scholarly journals Estradiol increases IP3 by a nongenomic mechanism in the smooth muscle cells from the rat oviduct

Reproduction ◽  
2015 ◽  
Vol 150 (4) ◽  
pp. 331-341 ◽  
Author(s):  
Patricia Reuquén ◽  
María L Oróstica ◽  
Israel Rojas ◽  
Patricia Díaz ◽  
Alexis Parada-Bustamante ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Contractile Activity ◽  
Primary Cultures ◽  
Muscle Cells ◽  
Calcium Calmodulin Dependent ◽  
Nongenomic Action ◽  
Dependent Protein ◽  
Egg Transport ◽  
Camkii Activation

Estradiol (E2) accelerates egg transport by a nongenomic action, requiring activation of estrogen receptor (ER) and successive cAMP and IP3production in the rat oviduct. Furthermore, E2increases IP3production in primary cultures of oviductal smooth muscle cells. As smooth muscle cells are the mechanical effectors for the accelerated oocyte transport induced by E2in the oviduct, herein we determined the mechanism by which E2increases IP3in these cells. Inhibition of protein synthesis by Actinomycin D did not affect the E2-induced IP3increase, although this was blocked by the ER antagonist ICI182780 and the inhibitor of phospholipase C (PLC) ET-18-OCH3. Immunoelectron microscopy for ESR1 or ESR2 showed that these receptors were associated with the plasma membrane, indicating compatible localization with E2nongenomic actions in the smooth muscle cells. Furthermore, ESR1 but not ESR2 agonist mimicked the effect of E2on the IP3level. Finally, E2stimulated the activity of a protein associated with the contractile tone, calcium/calmodulin-dependent protein kinase II (CaMKII), in the smooth muscle cells. We conclude that E2increases IP3by a nongenomic action operated by ESR1 and that involves the activation of PLC in the smooth muscle cells of the rat oviduct. This E2effect is associated with CaMKII activation in the smooth muscle cells, suggesting that IP3and CaMKII are involved in the contractile activity necessary to accelerate oviductal egg transport.

scholarly journals Estradiol increases cAMP in the oviductal secretory cells through a nongenomic mechanism

Reproduction ◽  
2014 ◽  
Vol 148 (3) ◽  
pp. 285-294 ◽  
Author(s):  
María L Oróstica ◽  
John Lopez ◽  
Israel Rojas ◽  
Jocelyn Rocco ◽  
Patricia Díaz ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Primary Cultures ◽  
Muscle Cells ◽  
Secretory Cells ◽  
Nongenomic Action ◽  
Confocal Immunofluorescence ◽  
Cellular Phenotypes ◽  
Egg Transport

In the rat oviduct, estradiol (E2) accelerates egg transport by a nongenomic action that requires previous conversion of E2to methoxyestrogens via catechol-O-methyltranferase (COMT) and activation of estrogen receptor (ER) with subsequent production of cAMP and inositol triphosphate (IP3). However, the role of the different oviductal cellular phenotypes on this E2nongenomic pathway remains undetermined. The aim of this study was to investigate the effect of E2on the levels of cAMP and IP3 in primary cultures of secretory and smooth muscle cells from rat oviducts and determine the mechanism by which E2increases cAMP in the secretory cells. In the secretory cells, E2increased cAMP but not IP3, while in the smooth muscle cells E2decreased cAMP and increased IP3. Suppression of protein synthesis by actinomycin D did not prevent the E2-induced cAMP increase, but this was blocked by the ER antagonist ICI 182 780 and the inhibitors of COMT OR 486, G protein-α inhibitory (Gαi) protein pertussis toxin and adenylyl cyclase (AC) SQ 22536. Expression of the mRNA for the enzymes that metabolizes estrogens,Comt,Cyp1a1, andCyp1b1was found in the secretory cells, but this was not affected by E2. Finally, confocal immunofluorescence analysis showed that E2induced colocalization between ESR1 (ERα) and Gαiin extranuclear regions of the secretory cells. We conclude that E2differentially regulates cAMP and IP3 in the secretory and smooth muscle cells of the rat oviduct. In the secretory cells, E2increases cAMP via a nongenomic action that requires activation of COMT and ER, coupling between ESR1 and Gαi, and stimulation of AC.

