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.

Role of α1β1-integrin in arterial stiffness and angiotensin-induced arterial wall hypertrophy in mice

2007 ◽  
Vol 293 (4) ◽  
pp. H2597-H2604 ◽  
Author(s):  
Huguette Louis ◽  
Augustine Kakou ◽  
Veronique Regnault ◽  
Carlos Labat ◽  
Aude Bressenot ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Arterial Stiffness ◽  
Mechanical Strength ◽  
P38 Mapk ◽  
Smooth Muscle Actin ◽  
Wall Stress ◽  
Integrin Expression ◽  
Ang Ii ◽  
Cross Sectional

We examined the arterial phenotype of mice lacking α1-integrin (α1−/−) at baseline and after 4 wk of ANG II or norepinephrine (NE) administration. Arterial mechanical properties were determined in the carotid artery (CA). Integrin expression, MAPK kinases, and focal adhesion kinase (FAK) were assessed in the aorta. No change in arterial pressure was observed in α1−/− mice. Elastic modulus-wall stress curves were similar in α1−/− and α1+/+ animals, indicating no change in arterial stiffness. The rupture pressure was lower in α1−/− mice, demonstrating decreased mechanical strength. Lack of α1-integrin was accompanied by an increase in β1-, αv-, and α5-integrins but no change in α2-integrin. ANG II increased medial cross-sectional area of the CA in α1+/+, but not α1−/−, mice, whereas equivalent pressor doses of NE did not produce a significant increase in either group. In α1+/+ mice, ANG II induced α1-integrin expression and smooth muscle cell (SMC) hypertrophy in the CA in association with increased aortic expression of α-smooth muscle actin and smooth muscle myosin heavy chain and phosphorylation of ERK1/2, p38 MAPK, and FAK. ANG II did not induce SMC hypertrophy or phosphorylation of p38 MAPK and FAK in α1−/− mice. A functional anti-α1-integrin antibody inhibited in vitro the ANG II-induced phosphorylation of FAK and p38 MAPK. In conclusion, α1−/− mice exhibit a reduced mechanical strength at baseline and a lack of ANG II-induced SMC hypertrophy. These results emphasize the importance of α1β1-integrin in p38 MAPK and FAK phosphorylation during vascular hypertrophy in response to ANG II.

scholarly journals Cutaneous myofibroblastic fibrosarcoma in a margay (Leopardus wiedii): a case report

2020 ◽  
Vol 13 (3) ◽  
pp. 597-601
Author(s):  
Raúl Bermúdez-Salas ◽  
Natalia Campos ◽  
Daniel Barrantes ◽  
Randall Arguedas ◽  
Alejandro Alfaro-Alarcón
Keyword(s):  
Smooth Muscle ◽  
Case Report ◽  
Smooth Muscle Actin ◽  
Histopathological Analysis ◽  
Muscle Actin ◽  
First Report ◽  
Mesenchymal Neoplasm

A routine check-up was performed on a captive 14-year-old female margay (Leopardus wiedii), a cutaneous mass was detected on the ventral thorax. The mass was surgically removed and sent for histopathological analysis. Histologically, the mass was a poorly-demarcated, highly cellular, infiltrative and unencapsulated mesenchymal neoplasm. Immunohistochemical labeling for smooth muscle actin and vimentin were positive, while desmin and cytokeratin were negative which is consistent with a myofibroblastic fibrosarcoma. This type of tumor has been diagnosed in wild felines, however this seems to be the first report of its occurrence in this L. wiedii. Wildlife oncology studies should be performed to promote our understanding of cancer in a species.

Prostatic Rhabdomyoma in a Toddler: A Case Report With Molecular Characterization

2021 ◽  
pp. 109352662110469
Author(s):  
Paola X. De la Iglesia Niveyro ◽  
J. Pandolfi ◽  
F. Jauk ◽  
T. Kreindel ◽  
P. Lobos
Keyword(s):  
Differential Diagnosis ◽  
Smooth Muscle ◽  
Case Report ◽  
Next Generation Sequencing ◽  
Smooth Muscle Actin ◽  
Muscle Actin ◽  
Ultrasound Evaluation ◽  
Microscopic Evaluation ◽  
Generation Sequencing

