scholarly journals Endothelin as a local regulating factor in the bovine oviduct

2016 ◽  
Vol 28 (6) ◽  
pp. 673 ◽  
Author(s):  
Yuki Yamamoto ◽  
Misa Kohka ◽  
Yoshihiko Kobayashi ◽  
Izabela Woclawek-Potocka ◽  
Kiyoshi Okuda
Keyword(s):  
Smooth Muscle ◽  
Epithelial Cells ◽  
Smooth Muscle Cells ◽  
Mrna Expression ◽  
Muscle Cells ◽  
Target Site ◽  
Ovarian Steroids

Endothelin (EDN) is a possible regulating factor of oviductal motility, which is important for the transport of gametes and embryo. To clarify the factors that control the secretion of EDN in the bovine oviduct, the expression of EDNs, EDN-converting enzymes (ECEs) and EDN receptors (EDNRs) were investigated. All isoforms of EDN (EDN1–3), ECE (ECE1 and ECE2) and EDNR (EDNRA and EDNRB) were immunolocalised in the epithelial cells of the ampulla and the isthmus. EDNRs were also immunolocalised in smooth-muscle cells. The mRNA expression of EDN2 and ECE2 was higher in cultured ampullary oviductal epithelial cells than in isthmic cells. The expression of EDN1, EDN2 and ECE2 in the ampullary tissue was highest on the day of ovulation. Oestradiol-17β increased EDN2 and ECE1 expression, while progesterone increased only ECE1 expression in cultured ampullary epithelial cells. These results indicate that EDNs are produced by epithelial cells and their target site is smooth-muscle and epithelial cells, and suggest that ovarian steroids are regulators of endothelin synthesis in ampullary oviductal epithelial cells.

Norepinephrine transport by the extraneuronal monoamine transporter in human bronchial arterial smooth muscle cells

2003 ◽  
Vol 285 (4) ◽  
pp. L829-L837 ◽  
Author(s):  
Gabor Horvath ◽  
Zoltan Sutto ◽  
Aliza Torbati ◽  
Gregory E. Conner ◽  
Matthias Salathe ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Mrna Expression ◽  
Binding Site ◽  
Membrane Binding ◽  
Muscle Cells ◽  
Arterial Smooth Muscle ◽  
Extraneuronal Monoamine Transporter ◽  
Arterial Smooth Muscle Cells ◽  
Specific Membrane

Inhaled glucocorticosteroids (GSs) cause acute, α1-adrenoreceptor (AR)-mediated bronchial vasoconstriction. After release from sympathetic nerves, norepinephrine (NE) must be taken up into cells for deactivation by intracellular enzymes. Because postsynaptic cellular NE uptake is steroid sensitive, GSs could increase NE concentrations at α1-AR, causing vasoconstriction. We therefore evaluated mRNA expression of different NE transporters in human bronchial arterial smooth muscle and pharmacologically characterized NE uptake into these cells. RT-PCR demonstrated mRNA expression of the extraneuronal monoamine transporter (EMT) and organic cation transporter 1 (OCT-1). Fluorometric uptake assay showed time (within minutes)- and concentration-dependent NE uptake by freshly isolated bronchial arterial smooth muscle cells (SMC) with an estimated Km of 240 μM. Corticosterone and O-methylisoprenaline (1 μM each), but not desipramine, inhibited NE uptake, a profile indicative of NE uptake by EMT, but not OCT-1. Budesonide and methylprednisolone inhibited uptake with IC50 values of 0.9 and 5.6 μM, respectively. Corticosterone's action was reversible and not sensitive to RU-486 (GS receptor antagonist), actinomycin D (transcription inhibitor), or cycloheximide (protein synthesis inhibitor). Corticosterone made membrane impermeant by coupling to BSA also blocked NE uptake. Immunocytochemistry indicated a specific membrane binding site for corticosterone on bronchial arterial SMC. These data demonstrate that although human bronchial arterial SMC express OCT-1 and EMT, EMT is the predominant plasma membrane transporter for NE uptake. This process can be inhibited by GSs, likely via a specific membrane binding site. This nongenomic GS action (increasing NE concentrations at α1-AR) could explain acute bronchial vasoconstriction caused by inhaled GSs.

