scholarly journals Spontaneous activity in peripheral diaphragmatic lymphatic loops

2013 ◽  
Vol 305 (7) ◽  
pp. H987-H995 ◽  
Author(s):  
Andrea Moriondo ◽  
Eleonora Solari ◽  
Cristiana Marcozzi ◽  
Daniela Negrini
Keyword(s):  
Vessel Wall ◽  
Wistar Rats ◽  
Smooth Muscle Actin ◽  
Lymphatic Vessels ◽  
Muscle Actin ◽  
Complex Interplay ◽  
Vessel Lumen ◽  
Spontaneous Contractions ◽  
First Time

The spontaneous contractility of FITC-dextran-filled lymphatics at the periphery of the pleural diaphragm was documented for the first time “in vivo” in anesthetized Wistar rats. We found that lymphatic segments could be divided into four phenotypes: 1) active, displaying rhythmic spontaneous contractions (51.8% of 197 analyzed sites); 2) stretch-activated, whose contraction was triggered by passive distension of the vessel lumen (4.1%); 3) passive, which displayed a completely passive distension (4.5%); and 4) inert, whose diameter never changed over time (39.6%). Smooth muscle actin was detected by immunofluorescence and confocal microscopy in the vessel walls of active but also of inert sites, albeit with a very different structure within the vessel wall. Indeed, while in active segments, actin was arranged in a dense mesh completely surrounding the lumen, in inert segments actin decorated the vessels wall in sparse longitudinal strips. When located nearby along the same lymphatic loop, active, stretch-activated, and passive sites were always recruited in temporal sequence starting from the active contraction. The time delay was ∼0.35 s between active and stretch-activated and 0.54 s between stretch-activated and passive segments, promoting a uniform lymph flux of ∼150/200 pl/min. We conclude that, unlike more central diaphragmatic lymphatic vessels, loops located at the extreme diaphragmatic periphery do require an intrinsic pumping mechanism to propel lymph centripetally, and that such an active lymph propulsion is attained by means of a complex interplay among sites whose properties differ but are indeed able to organize lymph flux in an ordered fashion.

scholarly journals Microvascular fragment spheroids: Three-dimensional vascularization units for tissue engineering and regeneration

2021 ◽  
Vol 12 ◽  
pp. 204173142110355
Author(s):  
Lisa Nalbach ◽  
Danièle Müller ◽  
Selina Wrublewsky ◽  
Wolfgang Metzger ◽  
Michael D Menger ◽  
...  
Keyword(s):  
Tissue Engineering ◽  
Cell Function ◽  
Smooth Muscle Actin ◽  
Three Dimensional ◽  
Stromal Vascular Fraction ◽  
Muscle Actin ◽  
Tissue Constructs ◽  
First Time ◽  
Tissue Defects

Adipose tissue-derived microvascular fragments (MVF) serve as vascularization units in tissue engineering and regenerative medicine. Because a three-dimensional cellular arrangement has been shown to improve cell function, we herein generated for the first time MVF spheroids to investigate whether this further increases their vascularization potential. These spheroids exhibited a morphology, size, and viability comparable to that of previously introduced stromal vascular fraction (SVF) spheroids. However, MVF spheroids contained a significantly higher number of CD31-positive endothelial cells and α-smooth muscle actin (SMA)-positive perivascular cells, resulting in an enhanced angiogenic sprouting activity. Accordingly, they also exhibited an improved in vivo vascularization and engraftment after transplantation into mouse dorsal skinfold chambers. These findings indicate that MVF spheroids are superior to SVF spheroids and, thus, may be highly suitable to improve the vascularization of tissue defects and implanted tissue constructs.