We present a 29-month-old male patient in follow-up due to pyelocaliceal dilation with a prostatic nodule incidentally found during ultrasound evaluation. Cysto video endoscopy was performed and a prostate biopsy, obtained. Microscopic evaluation showed a haphazardly distributed population of muscular cells with cross striations without evidence of mitosis or necrosis. Immunohistochemistry was positive for myogenin and desmin and negative for smooth muscle actin. Next generation sequencing was performed without finding any pathogenic variant or fusion in the tumor RNA. The patient received no further treatment, remained asymptomatic and continues in follow up, 3 years after initial diagnosis. We report a case of prostate rhabdomyoma in a toddler, an exceptional location that raises concern about differential diagnosis with its malignant counterpart, rhabdomyosarcoma, especially at this age.

scholarly journals Procyanidin B2 Reduces Vascular Calcification through Inactivation of ERK1/2-RUNX2 Pathway

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 916
Author(s):  
Yingquan Liang ◽  
Guilan Chen ◽  
Feng Zhang ◽  
Xiaoxiao Yang ◽  
Yuanli Chen ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Calcification ◽  
Aortic Root ◽  
Smooth Muscle Actin ◽  
Bone Morphogenetic Protein 2 ◽  
Plaque Burden ◽  
Runx2 Expression ◽  
Plaque Instability ◽  
Related Transcription Factor

Vascular calcification is strongly associated with atherosclerotic plaque burden and plaque instability. The activation of extracellular signal-regulated kinase 1/2 (ERK1/2) increases runt related transcription factor 2 (RUNX2) expression to promote vascular calcification. Procyanidin B2 (PB2), a potent antioxidant, can inhibit ERK1/2 activation in human aortic smooth muscle cells (HASMCs). However, the effects and involved mechanisms of PB2 on atherosclerotic calcification remain unknown. In current study, we fed apoE-deficient (apoE−/−) mice a high-fat diet (HFD) while treating the animals with PB2 for 18 weeks. At the end of the study, we collected blood and aorta samples to determine atherosclerosis and vascular calcification. We found PB2 treatment decreased lesions in en face aorta, thoracic, and abdominal aortas by 21.4, 24.6, and 33.5%, respectively, and reduced sinus lesions in the aortic root by 17.1%. PB2 also increased α-smooth muscle actin expression and collagen content in lesion areas. In the aortic root, PB2 reduced atherosclerotic calcification areas by 75.8%. In vitro, PB2 inhibited inorganic phosphate-induced osteogenesis in HASMCs and aortic rings. Mechanistically, the expression of bone morphogenetic protein 2 and RUNX2 were markedly downregulated by PB2 treatment. Additionally, PB2 inhibited ERK1/2 phosphorylation in the aortic root plaques of apoE−/− mice and calcified HASMCs. Reciprocally, the activation of ERK1/2 phosphorylation by C2-MEK1-mut or epidermal growth factor can partially restore the PB2-inhibited RUNX2 expression or HASMC calcification. In conclusion, our study demonstrates that PB2 inhibits vascular calcification through the inactivation of the ERK1/2-RUNX2 pathway. Our study also suggests that PB2 can be a potential option for vascular calcification treatment.

Rapid growth of myxoid leiomyosarcoma of the vulva during pregnancy: a case report

2004 ◽  
Vol 14 (1) ◽  
pp. 172-175 ◽  
Author(s):  
A. R. Di Gilio ◽  
G. Cormio ◽  
L. Resta ◽  
C. Carriero ◽  
V. Loizzi ◽  
...  
Keyword(s):  
Differential Diagnosis ◽  
Smooth Muscle ◽  
Case Report ◽  
Lymph Node ◽  
Cesarean Section ◽  
Recurrent Disease ◽  
Node Dissection ◽  
Smooth Muscle Tumors ◽  
Vulvar Mass

Smooth muscle tumors arising in the vulva are rare. Leiomyosarcoma is the most common variant of vulvar sarcoma, and very few cases have been reported during pregnancy. A 36-year-old woman presented with a progressively enlarging vulvar mass during pregnancy, diagnosed as a Bartholin's gland cyst. The lesion was resected at 38 weeks of gestation during cesarean section and diagnosis of myxoid leiomyosarcoma of the vulva was made. Six weeks later the patients were referred to our center and submitted to wide vulvar excision with groin lymph node dissection that revealed the presence of a small residual focus of leiomyosarcoma. At 30 months of follow-up the patient was well without any sign of recurrent disease. Leiomyosarcoma should be included in the differential diagnosis of vulvar masses; progressively enlarging vulvar lesion should be biopsied even during pregnancy. Leiomyosarcoma should be considered in the differential diagnosis of vulvar mass.