Phenotype modulation in primary cultures of aortic smooth muscle cells from streptozotocin-diabetic rats

1998 ◽  
Vol 63 (4) ◽  
pp. 225-236 ◽  
Author(s):  
Pascale Etienne ◽  
Núria Parés-Herbuté ◽  
Louis Monnier ◽  
Herisoa Rabesandratana ◽  
Laurence Mani-Ponset ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Primary Cultures ◽  
Muscle Cells ◽  
Diabetic Rats ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle ◽  
Streptozotocin Diabetic Rats

Density-dependent hyperpolarization in cultured aortic smooth muscle cells

1989 ◽  
Vol 256 (3) ◽  
pp. C644-C651 ◽  
Author(s):  
M. G. Blennerhassett ◽  
M. S. Kannan ◽  
R. E. Garfield
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Continuous Process ◽  
Primary Cultures ◽  
Muscle Cells ◽  
Sprague Dawley ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle ◽  
Wistar Kyoto

The membrane potential (Em) of cultured aortic smooth muscle cells from Sprague-Dawley (SD), Wistar-Kyoto (WKY), and spontaneously hypertensive (SHR) rats was measured in proliferating primary cultures. Em of SD cells in high-density cultures was -51 to -58 mV, whereas that of low-density cultures (1-2 days) was -30 mV. This difference was due to a continuous process of hyperpolarization during proliferation in culture. Em of WKY and SHR hyperpolarized similarly, from -12 to -42 and -38 mV, respectively. Hyperpolarization of Em of SD, WKY, and SHR cells was related to cell density rather than time in culture. Em may be a sensitive and significant indicator of the changes in the differentiated state expressed by proliferating smooth muscle in vitro.

Phenotype modulation in primary cultures of smooth-muscle cells from rat aorta

1986 ◽  
Vol 32 (2) ◽  
pp. 173-180 ◽  
Author(s):  
Maria Sjölund ◽  
Kjell Madsen ◽  
Klaus von der Mark ◽  
Johan Thyberg
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Primary Cultures ◽  
Muscle Cells ◽  
Rat Aorta

scholarly journals Inhibitory effects of cnidium components on proliferation of mouse aortic smooth muscle cells in primary cultures

1988 ◽  
Vol 46 ◽  
pp. 185
Author(s):  
Masayasu Kimura ◽  
Shinjiro Kobayashi ◽  
Kouhei Notoya ◽  
Yasuhiko Mimura ◽  
Jun Suzuki ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Primary Cultures ◽  
Muscle Cells ◽  
Inhibitory Effects ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle

scholarly journals cGMP-dependent protein kinase I in vascular smooth muscle cells improves ischemic stroke outcome in mice

2019 ◽  
Vol 39 (12) ◽  
pp. 2379-2391
Author(s):  
Maria Shvedova ◽  
Maxim M Litvak ◽  
Jesse D Roberts ◽  
Dai Fukumura ◽  
Tomoaki Suzuki ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Ischemic Stroke ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Infarct Volume ◽  
Muscle Cells ◽  
Dependent Protein Kinase ◽  
Cgmp Dependent Protein Kinase ◽  
Dependent Protein

Recent works highlight the therapeutic potential of targeting cyclic guanosine monophosphate (cGMP)-dependent pathways in the context of brain ischemia/reperfusion injury (IRI). Although cGMP-dependent protein kinase I (cGKI) has emerged as a key mediator of the protective effects of nitric oxide (NO) and cGMP, the mechanisms by which cGKI attenuates IRI remain poorly understood. We used a novel, conditional cGKI knockout mouse model to study its role in cerebral IRI. We assessed neurological deficit, infarct volume, and cerebral perfusion in tamoxifen-inducible vascular smooth muscle cell-specific cGKI knockout mice and control animals. Stroke experiments revealed greater cerebral infarct volume in smooth muscle cell specific cGKI knockout mice (males: 96 ± 16 mm3; females: 93 ± 12 mm3, mean±SD) than in all control groups: wild type (males: 66 ± 19; females: 64 ± 14), cGKI control (males: 65 ± 18; females: 62 ± 14), cGKI control with tamoxifen (males: 70 ± 8; females: 68 ± 10). Our results identify, for the first time, a protective role of cGKI in vascular smooth muscle cells during ischemic stroke injury. Moreover, this protective effect of cGKI was found to be independent of gender and was mediated via improved reperfusion. These results suggest that cGKI in vascular smooth muscle cells should be targeted by therapies designed to protect brain tissue against ischemic stroke.

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