scholarly journals LPS-mediated effects and spatio-temporal expression of TLR2 and TLR4 in the bovine corpus luteum

Reproduction ◽  
2016 ◽  
Vol 151 (4) ◽  
pp. 391-399 ◽  
Author(s):  
J Lüttgenau ◽  
K Herzog ◽  
K Strüve ◽  
S Latter ◽  
A Boos ◽  
...  

When given intravenously (iv), lipopolysaccharide (LPS) transiently suppresses the structure and function of the bovine corpus luteum (CL). This is associated with increased release of prostaglandin (PG) F2α metabolite. The underlying regulatory mechanisms of this process remain, however, obscure. Therefore, the aims of this study were: i) to investigate the expression of the LPS receptor toll-like receptor 4 (TLR4) and 2 (TLR2) in the bovine CL during early, mid- and late luteal phases; and ii) to further dissect the mechanisms of LPS-mediated suppression of luteal function. As revealed by semi-quantitative qPCR and immunohistochemistry, both receptors were detectable throughout the luteal lifespan. Their mRNA levels increased from the early toward the mid-luteal phase; no further changes were observed thereafter. The TLR4 protein seemed more highly represented than TLR2. The cellular localization of TLRs was in blood vessels; weaker signals were observed in luteal cells. Additionally, cows were treated either with LPS (iv, 0.5 μg/kg BW) or with saline on Day 10 after ovulation. Samples were collected 1200 h after treatment and on Day 10 of the respective subsequent (untreated) cycle. The mRNA expression of several possible regulatory factors was investigated, revealing the suppression of PGF2α receptor (PTGFR), STAR protein and 3β-hydroxysteroid dehydrogenase, compared with controls and subsequent cycles. The expression of TLR2 and TLR4, interleukin 1α (IL1A) and 1β (IL1B) and of PGF2α and PGE2 synthases (HSD20A and mPTGES respectively) was increased. The results demonstrate the presence of TLR2 and TLR4 in the bovine CL, and implicate their possible involvement in the deleterious effects of LPS on its function.

Author(s):  
Gabriella dos Santos Velho ◽  
Monique Tomazele Rovani ◽  
Rogério Ferreira ◽  
Bernardo Garziera Gasperin ◽  
André Gustavo Cabrera Dalto

Reproduction ◽  
2015 ◽  
Vol 150 (3) ◽  
pp. 217-225 ◽  
Author(s):  
Koumei Shirasuna ◽  
Haruka Matsumoto ◽  
Shuichi Matsuyama ◽  
Koji Kimura ◽  
Heinrich Bollwein ◽  
...  

When pregnancy is established, interferon tau (IFNT), a well-known pregnancy recognition signal in ruminants, is secreted by embryonic trophoblast cells and acts within the uterus to prepare for pregnancy. IFNT acts as an endocrine factor on the corpus luteum (CL) to induce refractory ability against the luteolytic action of PGF2α. Hypothesising that IFNT may influence not only the uterine environment but also the CL in cows via local or peripheral circulation, we investigated qualitative changes in the CL of pregnant cows during the maternal recognition period (day 16) and the CL of non-pregnant cows. The CL of pregnant animals had a higher number of neutrophils, and the expression of interleukin 8 (IL8) mRNA and its protein was higher as well as compared with the CL of non-pregnant animals. Although IFNT did not affect progesterone (P4) secretion and neutrophil migration directly, it stimulated IL8 mRNA expression on luteal cells (LCs), influencing the neutrophils, resulting in the increased migration of IFNT-activated neutrophils. Moreover, both IFNT-activated neutrophils and IL8 increased P4 secretion from LCs in vitro. Our novel finding was the increase in neutrophils and IL8 within the CL of pregnant cows, suggesting the involvement of IFNT function within the CL toward establishment of pregnancy in cows. The present results suggest that IFNT upregulates neutrophil numbers and function via IL8 on LCs in the CL of early pregnant cows and that both neutrophils and IL8, stimulated by IFNT, are associated with an increase in P4 concentrations during the maternal recognition period in cows.