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.

scholarly journals The Functional Role of Zinc Finger E Box-Binding Homeobox 2 (Zeb2) in Promoting Cardiac Fibroblast Activation

2018 ◽  
Vol 19 (10) ◽  
pp. 3207 ◽  
Author(s):  
Fahmida Jahan ◽  
Natalie Landry ◽  
Sunil Rattan ◽  
Ian Dixon ◽  
Jeffrey Wigle
Keyword(s):  
Smooth Muscle ◽  
Zinc Finger ◽  
Cardiac Fibrosis ◽  
Smooth Muscle Actin ◽  
Critical Role ◽  
Cardiac Fibroblast ◽  
In Vivo Studies ◽  
Fibroblast Activation ◽  
E Box

Following cardiac injury, fibroblasts are activated and are termed as myofibroblasts, and these cells are key players in extracellular matrix (ECM) remodeling and fibrosis, itself a primary contributor to heart failure. Nutraceuticals have been shown to blunt cardiac fibrosis in both in-vitro and in-vivo studies. However, nutraceuticals have had conflicting results in clinical trials, and there are no effective therapies currently available to specifically target cardiac fibrosis. We have previously shown that expression of the zinc finger E box-binding homeobox 2 (Zeb2) transcription factor increases as fibroblasts are activated. We now show that Zeb2 plays a critical role in fibroblast activation. Zeb2 overexpression in primary rat cardiac fibroblasts is associated with significantly increased expression of embryonic smooth muscle myosin heavy chain (SMemb), ED-A fibronectin and α-smooth muscle actin (α-SMA). We found that Zeb2 was highly expressed in activated myofibroblast nuclei but not in the nuclei of inactive fibroblasts. Moreover, ectopic Zeb2 expression in myofibroblasts resulted in a significantly less migratory phenotype with elevated contractility, which are characteristics of mature myofibroblasts. Knockdown of Zeb2 with siRNA in primary myofibroblasts did not alter the expression of myofibroblast markers, which may indicate that Zeb2 is functionally redundant with other profibrotic transcription factors. These findings add to our understanding of the contribution of Zeb2 to the mechanisms controlling cardiac fibroblast activation.

scholarly journals A translational cellular model for the study of peritubular cells of the testis

Reproduction ◽  
2020 ◽  
Vol 160 (2) ◽  
pp. 259-268 ◽  
Author(s):  
Nina Schmid ◽  
Annika Missel ◽  
Stoyan Petkov ◽  
Jan B Stöckl ◽  
Florian Flenkenthaler ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Replicative Senescence ◽  
Smooth Muscle Actin ◽  
Proteome Analysis ◽  
Inflammatory Factors ◽  
Seminiferous Tubules ◽  
Cellular Model ◽  
Mechanistic Studies ◽  
Peritubular Cells

Testicular peritubular cells (TPCs) are smooth muscle-like cells, which form a compartment surrounding the seminiferous tubules. Previous studies employing isolated human testicular peritubular cells (HTPCs) indicated that their roles in the testis go beyond sperm transport and include paracrine and immunological contributions. Peritubular cells from a non-human primate (MKTPCs), the common marmoset monkey, Callithrix jacchus, share a high degree of homology with HTPCs. However, like their human counterparts these cells age in vitro and replicative senescence limits in-depth functional or mechanistic studies. Therefore, a stable cellular model was established. MKTPCs of a young adult animal were immortalized by piggyBac transposition of human telomerase (hTERT), that is, without the expression of viral oncogenes. Immortalized MKTPCs (iMKTPCs) grew without discernable changes for more than 50 passages. An initial characterization revealed typical genes expressed by peritubular cells (androgen receptor (AR), smooth-muscle actin (ACTA2), calponin (CNN1)). A proteome analysis of the primary MKTPCs and the derived immortalized cell line confirmed that the cells almost completely retained their phenotype. To test whether they respond in a similar way as HTPCs, iMKTPCs were challenged with forskolin (FSK) and ATP. As HTPCs, they showed increased expression level of the StAR protein (StAR) after FSK stimulation, indicating steroidogenic capacity. ATP increased the expression of pro-inflammatory factors (e.g. IL1B; CCL7), as it is the case in HTPCs. Finally, we confirmed that iMKTPCs can efficiently be transfected. Therefore, they represent a highly relevant translational model, which allows mechanistic studies for further exploration of the roles of testicular peritubular cells.