Thrombin induces endothelin expression in arterial smooth muscle cells

2000 ◽  
Vol 278 (5) ◽  
pp. H1606-H1612 ◽  
Author(s):  
Delphine Lepailleur-Enouf ◽  
Olivier Valdenaire ◽  
Monique Philippe ◽  
Martine Jandrot-Perrus ◽  
Jean-Baptiste Michel
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Map Kinase ◽  
Mrna Expression ◽  
Protein Tyrosine Kinase ◽  
Muscle Cells ◽  
Transcriptional Level ◽  
Peroxisome Proliferator ◽  
Extracellular Medium ◽  
Map Kinase Kinase

Thrombin has been shown to stimulate endothelin release by endothelial cells, but the ability of thrombin to induce endothelin in nonendothelial cells is less well-known. Incubation of rat aortic smooth muscle cells with thrombin resulted in a stimulation of preproendothelin-1 (preproET-1) mRNA expression. This induction of preproET-1 mRNA expression by thrombin was accompanied by the release of immunoreactive peptide ET-1 into the extracellular medium. The synthetic thrombin receptor activator peptide (TRAP) confirmed ligand-specific receptor action to induce preproET-1 mRNA. Nuclear run-on analysis revealed that the transcriptional rate of preproET-1 mRNA increases twofold after 1 h of incubation with thrombin. In cells treated with thrombin, the half-life of preproET-1 mRNA was identical to that in untreated control cells. These results demonstrated that thrombin regulates endothelin synthesis at a transcriptional level but does not influence mRNA stability. Inhibition of protein kinase C (PKC) with selective inhibitors (chelerythrine and bisindolylmaleimide I) before thrombin stimulation failed to significantly inhibit preproET-1 gene expression. Inhibition of mitogen-activated protein (MAP) kinase kinase and protein tyrosine kinase decreased preproET-1 mRNA expression in thrombin-stimulated smooth muscle cells. Furthermore, addition of an activator of peroxisome proliferator-activated receptors-α (PPARα), fenofibrate, prevented the preproET-1 gene induction in response to thrombin. These results demonstrated that thrombin-induced endothelin gene transcription involved MAP kinase kinase rather than the PKC cascade in smooth muscle cells, which was repressed by PPARα stimulation.

Laser-assisted microdissection and real-time PCR detect anti-inflammatory effect of perfluorocarbon

2003 ◽  
Vol 285 (1) ◽  
pp. L55-L62 ◽  
Author(s):  
Katharina von der Hardt ◽  
Michael Andreas Kandler ◽  
Ludger Fink ◽  
Ellen Schoof ◽  
Jörg Dötsch ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Mrna Expression ◽  
Vascular Smooth Muscle Cells ◽  
Alveolar Macrophages ◽  
Real Time Pcr ◽  
Muscle Cells ◽  
Cell Types ◽  
Anti Inflammatory ◽  
Inflammatory Effect

The aim of this study was to identify cell types involved in the anti-inflammatory effect of ventilation with perfluorocarbon in vivo. Fifteen anesthetized, surfactant-depleted piglets received either aerosolized perfluorocarbon (Aerosol-PFC), partial liquid ventilation (rLV) at functional residual capacity (FRC) volume (FRC-PLV), or intermittent mandatory ventilation (control). After laser-assisted microdissection of different lung cell types, mRNA expression of IL-8 and ICAM-1 was determined using TaqMan real-time PCR normalized to hypoxanthine phosphoribosyltransferase (HPRT). IL-8 mRNA expression (means ± SE; control vs. Aerosol-PFC) was 356 ± 142 copies IL-8 mRNA/copy HPRT mRNA vs. 3.5 ± 1.8 in alveolar macrophages ( P <0.01); 208 ± 108 vs. 2.7 ± 0.8 in bronchiolar epithelial cells ( P <0.05); 26 ± 11 vs. 0.7 ± 0.2 in alveolar septum cells ( P <0.01); 2.8 ± 1.0 vs. 0.8 ± 0.4 in bronchiolar smooth muscle cells ( P <0.05); and 1.1 ± 0.4 vs. 0.2 ± 0.05 in vascular smooth muscle cells ( P <0.05). With FRC-PLV, IL-8/HPRT mRNA expression was significantly lower in macrophages, bronchiolar epithelial, and vascular smooth muscle cells. ICAM-1 mRNA expression in vascular endothelial cells remained unchanged. Predominantly, alveolar macrophages and bronchiolar epithelial cells were involved in the inflammatory pulmonary process. The anti-inflammatory effect of Aerosol-PFC was most pronounced.

scholarly journals Fibulin-3 Attenuates Phosphate-Induced Vascular Smooth Muscle Cell Calcification by Inhibition of Oxidative Stress

2018 ◽  
Vol 46 (4) ◽  
pp. 1305-1316 ◽  
Author(s):  
Trang T. D. Luong ◽  
Nadeshda Schelski ◽  
Beate Boehme ◽  
Manousos Makridakis ◽  
Antonia Vlahou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Mrna Expression ◽  
Vascular Calcification ◽  
Muscle Cells ◽  
Additional Treatment ◽  
Calcium Deposition