1999 ◽  
Vol 7 (1) ◽  
pp. 11-25 ◽  
Author(s):  
Richard Ivell

The notion of an oxytocic principle residing within the ovary is not new. In as early as 1910, Ott and Scott showed that an extract of bovine corpus luteum could induce milk letdown and uterine contraction. However, it took a further 70 years before the identification of this principle with the nonapeptide hormone oxytocin (OT) was made at the peptide and mRNA levels. This was followed by the identification of the peptide in ovarian tissues and ovarian venous blood from a wide variety of species, including humans, monkeys, pigs and ruminants (reviewed in 7, 8). For the majority of non-ruminant species the levels of expression of the peptide and its specific mRNA are relatively low, implying that whatever function the ovarian hormone has in these species, it is most likely to be at the local, paracrine level. Ruminants are an exception. Cows and sheep both produce very high levels of OT and OT-mRNA – the latter attaining concentrations of approximately 1% of all transcripts – within the corpus luteum of the early oestrous cycle. In ruminants, evolution has culminated in a systemic link between ovarian OT production and OT receptors in the endometrium of the uterus, inducing there the production of prostaglandin-F2∞ (PGF2∞) which completes a positive feedback loop to the ovary by stimulating further OT release (reviewed in 10). It is important to note, however, that natural selection can only act on a preexisting system. In this case, it has developed a systemic endocrine pathway in ruminants from a local ovarian OT system present probably in all mammals. There is even evidence for OT-related peptides, such as mesotocin and vasotocin, within the ovaries of marsupials and chicken, though their function is not known.


2022 ◽  
Vol 8 ◽  
Author(s):  
Agnieszka W. Jonczyk ◽  
Katarzyna K. Piotrowska-Tomala ◽  
Dariusz J. Skarzynski

We investigated the effects of different doses of dinoprost injected directly into the bovine corpus luteum (CL) on (i) concentrations of progesterone (P4) and oxytocin (OT) in peripheral blood and (ii) mRNA levels of steroidogenic acute regulatory protein (STAR), cytochrome P450 family 11 subfamily A member 1 (P450scc), hydroxy-delta-5-steroid dehydrogenase, 3 β- and steroid delta-isomerase 1 (HSD3B), and receptor-interacting protein kinases 1 and 3 (RIPK1, RIPK3) in CL tissue. Moreover, we examined the effects of dinoprost, injected intra-CL or administered intramuscularly (IM), on CL secretory function and on indicators of CL vascular network status: luteal tissue area (LTA), CL blood flow (CLBF), and the CLBF:LTA ratio (Adj. CLBF), in cows at the early and mid-luteal phases. In the Experiment 1, cows (day 10 of the cycle) were allocated to (i) an intra-CL injection of saline (control; n = 3); (ii) an intra-CL injection of dinoprost (1.25 mg; 2.5 mg, or 5 mg; n = 3 for each dose); (iii) an IM administration of saline (control; n = 3); or (iv) an IM administration of dinoprost (25 mg; positive control; n = 3). Concentrations of OT and P4 were measured in plasma samples. The mRNA expression of steroidogenesis- or necroptosis-related factors was determined in CL tissue 4 h after treatments. In Experiment 2, cows on day 4 (n = 12) or day 10 (n = 12) were allocated to (i) an intra-CL injection of dinoprost (2.5 mg/0.5 ml; n = 6), or (ii) IM administration of dinoprost (25 mg/5 ml; n = 6). Concentrations of P4 were measured in plasma samples. Luteal tissue area, CLBF, and Adj. CLBF were assessed based on color Doppler ultrasonography. An intra-CL injection of dinoprost increased OT and decreased P4 levels in the jugular vein (JV) in a dose-dependent manner in cows at the mid-luteal phase. Increased CLBF and Adj. CLBF, accompanied by reduced P4 levels, were observed 2 h after intra-CL dinoprost injection in middle-stage CL. Decreased STAR and increased RIPK1 and RIPK3 mRNA levels confirmed that 2.5 mg dinoprost injected directly into CL is the minimum dose that induces luteolytic cascade. Injection of dinoprost directly into the CL (at a dosage lower than recommended for peripheral application) results in a pattern similar to IM dinoprost administration.


1997 ◽  
Vol 44 (4) ◽  
pp. 781-789 ◽  
Author(s):  
B Kaminska ◽  
R K Filipkowski ◽  
I W Biedermann ◽  
D Konopka ◽  
D Nowicka ◽  
...  

