scholarly journals Histopathological analysis of in vivo specimens of recurrent aneurysms after coil embolization

2021 ◽  
pp. neurintsurg-2021-017872
Author(s):  
Chao Wang ◽  
Mengxing Li ◽  
Huiyuan Chen ◽  
Xinjian Yang ◽  
Ying Zhang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Coil Embolization ◽  
Immunohistochemical Staining ◽  
Cell Damage ◽  
Smooth Muscle Actin ◽  
Inflammatory Cells ◽  
Scar Tissue ◽  
Histopathological Analysis ◽  
Aneurysm Wall

BackgroundAneurysm recurrence after coil embolization remains a challenging problem.ObjectiveTo determine the histopathological features of recurrent aneurysm specimens and explore the mechanism of aneurysm recurrence.MethodsNine aneurysm specimens were collected from eight patients who underwent clipping for aneurysm recurrence within 2 years after embolization. All specimens were sectioned and embedded in resin, stained with hematoxylin-eosin (H&E), Masson stain, and immunohistochemical staining for smooth muscle actin (SMA) and CD68+ antibodies, and were examined under light microscopy.ResultsFive aneurysms were surgically clipped owing to post-embolic subarachnoid hemorrhage, while the other four aneurysms had dangerous recanalization detected on follow-up imaging. Five aneurysms had self-growth and four aneurysms had coil compactions. Gross observation showed that each recurrent aneurysm was wrapped by a thrombus and the aneurysm wall; some coils protruded from the pseudocapsule in some ruptured aneurysms. Microscopically, H&E staining showed that three types of thrombi (fresh thrombus, granulation tissue, and scar tissue) coexisted in one section. In addition, characteristic unstable and unorganized thrombi with empty spaces were found in the neck cavity. Immunohistochemical staining showed that the SMA stain was discontinued and incomplete, and CD68+ antibody and H&E staining revealed inflammatory infiltrate in the aneurysm wall.ConclusionThe coexistence of three types of thrombi is the main characteristic of recurrent aneurysms. The formation of stable thrombus may be one of the key points of aneurysm recurrence. Smooth muscle cell damage and infiltration of inflammatory cells in the aneurysm wall probably contribute to the recanalization.

scholarly journals Characterizing patterns of endothelialization following coil embolization: a whole-mount, dual immunostaining approach

2015 ◽  
Vol 8 (4) ◽  
pp. 402-406 ◽  
Author(s):  
Daying Dai ◽  
Yong-Hong Ding ◽  
Issa Rezek ◽  
David F Kallmes ◽  
Ramanathan Kadirvel
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Coil Embolization ◽  
Smooth Muscle Actin ◽  
Central Area ◽  
Immunohistochemical Analysis ◽  
Inflammatory Cells ◽  
Parent Artery ◽  
Aneurysm Neck ◽  
Platinum Coil

BackgroundThe extent, rate, and source of endothelialization following coil embolization of saccular aneurysms remains poorly understood. We performed a whole tissue mount, dual immunohistochemical analysis of experimental aneurysms to characterize the state of endothelialization over time after platinum coil embolization.Method and materialElastase-induced rabbit aneurysms were created and treated with bare platinum coils. Samples were harvested at 4 and 8 weeks (n=6 for each). En face whole tissue mount staining with antibodies to CD31 and α-smooth muscle actin was used to identify endothelial cells and smooth muscle cells, respectively. Sytox green stain was used to demonstrate nuclear morphology for identification of inflammatory cells. The extent of endothelialization was measured in relation to the aneurysm neck–parent artery interface.ResultsAt 4 weeks after coil embolization, very localized membranous tissue and neoendothelial cells were detected on the coil loops immediately adjacent to the parent artery–neck interface, but the remainder of the coil loops remained devoid of endothelial cells. At 8 weeks neoendothelial cells were more confluent over the coils than at 4 weeks, and extended up to 900 µm from the parent artery–neck interface. However, the surfaces of the coils farther away than this region harbored no endothelial cells. Scattered inflammatory cells, including neutrophils and monocytes, were seen on the coil surface at the neck central area, where the coil surface was bare at the 4 and 8 weeks’ follow-up.ConclusionsPlatinum coil embolization supports gradual but limited endothelialization, where endothelial cells migrate directly from the adjacent parent artery.