Follicle development in cryopreserved bitch ovarian tissue grafted to immunodeficient mouse

2012 ◽  
Vol 24 (3) ◽  
pp. 461 ◽  
Author(s):  
L. Commin ◽  
S. Buff ◽  
E. Rosset ◽  
C. Galet ◽  
A. Allard ◽  
...  
Keyword(s):  
Stromal Cells ◽  
Histological Analysis ◽  
Smooth Muscle Actin ◽  
Ovarian Tissue ◽  
Follicular Development ◽  
Slow Freezing ◽  
Angiogenic Factor ◽  
Muscle Actin ◽  
Once Daily

The present study evaluated: (1) in vivo follicular development in canine ovarian tissue after slow freezing and xenotransplantation; and (2) the use of erythropoietin (EPO) as an angiogenic factor to optimise the transplantation procedure. Frozen–thawed ovarian tissue from five bitches was grafted into severe combined immunodeficient (SCID) mice (n = 47) treated with or without EPO (500 IU kg–1, once daily for 3 days) (Groups A and B, respectively) and analysed after 0, 1, 8 or 16 weeks. Follicle grade, follicle density, follicle morphology and stromal cells density were assessed by histological analysis, whereas vascularisation of the graft was quantified by immunohistochemistry with anti-α-smooth muscle actin antibody. Despite a massive loss of follicles after grafting, secondary follicle density was higher at 8 and 16 weeks than at 1 week regardless of EPO treatment. EPO significantly improved early follicle morphology and stromal cell density after 8 weeks and blood vessel density at 16 weeks after transplantation (P < 0.05). Intact secondary follicles with more than three granulosa cells layers were observed 16 weeks after transplantation. The results suggest that canine ovarian tissue can be successfully preserved by our slow-freezing protocol because the tissue showed follicular growth after xenotransplantation. EPO treatment did not lessen the massive loss of follicles after transplantation.

Abstract 228: Activation of the Free Fatty Acid Receptor GPR120 Prevents Fibrosis in NIH3T3 Cells and Primary Cardiac Fibroblasts

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Qingwen Qian ◽  
Tim D O'Connell
Keyword(s):  
Heart Failure ◽  
Cardiac Fibroblasts ◽  
Smooth Muscle Actin ◽  
Fibroblast Proliferation ◽  
Muscle Actin ◽  
3T3 Cells ◽  
Nih3t3 Cells ◽  
Actin Expression ◽  
Nih 3T3 ◽  
First Time

Fibrosis significantly contributes to contractile dysfunction and pathologic ventricular remodeling in heart failure. Recently, we showed for the first time that ω3-polyunsaturated fatty acids (ω-PUFAs) prevent fibrosis and cardiac dysfunction in pressure-overload induced heart failure through inhibition of collagen expression, fibroblast proliferation, and fibroblast-to-myofibroblast transformation. In cultured cardiac fibroblasts, we found that ω3-PUFAs induced eNOS activity to prevent TGFβ1-Smad2/3 pro-fibrotic signaling. Mechanistically, ω3-PUFAs are thought to regulate ion channels or to incorporate into the membrane and alter the properties of lipid-rafts, but how a fatty acid might activate eNOS is unknown. Recently, GPR40 and GPR120 were identified as receptors for long-chain fatty acids (FFARs). Here, we examined GPR120 regulation of cardiac fibrosis. Among the FFARs, GPR40, 41, 43, 84, and 120, GPR120 mRNA was expressed at highest level in whole heart. Furthermore, we detected GPR120 expression in isolated cardiac myocytes and fibroblasts, as well as NIH3T3 mouse embryonic fibroblasts. To determine if activation of GPR120 was sufficient to prevent fibrosis, we tested the ability of the GPR120 agonist GW9508 to prevent TGFβ1-induced fibrosis in both NIH3T3 cells and primary cultures of cardiac fibroblasts. In both NIH3T3 cells and primary cardiac fibroblasts, TGFβ1 (1 ng/ml) induced a pro-fibrotic response indicated by increased fibroblast proliferation, α-smooth muscle actin expression, and collagen I expression. In both cell types, pre-treatment with GW9508 significantly inhibited TGFβ1-induced proliferation (63% in NIH 3T3 cells and 52% in cardiac fibroblasts, respectively), α-smooth muscle actin expression (78% in NIH 3T3 cells, 90% in cardiac fibroblasts), and collagen I expression. In summary, our results demonstrate for the first time, that GPR120 signaling in the heart prevents fibrosis.

scholarly journals Conjunctival stromal tumour (COST): anterior-segment OCT findings

