS. Incubation with Stx2 did not influence the amount of CD46 or CD55 on the surface of HK-2 and GEnC cells, as determined by fluorescence-activated cell sorter analysis. In contrast, CD59 was significantly reduced by half on GEnC cells, but the reduction on HK-2 cells was less pronounced. With increasing amounts of Stx2, reduction of CD59 also reached significance in HK-2 cells. Enzyme-linked immunosorbent assay analyses showed that CD59 was not present in the supernatant of Stx2-treated cells, implying that CD59 reduction was not caused by cleavage from the cell surface. In fact, reverse transcription-quantitative PCR analyses showed downregulation of CD59 mRNA as the likely reason for CD59 cell surface reduction. In addition, a significant increase in terminal complement complex deposition on HK-2 cells was observed after treatment with Stx2, as a possible consequence of CD59 downregulation. In summary, Stx2 downregulates CD59 mRNA and protein levels on tubular epithelial and glomerular endothelial cells, and this downregulation likely contributes to complement activation and kidney destruction in EHEC-associated HUS.

MO761THE CONTRIBUTION OF HIGH-PHOSPHORUS IN EXTRACELLULAR MATRIX ACCUMULATION OF VALVULAR CALCIFICATION IN CHRONIC KIDNEY DISEASE

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Liting Wang ◽  
Yuxia Zhang ◽  
Yujia Wang ◽  
Rining Tang
Keyword(s):  
Chronic Kidney Disease ◽  
Extracellular Matrix ◽  
Endothelial Cells ◽  
Kidney Disease ◽  
Early Stage ◽  
Umbilical Vein ◽  
Akt Pathway ◽  
Protein Levels ◽  
Valvular Calcification ◽  
High Phosphorus

Abstract Background and Aims The characteristics of valvular calcification (VC) in early stage are extracellular matrix (ECM) accumulation and muti-cells activation. In our previous work, we found high-phosphorus (HP) diet aggravated ECM accumulation in both aortic valve and mitral valve in rats with chronic kidney disease (CKD). However, the underlying mechanism of HP contribution in ECM accumulation of CKD-induced VC is still unknown. Method canine valvular interstitial cells (VICs), valvular endothelial cells (VECs) and human umbilical vein endothelial cells (HUVECs) were used in this study. CKD mice (C57b and Tek-EGFP-PolyA) was build by 0.2% adenine-diet for 6 weeks and HP diet/NP diet for 10 weeks. Results As for VICs, HP induced qVICs transfer into aVICs, not oVICs, which was characterized with upregulated level of smoothelin and viemitin. There was no calcium accumulation was observed, suggesting that VICs do not have the ability to synthesize calcium crystals under pure HP intervention. As for VECs, aVICs activated by HP induced VECs EndMT in a transwell-assay, which was characterized with decreasing protein levels of endothelial markers (CD31, vWF, VE-cadherin) and increasing protein levels of mesenchymal makers (α-SMA, FSP1, N-cadherin). Then, IL-8 was found as the main factor releasing from VICs to induce VECs EndMT. In vitro, the concentration of IL-8 in the lower chamber could reach 2-4ng/ml. Reparixin was used to inhibit IL-8 receptor of VECs, which could relive aVICs-induced EndMT. In vivo, the expression of valve CXCL-2 (the mouse IL8 functional homolog) was increased in HP-diet compared with NP-diet, though the serum level of CXCL-2 was similar between two groups. AAV9-sm22a-CXCL-2 and Reparixin could inhibit VECs EndMT by inhibiting VICs relasing CXCL-2 and inhibiting VECs IL-8 receptor in CKD mice of Tek-EGFP-PolyA respectively. Then, IL-8 was found to induced VECs EndMT by miR-214-3p/PTEN/Akt pathway. Inhibiting EndMT by blocking IL-8/miR-214-3p could alleviate ECM accumulation. Conclusion HP could induce qVICs transfer into aVICs, and aVICs could cause VECs EndMT via IL-8/miR-214-3p/PTEN/Akt pathway. Both take part in ECM accumulation in CKD-induced VC.

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