scholarly journals Large intraperitoneal lipoleiomyoma in a pre-menopausal woman: a case report

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Sara L. Schaefer ◽  
Amy L. Strong ◽  
Sheena Bahroloomi ◽  
Jichang Han ◽  
Michella K. Whisman ◽  
...  
Keyword(s):  
Differential Diagnosis ◽  
Smooth Muscle ◽  
Case Report ◽  
Smooth Muscle Actin ◽  
Abdominal Mass ◽  
Histopathological Analysis ◽  
Menopausal Woman ◽  
En Bloc ◽  
Cross Sectional

Abstract Background Lipoleiomyoma is a rare, benign variant of the commonplace uterine leiomyoma. Unlike leiomyoma, these tumors are composed of smooth muscle cells admixed with mature adipose tissue. While rare, they are most frequently identified in the uterus, but even more infrequently have been described in extrauterine locations. Case presentation We describe a case report of a 45-year-old woman with a history of in vitro fertilization pregnancy presenting 6 years later with abdominal distention and weight loss found to have a 30-cm intra-abdominal lipoleiomyoma. While cross-sectional imaging can narrow the differential diagnosis, histopathological analysis with stains positive for smooth muscle actin, desmin, and estrogen receptor, but negative for HMB-45 confirms the diagnosis of lipoleiomyoma. The large encapsulated tumor was resected en bloc. The patients post-operative course was uneventful and her symptoms resolved. Conclusions Lipoleiomyoma should be considered on the differential diagnosis in a woman with a large intra-abdominal mass. While considered benign, resection should be considered if the mass is symptomatic, and the diagnosis is unclear or there is a concern for malignancy.

Abstract 38: Rbp-j Regulates the Genetic Program of the Myo-epithelioid JG Cell

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Ruth M Castellanos Rivera ◽  
Ellen S. Pentz ◽  
Kenneth W. Gross ◽  
Silvia Medrano ◽  
Jing Yu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Fluorescent Protein ◽  
Smooth Muscle Actin ◽  
Artificial Chromosome ◽  
Specific Protein ◽  
Genetic Program ◽  
Cell Phenotype ◽  
Gfp Expression ◽  
Renin Gene

RBP-J , the major downstream effector of Notch signaling, is necessary to maintain the number of juxtaglomerular (JG) cells. In addition, RBP-J regulates the plasticity of arteriolar smooth muscle cells to adopt the renin cell phenotype when homeostasis is threatened. We hypothesized that RBP-J acts as an on/off switch controlling the expression of genes that determine the renin phenotype. To determine whether RBP-J directly affects renin gene expression, we generated mice harboring a bacterial artificial chromosome (BAC) transgene with green fluorescent protein (GFP) under the control of the renin gene carrying a mutation in its RBP-J- binding site (Mut-BAC). Mut-BAC mice had markedly reduced GFP expression to 12.9 % ±0.01 (n=3) of the control (Wt-BAC) and a diminished response to homeostatic challenges: mut-BAC mice had a reduced number of GFP positive JG areas per total number of glomeruli (Wt-BAC: 25.1 % ±3.0, n=3; Mut-BAC: 9.3 % ±1.4, n=2, p<0.02) and no GFP expression along the arterioles. To determine whether the decrease in the number of JG cells in mice lacking RBP-J (cKO) was due to a diminished endowment of renin progenitor cells, we traced the fate of cells derived from the renin lineage by generating mice ( RBP-J fl/fl ; Ren1d +/cre ; R26R +/- ) in which cells lacking RBP-J simultaneously expressed β-galactosidase (β-gal). The pattern of β-gal in cKO and control kidneys was identical, indicating that cells derived from the renin lineage did not die but instead changed their phenotype. Next we investigated the phenotype adopted by the cells derived from the renin lineage. Expression of α-smooth muscle actin and smoothelin (a marker of mature smooth muscle) was significantly decreased to 41 % ±7.0 (n=2) and 44 % ±8.8 (n=2) respectively with respect to controls (p<0.01). In addition, mutant JG cells in vivo did not express genes characteristic of the renin phenotype such as renin, calponin1, Nfat and Akr1b7 expressing instead fibroblast-specific protein 1 indicating the adoption of a fibroblast-like phenotype. Results indicate that RBP-J directly governs a genetic program that controls the dual endocrine-contractile phenotype of the JG cell, which is crucial to maintain blood pressure and fluid-electrolyte homeostasis.