2019 ◽  
Vol 12 (11) ◽  
pp. e230348 ◽  
Author(s):  
Joyeeta Das ◽  
Samar K Basak ◽  
Nibedita Das
Keyword(s):  
Optical Coherence Tomography ◽  
Smooth Muscle ◽  
Smooth Muscle Actin ◽  
Anterior Segment ◽  
Stromal Tumour ◽  
Muscle Actin ◽  
Anterior Segment Oct ◽  
Collagenous Material ◽  
First Time ◽  
Conjunctival Myxoma

Conjunctival stromal tumour (COST) is a recently described rare conjunctival tumour of mesenchymal origin with only four publications describing a handful of cases thus far. In this report, we describe the anterior-segment optical coherence tomography (AS-OCT) characteristics in a case of COST for the first time, in addition to the clinical and histopathological characteristics. The AS-OCT showed an elevated, dome-shaped hyporeflective homogenous lesion in the conjunctival stroma lined by hyperreflective outer layer with mild posterior shadowing, consistent with histological description of a paucicellular tumour with large myxoid collagenous material inside. Immunohistochemistry showed positive CD34 and vimentin but negative S100 and smooth muscle actin, thereby differentiating it from conjunctival myxoma.

scholarly journals β-Catenin is required for endothelial-mesenchymal transformation during heart cushion development in the mouse

2004 ◽  
Vol 166 (3) ◽  
pp. 359-367 ◽  
Author(s):  
Stefan Liebner ◽  
Anna Cattelino ◽  
Radiosa Gallini ◽  
Noemi Rudini ◽  
Monica Iurlaro ◽  
...  
Keyword(s):  
Wnt Signaling ◽  
Heart Development ◽  
Transcriptional Activity ◽  
Ex Vivo ◽  
Smooth Muscle Actin ◽  
Muscle Actin ◽  
Endocardial Cushions ◽  
Smad Phosphorylation ◽  
Mesenchymal Transformation

During heart development endocardial cells within the atrio-ventricular (AV) region undergo TGFβ-dependent epithelial-mesenchymal transformation (EMT) and invade the underlying cardiac jelly. This process gives rise to the endocardial cushions from which AV valves and part of the septum originate. In this paper we show that in mouse embryos and in AV explants TGFβ induction of endocardial EMT is strongly inhibited in mice deficient for endothelial β-catenin, leading to a lack of heart cushion formation. Using a Wnt-signaling reporter mouse strain, we demonstrated in vivo and ex vivo that EMT in heart cushion is accompanied by activation of β-catenin/TCF/Lef transcriptional activity. In cultured endothelial cells, TGFβ2 induces α-smooth muscle actin (αSMA) expression. This process was strongly reduced in β-catenin null cells, although TGFβ2 induced smad phosphorylation was unchanged. These data demonstrate an involvement of β-catenin/TCF/Lef transcriptional activity in heart cushion formation, and suggest an interaction between TGFβ and Wnt-signaling pathways in the induction of endothelial-mesenchymal transformation.

scholarly journals Combination of 13-Cis Retinoic Acid and Lovastatin: Marked Antitumor Potential In Vivo in a Pheochromocytoma Allograft Model in Female Athymic Nude Mice

Endocrinology ◽  
2014 ◽  
Vol 155 (7) ◽  
pp. 2377-2390 ◽  
Author(s):  
Svenja Nölting ◽  
Alessio Giubellino ◽  
Yasin Tayem ◽  
Karen Young ◽  
Michael Lauseker ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Retinoic Acid ◽  
Smooth Muscle Actin ◽  
Treated Group ◽  
Muscle Actin ◽  
Tumor Mass ◽  
Viable Tumor ◽  
Over Time