Kainate is a glutamate analog that produces neuronal excitation resulting in seizures within hours following its intraperitoneal injection into adult rats. Then, at 2-3 days after the treatment, neurodegeneration of apoptotic character can be observed in limbic system. As a consequence, plastic reorganization and glial reactivation phenomena occur. These physiological and pathological responses are reflected by specific changes in gene expression, that can be dissected according to their spatio-temporal patterns. The early phase of gene expression observed in all hippocampal subfields appears to reflect a sudden burst of spiking activity. Changes in mRNA levels restricted to dentate gyrus are suggestive of a link to neuronal plasticity. The late gene expression response implies its correlation either to neuronal cell death or glial reactivation, depending on cellular localization of gene products. Thus analysis of the temporal and spatial gene expression pattern in the hippocampus after kainate treatment may provide clues revealing specific phenomena to which gene expression could be attributed.


2001 ◽  
Vol 47 (5) ◽  
pp. 283-294 ◽  
Author(s):  
Masahiko NISHIGAI ◽  
Akiko TAKAMURA ◽  
Hideo KAMOMAE ◽  
Tomomi TANAKA ◽  
Yoshihiro KANEDA

2010 ◽  
Vol 24 (2) ◽  
pp. 370-380 ◽  
Author(s):  
Natalia Di Pietro ◽  
Valentine Panel ◽  
Schantel Hayes ◽  
Alessia Bagattin ◽  
Sunitha Meruvu ◽  
...  

Abstract The serum and glucocorticoid-inducible kinase 1 (SGK1) is an inducible kinase the physiological function of which has been characterized primarily in the kidney. Here we show that SGK1 is expressed in white adipose tissue and that its levels are induced in the conversion of preadipocytes into fat cells. Adipocyte differentiation is significantly diminished via small interfering RNA inhibition of endogenous SGK1 expression, whereas ectopic expression of SGK1 in mesenchymal precursor cells promotes adipogenesis. The SGK1-mediated phenotypic effects on differentiation parallel changes in the mRNA levels for critical regulators and markers of adipogenesis, such as peroxisome proliferator-activated receptor γ, CCAAT enhancer binding protein α, and fatty acid binding protein aP2. We demonstrate that SGK1 affects differentiation by direct phosphorylation of Foxo1, thereby changing its cellular localization from the nucleus to the cytosol. In addition we show that SGK1−/− cells are unable to relocalize Foxo1 to the cytosol in response to dexamethasone. Together these results show that SGK1 influences adipocyte differentiation by regulating Foxo1 phosphorylation and reveal a potentially important function for this kinase in the control of fat mass and function.


2009 ◽  
Vol 115 (1-4) ◽  
pp. 18-28 ◽  
Author(s):  
Luiz Gustavo B. Siqueira ◽  
Ciro A.A. Torres ◽  
Lincoln S. Amorim ◽  
Eliza D. Souza ◽  
Luiz Sérgio A. Camargo ◽  
...  

2012 ◽  
Vol 80 (8) ◽  
pp. 2868-2877 ◽  
Author(s):  
Gaoyan Tang ◽  
Teresa Ruiz ◽  
Keith P. Mintz

ABSTRACTAggregatibacter actinomycetemcomitansis hypothesized to colonize through the interaction with collagen and establish a reservoir for further dissemination. The trimeric adhesin EmaA ofA. actinomycetemcomitansbinds to collagen and is modified with sugars mediated by an O-antigen polysaccharide ligase (WaaL) that is associated with lipopolysaccharide (LPS) biosynthesis (G. Tang and K. Mintz, J. Bacteriol.192:1395–1404, 2010). This investigation characterized the function and cellular localization of EmaA glycosylation. The interruption of LPS biogenesis by using genetic and pharmacological methods changed the amount and biophysical properties of EmaA molecules in the outer membrane. InrmlCandwaaLmutant strains, the membrane-associated EmaA was reduced by 50% compared with the wild-type strain, without changes in mRNA levels. The membrane-associated EmaA protein levels were recovered by complementation with the corresponding O-polysaccharide (O-PS) biosynthetic genes. In contrast, another trimeric autotransporter, epithelial adhesin ApiA, was not affected in the same mutant background. The inhibition of undecaprenyl pyrophosphate recycling by bacitracin resulted in a similar decrease in the membrane-associated EmaA protein. This effect was reversed by removal of the compound. A significant decrease in collagen binding activity was observed in strains expressing the nonglycosylated form of EmaA. Furthermore, the electrophoretic mobility shifts of the EmaA monomers found in the O-PS mutant strains were associated only with the membrane-associated protein and not with the cytoplasmic pre-EmaA protein, suggesting that this modification does not occur in the cytoplasm. The glycan modification of EmaA appears to be required for collagen binding activity and protection of the protein against degradation by proteolytic enzymes.


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