Abstract 064: The Lipoxigenase Inhibitor Nordihydroguaiaretic Acid Prevents the Development of Hypoxia-Induced Pulmonary Hypertension in Mice

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Andrea Iorga ◽  
Gabriel Wong ◽  
Denise Mai ◽  
Jingyuan Li ◽  
Salil Sharma ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Smooth Muscle ◽  
Smooth Muscle Actin ◽  
Nordihydroguaiaretic Acid ◽  
Treated Group ◽  
Oxidation Products ◽  
Lipoxygenase Inhibitor ◽  
Human Pulmonary Artery

Pulmonary hypertension (PH) is a chronic lung disease characterized by progressively elevated pulmonary arterial pressures and severe pulmonary vascular remodeling resulting from interactions between oxidized lipoprotein deposition and increased endothelial proliferation. Previously we have shown increased plasma levels of biological oxidation products such as hydroxyoctadecadienoic acids (HODEs) and hydroxyeicosatetraenoic acids (HETEs) in the rat monocrotaline model of PH. Here we investigated the role of HETEs and HODEs in the development of PH and whether their inhibition with the lipoxygenase inhibitor nordihydroguaiaretic acid (NDGA) attenuates the progression of PH. Mice were placed in a hypoxic chamber with O2 concentrations of ≤10% for 21 days and either left untreated to develop PH (n=7) or treated with NDGA daily (10mg/kg/day, i.p., n=4) from day 1. Direct RV catheterization was terminally performed to record RV pressure (RVP). Pulmonary arteriolar thickening and oxidized lipid deposition were assessed by staining lung sections with Masson’s Trichrome or with α-smooth muscle actin and E-06 (marker for oxidized low-density lipoproteins). In vitro, human pulmonary artery smooth muscle cell (hPASMC) proliferation was assessed by MTT assays in the absence or presence of 12-HETE (100ng/ml), 9-HODE (1µg/ml) and 13-HODE (1µg/ml) alone or together with NDGA (10, 25 and 50µM). In-vitro, HETE/HODE treatment increased hPASMC proliferation ~ 2-fold when compared to untreated cells and NDGA significantly inhibited the proliferative effects of all three oxidized lipids. In-vivo, NDGA treatment prevented the development of PH. RVP was lower in the NDGA-treated group vs. the PH group (24.01±1.39mmHg vs. 36.91±5.74mmHg, p<0.05) and was comparable to control normoxic mice (20.93±2.52mmHg). RV hypertrophy index was significantly elevated in the PH mice versus control mice (0.38±0.03 vs. 0.28±0.02 (p<0.001), while NDGA treatment completely prevented the development of RV hypertrophy (0.28±0.04). Lung sections demonstrated arteriolar thickening and E-06 positive deposits in the PH group, which was prevented by NDGA therapy. We conclude that oxidized fatty acid deposition and accumulation might play a role in the development of PH.

Piloleiomyosarcoma in Seven Ferrets

2001 ◽  
Vol 38 (6) ◽  
pp. 710-711 ◽  
Author(s):  
B. H. Rickman ◽  
L. E. Craig ◽  
M. H. Goldschmidt
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Immunohistochemical Staining ◽  
Smooth Muscle Actin ◽  
Surgical Excision ◽  
Muscle Actin ◽  
Mustela Putorius ◽  
Nuclear Pleomorphism ◽  
Complete Surgical Excision

In each of seven ferrets ( Mustela putorius furo) with leiomyosarcoma, a single dermal mass was identified and biopsied. Each mass consisted of a well-demarcated but nonencapsulated proliferation of large spindle- to strap-shaped cells arranged in interwoven bundles. The cells resembled the smooth muscle cells of the adjacent arrector pili muscles, but with marked nuclear pleomorphism. Immunohistochemical staining for smooth muscle actin, desmin, and vimentin was positive and staining for myoglobin and cytokeratin was negative. Follow-up on three of the ferrets indicates that the prognosis is good following complete surgical excision.