Currently, there are no reliably effective therapeutic options for metastatic pheochromocytoma (PCC) and paraganglioma. Moreover, there are no therapies that may prevent the onset or progression of tumors in patients with succinate dehydrogenase type B mutations, which are associated with very aggressive tumors. Therefore, we tested the approved and well-tolerated drugs lovastatin and 13-cis-retinoic acid (13cRA) in vitro in an aggressive PCC mouse cell line, mouse tumor tissue-derived (MTT) cells, and in vivo in a PCC allograft nude mouse model, in therapeutically relevant doses. Treatment was started 24 hours before sc tumor cell injection and continued for 30 more days. Tumor sizes were measured from outside by caliper and sizes of viable tumor mass by bioluminescence imaging. Lovastatin showed antiproliferative effects in vitro and led to significantly smaller tumor sizes in vivo compared with vehicle treatment. 13cRA promoted tumor cell growth in vitro and led to significantly larger viable tumor mass and significantly faster increase of viable tumor mass in vivo over time compared with vehicle, lovastatin, and combination treatment. However, when combined with lovastatin, 13cRA enhanced the antiproliferative effect of lovastatin in vivo. The combination-treated mice showed slowest tumor growth of all groups with significantly slower tumor growth compared with the vehicle-treated mice and significantly smaller tumor sizes. Moreover, the combination-treated group displayed the smallest size of viable tumor mass and the slowest increase in viable tumor mass over time of all groups, with a significant difference compared with the vehicle- and 13cRA-treated group. The combination-treated tumors showed highest extent of necrosis, lowest median microvessel density and highest expression of α-smooth muscle actin. The combination of high microvessel density and low α-smooth muscle actin is a predictor of poor prognosis in other tumor entities. Therefore, this drug combination may be a well-tolerated novel therapeutic or preventive option for malignant PCC.

The correlation of in vivo burn scar contraction with the level of α-smooth muscle actin expression

Burns ◽  
2011 ◽  
Vol 37 (8) ◽  
pp. 1367-1377 ◽  
Author(s):  
Xue-Qing Wang ◽  
Olena Kravchuk ◽  
Clay Winterford ◽  
Roy M. Kimble
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Actin ◽  
Muscle Actin ◽  
Burn Scar ◽  
Actin Expression ◽  
Scar Contraction

? Isoform of smooth muscle actin is expressed in astrocytes in vitro and in vivo

1991 ◽  
Vol 28 (4) ◽  
pp. 601-606 ◽  
Author(s):  
E. Lecain ◽  
F. Alliot ◽  
M. C. Laine ◽  
B. Calas ◽  
B. Pessac
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Actin ◽  
Muscle Actin

scholarly journals Influence of Laminin Coating on the Autologous In Vivo Recellularization of Decellularized Vascular Protheses

Materials ◽  
2019 ◽  
Vol 12 (20) ◽  
pp. 3351 ◽  
Author(s):  
Mahfuza Toshmatova ◽  
Sentaro Nakanishi ◽  
Yukiharu Sugimura ◽  
Vera Schmidt ◽  
Artur Lichtenberg ◽  
...  
Keyword(s):  
Inflammatory Cell ◽  
Smooth Muscle Actin ◽  
Muscle Actin ◽  
Similar Extent ◽  
Alpha Smooth Muscle Actin ◽  
Promising Strategy ◽  
Biological Implants ◽  
Significant Acceleration ◽  
The Media

Decellularization of non-autologous biological implants reduces the immune response against foreign tissue. Striving for in vivo repopulation of aortic prostheses with autologous cells, thereby improving the graft biocompatibility, we examined surface coating with laminin in a standardized rat implantation model. Detergent-decellularized aortic grafts from donor rats (n = 37) were coated with laminin and systemically implanted into Wistar rats. Uncoated implants served as controls. Implant re-colonization and remodeling were examined by scanning electron microscopy (n = 10), histology and immunohistology (n = 18). Laminin coating persisted over eight weeks. Two weeks after implantation, no relevant neoendothelium formation was observed, whereas it was covering the whole grafts after eight weeks, with a significant acceleration in the laminin group (p = 0.0048). Remarkably, the intima-to-media ratio, indicating adverse hyperplasia, was significantly diminished in the laminin group (p = 0.0149). No intergroup difference was detected in terms of medial recellularization (p = 0.2577). Alpha-smooth muscle actin-positive cells originating from the adventitial surface invaded the media in both groups to a similar extent. The amount of calcifying hydroxyapatite deposition in the intima and the media did not differ between the groups. Inflammatory cell markers (CD3 and CD68) proved negative in coated as well as uncoated decellularized implants. The coating of decellularized aortic implants with bioactive laminin caused an acceleration of the autologous recellularization and a reduction of the intima hyperplasia. Thereby, laminin coating seems to be a promising strategy to enhance the biocompatibility of tissue-engineered vascular implants.

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