Background/Aims: Fibulin-3, an extracellular matrix glycoprotein, inhibits vascular oxidative stress and remodeling in hypertension. Oxidative stress is prevalent in chronic kidney disease (CKD) patients and is an important mediator of osteo-/chondrogenic transdifferentiation and calcification of vascular smooth muscle cells (VSMCs) during hyperphosphatemia. Therefore, the present study explored the effects of Fibulin-3 on phosphate-induced vascular calcification. Methods: Experiments were performed in primary human aortic smooth muscle cells (HAoSMCs) treated with control or with phosphate without or with additional treatment with recombinant human Fibulin-3 protein or with hydrogen peroxide as an exogenous source of oxidative stress. Results: Treatment with calcification medium significantly increased calcium deposition in HAoSMCs, an effect significantly blunted by additional treatment with Fibulin-3. Moreover, phosphate-induced alkaline phosphatase activity and mRNA expression of osteogenic and chondrogenic markers MSX2, CBFA1, SOX9 and ALPL were all significantly reduced by addition of Fibulin-3. These effects were paralleled by similar regulation of oxidative stress in HAoSMCs. Phosphate treatment significantly up-regulated mRNA expression of the oxidative stress markers NOX4 and CYBA, down-regulated total antioxidant capacity and increased the expression of downstream effectors of oxidative stress PAI-1, MMP2 and MMP9 as well as BAX/BLC2 ratio in HAoSMCs, all effects blocked by additional treatment with Fibulin-3. Furthermore, the protective effects of Fibulin-3 on phosphate-induced osteogenic and chondrogenic markers expression in HAoSMCs were reversed by additional treatment with hydrogen peroxide. Conclusions: Fibulin-3 attenuates phosphate-induced osteo-/ chondrogenic transdifferentiation and calcification of VSMCs, effects involving inhibition of oxidative stress. Up-regulation or supplementation of Fibulin-3 may be beneficial in reducing the progression of vascular calcification during hyperphosphatemic conditions such as CKD.

Urethral reconstruction using an amphiphilic tissue-engineered autologous polyurethane nanofiber scaffold with rapid vascularization function

2020 ◽  
Vol 8 (8) ◽  
pp. 2164-2174
Author(s):  
Yuqing Niu ◽  
Guochang Liu ◽  
Chuangbi Chen ◽  
Ming Fu ◽  
Wen Fu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Epithelial Cells ◽  
Smooth Muscle Cells ◽  
Phenotypic Expression ◽  
Muscle Cells ◽  
Urethral Reconstruction ◽  
Nanofiber Scaffold

We report the efficient application of a well-layered tubular amphiphilic nanofiber of a polyurethane copolymer (PU-ran) for the regulation the phenotypic expression of epithelial cells (ECs) and smooth muscle cells (SMCs) for vascularized urethral reconstruction.

scholarly journals Oncostatin M promotes biphasic tissue factor expression in smooth muscle cells: evidence for Erk-1/2 activation

Blood ◽  
2001 ◽  
Vol 97 (3) ◽  
pp. 692-699 ◽  
Author(s):  
Toshiya Nishibe ◽  
Graham Parry ◽  
Atsushi Ishida ◽  
Salim Aziz ◽  
Jacqueline Murray ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Dna Binding ◽  
Smooth Muscle Cells ◽  
Mrna Expression ◽  
Tissue Factor ◽  
Muscle Cells ◽  
Binding Activity ◽  
Oncostatin M ◽  
Dna Binding Activity ◽  
Atherosclerotic Lesions

Abstract Tissue factor (TF), a transmembrane glycoprotein, initiates the extrinsic coagulation cascade. TF is known to play a major role in mediating thrombosis and thrombotic episodes associated with the progression of atherosclerosis. Macrophages at inflammatory sites, such as atherosclerotic lesions, release numerous cytokines that are capable of modulating TF expression. This study examined the role of oncostatin M (OSM), a macrophage/ T-lymphocyte–restricted cytokine, in the expression of TF in vascular smooth muscle cells (SMCs). It is reported here that OSM stimulated a biphasic and sustained pattern of TF messenger RNA (mRNA). The effect of OSM on TF mRNA expression was regulated at the transcriptional level as determined by nuclear run-offs and transient transfection of a TF promoter-reporter gene construct. OSM-induced TF expression was regulated primarily by the transcription factor NF-κB. Activation of NF-κB by OSM did not require IκB-α degradation. Inhibition of MEK activity by U0126 prevented OSM-induced TF expression by suppressing NF-κB DNA binding activity as determined by gel-shift analysis. Further, inhibition of Erk-1/2 protein by antisense treatment resulted in suppression of TF mRNA expression, indicating a role for Erk-1/2 in modulating NF-κB DNA binding activity. These studies suggest that the induced expression of TF by OSM is primarily through the activation of NF-κB and that activation of NF-κB is regulated in part by the MEK/Erk-1/2 signal transduction pathway. This study indicates that OSM may play a key role in promoting TF expression in SMCs within atherosclerotic lesions.

Sign in / Sign up

Export Citation Format

Share Document