Upregulation of miR-133a by adiponectin inhibits pyroptosis pathway and rescues acute aortic dissection

2020 ◽  
Vol 52 (9) ◽  
pp. 988-997
Author(s):  
Haizhen Duan ◽  
Xiaojun Zhang ◽  
Renjie Song ◽  
Tongying Liu ◽  
Yuanyuan Zhang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Aortic Dissection ◽  
Acute Aortic Dissection ◽  
Smooth Muscle Actin ◽  
Middle Layer ◽  
Specific Protein ◽  
Receptor Protein ◽  
Mice Model

Abstract Acute aortic dissection (AAD) is a cardiovascular emergency caused by the formation of hematoma in the middle layer of the aortic wall. Adiponectin (APN) is an adipose tissue-specific protein that has anti-inflammation and anti-atherosclerosis functions. Pyroptosis, as an inflammatory cell death, depends on the activation of caspase1, while nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) is a typical representative of the pyroptosis pathway. In this study, we aimed to find whether APN affects the AAD process. The results showed that APN overexpression (OE) inhibited the AAD development and the levels of glucose, triglyceride, and total cholesterol in mice model. In addition, APN OE inhibited the productions of gasdermin D (GSDMD), NLRP3, caspase1, interleukin-1β (IL-1β), IL-18, and osteopontin (OPN), as well as α-smooth muscle actin (α-SMA) downregulation in vitro and in vivo. In addition, NLRP3 was found to be a target gene of miR-133a and miR-133a OE showed similar effects to APN OE in attenuating the LPS-induced productions of GSDMD, NLRP3, caspase1, IL-1β, IL-18, and OPN, as well as α-SMA downregulation in vascular smooth muscle cells (vSMCs). Moreover, the beneficial effects of APN OE were abolished by miR-133a knockdown in vSMCs. In conclusion, our present results indicated that the upregulation of miR-133a by APN inhibits pyroptosis pathway, which potentially rescues AAD.

scholarly journals Role of Mouse Cytochrome P450 Enzymes of the Cyp2abfgs Subfamilies in the Induction of Lung Inflammation by Cigarette Smoke Exposure

2019 ◽  
Vol 172 (1) ◽  
pp. 123-131
Author(s):  
Matthew Hartog ◽  
Qing-Yu Zhang ◽  
Xinxin Ding
Keyword(s):  
Cytochrome P450 ◽  
Tobacco Smoke ◽  
Lung Inflammation ◽  
Inflammatory Cells ◽  
Lavage Fluid ◽  
Cigarette Smoke Exposure ◽  
Histopathological Analysis ◽  
Cytochrome P450 Enzymes

Abstract Many constituents of tobacco smoke (TS) require bioactivation to exert toxic effects; however, few studies have examined the role of bioactivation enzymes in the adverse effects of TS exposure. This knowledge gap is a major source of uncertainty for risk assessment and chemoprevention efforts. Our aim is to test the hypothesis that cytochrome P450 (P450) enzyme-mediated bioactivation is essential to the development of TS exposure-induced lung toxicity, by determining the contributions of P450 enzymes in the mouse Cyp2abfgs gene subfamilies to environmental tobacco smoke (ETS)-induced lung inflammation. Adult female wildtype (WT) and Cyp2abfgs-null mice (both on C57BL/6J background) were exposed to filtered air or ETS, intermittently, for 1 or 2 weeks. Lung inflammation was assessed by quantification of inflammatory cells, cytokines, chemokines, and proteins in bronchoalveolar lavage fluid (BALF) and histopathological analysis. Glutathione (GSH) conjugates of 2 ETS constituents, naphthalene (NA), and 3-methylindole (3MI), were measured in mice exposed to ETS for 4 h. Persistent macrophagic and neutrophilic lung inflammation was observed in ETS-exposed WT mice; the extent of which was significantly reduced in ETS-exposed Cyp2abfgs-null mice. Levels of proinflammatory cytokines and chemokines, along with the total protein concentration, were increased in cell-free BALF from ETS-exposed WT mice, but not Cyp2abfgs-null mice. Additionally, GSH conjugates of NA and 3MI were detected in the lungs of WT, but not Cyp2abfgs-null, mice following ETS exposure. These results provide the first in vivo evidence that the mouse Cyp2abfgs gene cluster plays an important role in ETS-induced lung inflammation.

