scholarly journals Chlamydia muridarum infection differentially changes smooth muscle contractility and responses to prostaglandins in uterus and cervix

2018 ◽  
Author(s):  
Jia Ming Lee ◽  
Jemma R. Mayall ◽  
Anne Chevalier ◽  
Dirk Van Helden ◽  
Jay C. Horvat ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Mrna Expression ◽  
Reproductive Tract ◽  
Uterine Horn ◽  
Female Reproductive Tract ◽  
Muscle Contractility ◽  
Smooth Muscle Contractility ◽  
Contraction Amplitude ◽  
Chlamydia Muridarum ◽  
Reproductive Tract Infection

AbstractChlamydia trachomatis infection is a primary cause of reproductive tract diseases including chronic pelvic pain and infertility. Previous studies showed that this infection alters physiological activities in mouse oviducts. Whether this occurs in the uterus and cervix has never been investigated. This study characterized the physiological activity of the uterus and the cervix in a Chlamydia muridarum (Cmu) mouse model of reproductive tract infection. Uterine or cervix smooth muscle contractility, responses to oxytocin or prostaglandins (PGF2α and PGE2) and mRNA expression of oxytocin and PG receptors were assessed 14 days post infection. Cmu infection did not affect the contractions of the uterine horn but significantly decreased the contraction amplitude of the cervix. Cmu infection did not alter the responses of uterine horn or cervix to oxytocin, however PGF2α induced contractions of the uterine horn, but not the cervix, were significantly increased following Cmu infection. PGE2 contraction amplitude in both the uterine horn and cervix was unaffected by Cmu infection. An upregulation of Ptgfr and a down-regulation of Ptegr4 mRNA expression was observed in the uterine horn following Cmu infection. These results indicate that Cmu infection alters contractility and prostaglandin signalling in the female reproductive tract but the effects are localised to specific regions.

scholarly journals Chlamydia muridarum infection differentially alters smooth muscle function in mouse uterine horn and cervix

2020 ◽  
Vol 318 (6) ◽  
pp. E981-E994 ◽  
Author(s):  
Jia Ming Lee ◽  
Jemma R. Mayall ◽  
Anne Chevalier ◽  
Huw McCarthy ◽  
Dirk Van Helden ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Muscle Function ◽  
Reproductive Tract ◽  
Contractile Force ◽  
Uterine Horn ◽  
Chlamydia Muridarum ◽  
Chlamydia Trachomatis Infection ◽  
Messenger Ribonucleic Acid ◽  
Time Points ◽  
Smooth Muscle Function

Chlamydia trachomatis infection is a primary cause of reproductive tract diseases including infertility. Previous studies showed that this infection alters physiological activities in mouse oviducts. Whether this occurs in the uterus and cervix has never been investigated. This study characterized the physiological activities of the uterine horn and the cervix in a Chlamydia muridarum ( Cmu)-infected mouse model at three infection time points of 7, 14, and 21 days postinfection (dpi). Cmu infection significantly decreased contractile force of spontaneous contraction in the cervix (7 and 14 dpi; P < 0.001 and P < 0.05, respectively), but this effect was not observed in the uterine horn. The responses of the uterine horn and cervix to oxytocin were significantly altered by Cmu infection at 7 dpi ( P < 0.0001), but such responses were attenuated at 14 and 21 dpi. Cmu infection increased contractile force to prostaglandin (PGF2α) by 53–83% in the uterine horn. This corresponded with the increased messenger ribonucleic acid (mRNA) expression of Ptgfr that encodes for its receptor. However, Cmu infection did not affect contractions of the uterine horn and cervix to PGE2 and histamine. The mRNA expression of Otr and Ptger4 was inversely correlated with the mRNA expression of Il1b, Il6 in the uterine horn of Cmu-inoculated mice ( P < 0.01 to P < 0.001), suggesting that the changes in the Otr and Ptger4 mRNA expression might be linked to the changes in inflammatory cytokines. Lastly, this study also showed a novel physiological finding of the differential response to PGE2 in mouse uterine horn and cervix.

Surface ultrastructure of danazol treated rat endometrium: A SEM study

1983 ◽  
Vol 41 ◽  
pp. 556-557
Author(s):  
R.P. Apkarian ◽  
J.S. Sanfilippo
Keyword(s):  
Cross Sections ◽  
Reproductive Tract ◽  
Preliminary Investigation ◽  
Breast Disease ◽  
Distal Segment ◽  
Uterine Horn ◽  
Female Reproductive Tract ◽  
Ultrastructural Changes ◽  
Cycle Phase ◽  
Sprague Dawley

The synthetic androgen danazol, is an isoxazol derivative of ethisterone. It is utilized in the treatment of endometriosis, fibrocystic breast disease, and has a potential use as a contraceptive. A study was designed to evaluate the ultrastructural changes associated with danazol therapy in a rat model. The preliminary investigation of the distal segment of the rat uterine horn was undertaken as part of a larger study intended to elucidate the effects of danazol on the female reproductive tract.Cross-sections (2-3 mm in length) of the distal segment of the uterine horn from sixteen Sprague-Dawley rats were prepared for SEM. Ten rats in estrus served as controls and six danazol treated rats were noted to have alterations of the estrus cycle i.e. a lag in cycle phase or noncycling patterns. Specimens were fixed in 3% glutaraldehyde in 0.05M phosphate buffer containing CaCl2 at pH 7.0-7.4 and chilled to 4°C. After a brief wash in distilled water, specimens were passed through a graded series of ethanol, critical point dryed in CO2 from absolute ethanol, and coated with 6nm Au. Observations were made with an IS1-40 SEM operated at 15kV.

scholarly journals Complementary vasoactivity and matrix remodelling in arterial adaptations to altered flow and pressure

2008 ◽  
Vol 6 (32) ◽  
pp. 293-306 ◽  
Author(s):  
A Valentín ◽  
L Cardamone ◽  
S Baek ◽  
J.D Humphrey
Keyword(s):  
Smooth Muscle ◽  
Continuum Theory ◽  
Muscle Contractility ◽  
Smooth Muscle Contractility ◽  
Rates Of Change ◽  
Biomechanical Loading ◽  
Smooth Muscle Proliferation ◽  
And Function ◽  
Diverse Data ◽  
Induced Changes

Arteries exhibit a remarkable ability to adapt to sustained alterations in biomechanical loading, probably via mechanisms that are similarly involved in many arterial pathologies and responses to treatment. Of particular note, diverse data suggest that cell and matrix turnover within vasoaltered states enables arteries to adapt to sustained changes in blood flow and pressure. The goal herein is to show explicitly how altered smooth muscle contractility and matrix growth and remodelling work together to adapt the geometry, structure, stiffness and function of a representative basilar artery. Towards this end, we employ a continuum theory of constrained mixtures to model evolving changes in the wall, which depend on both wall shear stress-induced changes in vasoactive molecules (which alter smooth muscle proliferation and synthesis of matrix) and intramural stress-induced changes in growth factors (which alter cell and matrix turnover). Simulations show, for example, that such considerations help explain the different rates of experimentally observed adaptations to increased versus decreased flows as well as differences in rates of change in response to increased flows or pressures.

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