Summary: Polyamines are polycationic molecules that contain two or more amino groups (–NH₃⁺) and are present in all eukaryotic and prokaryotic cells. Polyamines are synthesized from arginine, ornithine, and proline, and from methionine as the methyl-group donor. In the traditional pathway for polyamine synthesis, arginase converts arginine into ornithine, which is decarboxylated by ornithine decarboxylase (ODC1) to generate putrescine. The latter is converted to spermidine and spermine. Recent studies have indicated the existence of ‘non-classical pathways’ for the generation of putrescine from arginine and proline in animal cells. Specifically, arginine decarboxylase (ADC) catalyzes the conversion of arginine into agmatine, which is hydrolyzed by agmatinase (AGMAT) to form putrescine. Additionally, proline is oxidized by proline oxidase to yield pyrroline-5-carboxylate, which undergoes transamination with glutamate to produce ornithine for decarboxylation by ODC1. Intracellular production of polyamines is controlled by antizymes binding to and inactivating ODC1. Polyamines exert effects that include stimulation of cell division and proliferation, gene expression for the survival of cells, DNA and protein synthesis, regulation of apoptosis, oxidative stress, angiogenesis, and cell–cell communication activity. Accordingly, polyamines are essential for early embryonic development and successful pregnancy outcome in mammals. In this paper the main concepts on the history, structure and molecular pathways of polyamines as well as their physiological role on angiogenesis, and reproductive physiology are reviewed.

Once initiated, invasion of trophoblast cells must be tightly regulated, particularly in early pregnancy. The mechanisms necessary for the invasion and migration of trophoblast cells are thought to be related to those involved in the invasive and metastatic properties of cancer cells. Quantitative PCR was used to measure, in trophoblast cells, the transcriptional expression profiles of four genes, INSL4, BRMS1, KiSS-1 and KiSS-1R, reported to be implicated in tumor invasion and metastasis. Laser capture microdissection and purification of trophoblast cells demonstrate that, as already known for INSL4, BRMS1, KiSS-1 and KiSS-1R are expressed by the trophoblast subset of placental tissues. Expression profiles of these genes studied in early placentas (7-9 weeks, n=55) and term placentas (n=11) showed that expression levels of BRMS1 are higher in term than in early placentas, while expression levels of KiSS-1R are higher in early than in term placentas. Low levels of expression of BRMS1 were observed in normal pregnancies, in molar pregnancies and in choriocarcinoma cell lines BeWo, JAR and JEG3 while, in striking contrast, the expression levels of INSL4, KiSS-1 and Kiss-1R were increased in both early placentas and molar pregnancies and were reduced in choriocarcinoma cells. These transcriptional expression profiles are in favor of a predominant role of INSL4, KiSS-1 and KiSS-1R in the control of the invasive and migratory properties of trophoblast cells.

In utero transmission of HIV‐1 has been demonstrated and may account for around 10–20% of all materno–fetal HIV‐1 transmission. The possible routes for such transmission are transannexial or transplacental. In both cases, the microenvironment (cytokines and chemokines) at the placental interface could be an important regulatory factor in viral transmission. We therefore performed explant cultures of placental villi, and isolated purified trophoblasts, from term placentae obtained from HIV‐1‐seropositive and HIV‐1‐seronegative women in order to assess and compare the cytokine and chemokine secretion profiles using ELISA and semiquantitative RT‐PCR. No major differences could be seen in the secretions of cytokines and chemokines at the level of whole placental tissue in HIV‐1‐positive and HIV‐1‐negative women. However, variations were observed in the expression of inflammatory cytokines and chemokines from trophoblastic cells, depending on the status of HIV‐1 infection of the mothers but not the babies, all of which remained uninfected. The significance of these data is discussed.

Maya-Pulgarin D, et al. J Vet Sci. 2017 Sep;18(3):407-414. https://doi.org/10.4142/jvs.2017.18.3.407

Subclinical Ruminal Acidosis (SARA) and Subclinical Ketosis (SCK) are two of the most prevalent metabolic diseases of dairy cows, with impacts on reproductive performance. There is scarce literature about these diseases in dairy regions in Colombia. In 29 randomly selected herds in Pasto, Colombia, 249 dairy cows were followed weekly for two months postpartum to determine: 1) incidence risk of SARA and SCK; and 2) effects of SARA and SCK on the occurrence of postpartum anestrus (PA) at two months. Samples from ruminal liquor and blood were obtained one time per cow during the first week postpartum to determine presence of SARA (pH < 5.6) and SCK (1.0-2.9 mmol/L of blood Beta-Hydroxy-Butyrate), respectively. PA diagnosis was determined with ultrasound. Pregnancy risks at 30 and 60 days post-breeding (and assumed embryo losses between these days) were determined. Risk factors associated with PA were estimated through a mixed multi-level multivariable logistic regression model, adjusting for clustering of cows within herds. The incidence risks of SARA and SCK were 23.3% and 46.2%, respectively. Simultaneous occurrence of SCK and SARA (SCASCK) was present in 5.2% of the cows. In the final multivariable model, the occurrence of SARA (Odds Ratio: OR = 39.4), SCK (OR = 47.4) and SCASCK (OR = 68.5) was associated with increased odds of PA. Feeding a transition period diet was associated with reduced odds of PA (OR = 0.15). Second parity cows had significantly lower odds of PA than first parity cows (OR = 0.21). In conclusion, inadequate pre-partum and postpartum nutritional management of the herds increased the occurrence of SARA and SCK, which had adverse effects on reproductive performance.