Leiomyomatous hamartoma of the incisive papilla

2002 ◽  
Vol 25 (2) ◽  
pp. 157-159 ◽  
Author(s):  
Luciana Corrêa ◽  
Mônica Lotufo ◽  
Marília Trierveiler Martins ◽  
Norberto Sugaya ◽  
Suzana Cantanhede Orsini Machado de Sousa
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Immunohistochemical Staining ◽  
Smooth Muscle Actin ◽  
Muscle Cells ◽  
Histological Diagnosis ◽  
Muscle Actin ◽  
Histological Findings ◽  
Spindle Cells ◽  
Congenital Epulis

A case of unusual hamartoma in a six-year-old otherwise healthy Brazilian girl is reported, with emphasis on histological and immunohistochemical features. A mass observed in the incisive papilla was detected whose appearance was similar to congenital epulis or fibroma. Histological findings showed interlacing fascicles of large spindle cells resembling smooth muscle cells. Immunohistochemical staining for desmin and for smooth-muscle actin was positive. The histological diagnosis was leiomyomatous hamartoma, based on clinical and microscopic observations.

Immunohistochemical Staining Characteristics of Canine Gastrointestinal Stromal Tumors

1997 ◽  
Vol 34 (4) ◽  
pp. 303-311 ◽  
Author(s):  
R. G. LaRock ◽  
P. E. Ginn
Keyword(s):  
Smooth Muscle ◽  
Small Intestine ◽  
Immunohistochemical Staining ◽  
Gastrointestinal Stromal Tumors ◽  
Smooth Muscle Actin ◽  
Muscle Actin ◽  
Stromal Tumors ◽  
S 100 ◽  
Microscopic Features ◽  
Microscopic Diagnosis

Sections from 35 formalin-fixed, paraffin-embedded, canine gastrointestinal stromal tumors consisting of 14 leiomyomas (five stomach, three small intestine, two colon, four rectum), 18 leiomyosarcomas (one stomach, five small intestine, nine cecum, three rectum), two undifferentiated sarcomas (two stomach), and one neurofibrosarcoma (small intestine) were examined for the expression of vimentin, S-100 protein, α-smooth muscle actin, and desmin via immunoperoxidase methodology using an avidin-biotin complex technique. The leiomyomas were 4/14 (29%) vimentin-positive, 3/14 (21%) S-100 protein-positive, 10/14 (71%) α-smooth muscle actin-positive and 13/14 (93%) desmin-positive. Leiomyosarcomas were 18/18 (100%) vimentin-positive, 11/18 (61%) S-100 protein-positive, 9/18 (50%) α-smooth muscle actin-positive, and 15/18 (83%) desmin-positive. The undifferentiated sarcomas were 2/2 (100%) vimentin-positive, 2/2 (100%) S-100 protein-positive, 1/2 (50%) α-smooth muscle actin-positive, and 0/2 (0%) desmin-positive. The neurofibrosarcoma was vimentin and S-100 protein-positive and α-smooth muscle actin- and desmin-negative. Thirty-one of thirty-five (89%) of all neoplasms demonstrated reactivity for either desmin and/or α-smooth muscle actin. S-100 protein reactivity occurred in 17/35 (49%) of all specimens. Lack of desmin and α-smooth muscle actin reactivity occurred in 4/35 (11%) of all specimens, all of which were vimentin-positive. The immunohistochemical results indicate that the majority of canine gastrointestinal stromal tumors (GIST) with light microscopic features of smooth muscle cells have immunohistochemical staining patterns supporting smooth muscle differentiation. Vimentin reactivity correlated with a light microscopic diagnosis of malignancy. The lack of smooth muscle cell markers in some tumors and the high percentage of cases positive for S-100 protein may suggest a more complex histogenesis or differentiation for subgroups of these tumors.

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