scholarly journals Case Report: A giant myopericytoma involving the occipital region of the scalp - a rare entity

F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 2905 ◽  
Author(s):  
Sunil Munakomi ◽  
Pramod Chaudhary
Keyword(s):  
Smooth Muscle ◽  
Case Report ◽  
Histological Examination ◽  
Rare Case ◽  
Smooth Muscle Actin ◽  
Positive Staining ◽  
Occipital Region ◽  
Rare Entity ◽  
Muscle Actin ◽  
Complete Excision

Herein we report a rare case of a giant myopericytoma presenting in a 16-year-old girl as a slowly progressive swelling involving the scalp in the occipital region. It was managed by complete excision. Histological examination of the lesion revealed  spindle-shaped cells forming characteristic rosettes around the blood vessels, and positive staining with smooth muscle actin.

Drebrin attenuates atherosclerosis by limiting smooth muscle cell transdifferentiation

2021 ◽  
Author(s):  
Jiao-Hui Wu ◽  
Lisheng Zhang ◽  
Igor Nepliouev ◽  
Leigh Brian ◽  
Taiqin Huang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Foam Cell ◽  
Atherosclerotic Lesion ◽  
Foam Cells ◽  
Actin Binding ◽  
Cross Sectional ◽  
Cell Transdifferentiation

Abstract Aims The F-actin-binding protein Drebrin inhibits smooth muscle cell (SMC) migration, proliferation and pro-inflammatory signaling. Therefore, we tested the hypothesis that Drebrin constrains atherosclerosis. Methods and results SM22-Cre+/Dbnflox/flox/Ldlr-/- (SMC-Dbn-/-/Ldlr-/-) and control mice (SM22-Cre+/Ldlr-/-, Dbnflox/flox/Ldlr-/-, and Ldlr-/-) were fed a Western diet for 14-20 weeks. Brachiocephalic arteries of SMC-Dbn-/-/Ldlr-/- mice exhibited 1.5- or 1.8-fold greater cross-sectional lesion area than control mice at 14 or 20 wk, respectively. Aortic atherosclerotic lesion surface area was 1.2-fold greater in SMC-Dbn-/-/Ldlr-/- mice. SMC-Dbn-/-/Ldlr-/- lesions comprised necrotic cores that were two-fold greater in size than those of control mice. Consistent with their bigger necrotic core size, lesions in SMC-Dbn-/- arteries also showed more transdifferentiation of SMCs to macrophage-like cells: 1.5- to 2.5-fold greater, assessed with BODIPY or with CD68, respectively. In vitro data were concordant: Dbn-/- SMCs had 1.7-fold higher levels of KLF4 and transdifferentiated to macrophage-like cells more readily than Dbnflox/flox SMCs upon cholesterol loading, as evidenced by greater up-regulation of CD68 and galectin-3. Adenovirally mediated Drebrin rescue produced equivalent levels of macrophage-like transdifferentiation in Dbn-/- and Dbnflox/flox SMCs. During early atherogenesis, SMC-Dbn-/-/Ldlr-/- aortas demonstrated 1.6-fold higher levels of reactive oxygen species than control mouse aortas. The 1.8-fold higher levels of Nox1 in Dbn-/- SMCs was reduced to WT levels with KLF4 silencing. Inhibition of Nox1 chemically or with siRNA produced equivalent levels of macrophage-like transdifferentiation in Dbn-/- and Dbnflox/flox SMCs. Conclusions We conclude that SMC Drebrin limits atherosclerosis by constraining SMC Nox1 activity and SMC transdifferentiation to macrophage-like cells. Translational perspective Drebrin is abundantly expressed in vascular smooth muscle cells (SMCs) and is up-regulated in human atherosclerosis. A hallmark of atherosclerosis is the accumulation of foam cells that secrete pro-inflammatory cytokines and contribute to plaque instability. A large proportion of these foam cells in humans derive from SMCs. We found that SMC Drebrin limits atherosclerosis by reducing SMC transdifferentiation to macrophage-like foam cells in a manner dependent on Nox1 and KLF4. For this reason, strategies aimed at augmenting SMC Drebrin expression in atherosclerotic plaques may limit atherosclerosis progression and enhance plaque stability by bridling SMC-to-foam-cell transdifferentiation.

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