Biomedical subjects

J C Cross

Publications and source records attributed to J C Cross.

59 records · Page 4Linked to original sources

PubMed1989

Porcine conceptuses secrete an interferon during the preattachment period of early pregnancy.

Maternal recognition of pregnancy in sheep and cattle is thought to be initiated by the conceptus secretory proteins ovine trophoblast protein-1 (oTP-1) and bovine trophoblast protein-1 (bTP-1), respectively. Recently, these proteins have been shown to be members of the interferon-alpha (IFN-alpha) family. In this study, we have examined whether pig conceptuses also produce IFN during early pregnancy. conceptuses were collected at Days 8, 10, 11, 12, 13, 15, and 17 of pregnancy and cultured in serum-free medium for 24 h. Day 11 conceptuses secreted a dominant 22,000-24,000 Mr cluster of acidic proteins (pI 5.2-5.4), that appeared to cross-react on immunoblots with antiserum against human IFN-alpha but not against oTP-1. Antiviral activity characteristic of an IFN was present in conceptus culture medium and uterine flushings from Day 11 through Day 17 of pregnancy, but was absent in flushings prior to Day 11 of pregnancy and in flushings from Day 12 nonpregnant gilts. The antiviral activity coeluted with a 22,000-24,000 Mr protein during partial purification through a gel filtration column. The activity was extremely labile, but could be restored by sequential protein denaturation, reduction, and renaturation. We conclude that production of IFN by early conceptuses is not restricted to ruminant species, and may therefore represent a more general phenomenon.

Animals↗

PubMed1987

Effects of progesterone and weaning on LH and FSH responses to naloxone in postpartum beef cows.

Two experiments were conducted to evaluate the effects of naloxone, an endogenous opioid receptor antagonist, on LH and FSH secretion in postpartum beef cows. In Experiment 1, 24 cows were divided into three equal groups. On day 15 postpartum, all cows were bled for 8 hr at 10 min intervals to evaluate LH secretory parameters. On day 18 postpartum, three treatments were administered: (a) saline at 0730 and 1130 hr; (b) 275 mg naloxone at 0730 and 1130 hr; (c) naloxone as in (b) above, plus this group was also treated with 50 mg progesterone (P4) twice daily from day 16 to day 19. In each treatment, jugular vein samples were collected at 10 min intervals from 0800 to 1600 hr. On day 19 the same treatments were administered at the same times, however, all cows were given 25 micrograms GnRH at 1200 hr to evaluate the LH secretory response. Naloxone increased mean LH concentration (P less than .05) and tended to increase pulse amplitude and frequency compared to controls. However, the most dramatic difference was due to P4 treatment which suppressed mean LH, pulse amplitude and frequency. Treatments had no effect on LH secretion in response to a 25 micrograms dose of GnRH. In Experiment 2, the effects of suckling on the naloxone response were examined in 16 postpartum cows. On day 21 postpartum, blood was collected at 10 min intervals for 8 hr and then calves were removed from half the cows. After 3 days of calf removal, all cows were sampled at 10 min intervals for 4 hr; then naloxone was injected after each 10 min sample at a dose rate of 200 mg/hr (33 mg per injection). Naloxone treatment and sampling continued for an additional 8 hr. Calf removal alone had very little effect on LH pulsatility. However, naloxone resulted in increased pulse frequency and mean LH compared to the control period. We conclude that LH release in the early postpartum cow is partially regulated by endogenous opioid peptides. We were unable to detect any effects on FSH secretion nor on pituitary sensitivity to exogenous GnRH.

Animals↗

PubMed1987

Absence of detectable phosphocreatine in rat luteal cells.

Previous studies from this laboratory showed that adenosine amplifies the action of luteinizing hormone (LH) severalfold in rat and human luteal cells by an intracellular, adenosine 5'-triphosphate (ATP)-linked process. The objective of this study was to evaluate the contribution of phosphocreatine (PCr) and creatine kinase (CK) to the dynamics of luteal ATP metabolism. Levels of PCr in luteinized rat ovaries were similar to those seen in liver but were approximately 1 and 7% of levels found in skeletal and heart muscle, respectively. In isolated rat luteal cells, little detectable PCr was seen after incubation in the presence or absence of adenosine, although cell ATP levels were increased twofold by adenosine treatment. The presence or absence of LH had no effect on either PCr or ATP levels in incubations of isolated luteal cells. Analysis of CK activity in tissue and cell homogenates showed that the specific activity of CK in luteal cells was in the same range as that seen in liver but less than 1/30 of that seen in skeletal muscle. From these studies we conclude that rat luteal cells contain little, if any, PCr and low levels of CK. Thus the rapid changes in ATP levels that are seen in rat luteal tissue and cells may occur because these cells have little capacity to buffer ATP levels with a reservoir of high-energy phosphate groups in the form of PCr.

Adenosine Triphosphate↗

PubMedDate not supplied

Genes governing placental development.

The placenta is essential for fetal growth because it promotes the delivery of nutrients and oxygen from the maternal circulation. In mice, many gene mutations disrupt formation of the placenta, with specific effects at different times and on different components. Studies of these mutations are beginning to provide insights into both the molecular pathways required for formation of different placental substructures and the nature of intercellular interactions, between trophoblast, mesenchymal and vascular components, that regulate placental development. Conserved gene expression patterns in humans should enable the elucidation of the molecular basis of human placental dysfunction.

Allantois↗

PubMedDate not supplied

Genes, development and evolution of the placenta.

Through studies of transgenic and mutant mice, it is possible to describe molecular pathways that control the development of all major trophoblast cell subtypes and structures of the placenta. For example, the proliferation of trophoblast stem cells is dependent on FGF signalling and downstream transcription factors Cdx2, Eomes and Err2. Several bHLH transcription factors regulate the progression from trophoblast stem cells to spongiotrophoblast and to trophoblast giant cells (Id1/2, Mash2, Hand1, Stra13). Intercellular actions critical for maintaining stable precursor cell populations are dependent on the gap junction protein Cx31 and the growth factor Nodal. Differentiation towards syncytiotrophoblast as well as the initiation of chorioallantoic (villous) morphogenesis is regulated by the Gcm1 transcription factor, and subsequent labyrinth development is dependent on Wnt, HGF and FGF signalling. These insights suggest that most of the genes that evolved to regulate placental development are either identical to ones used in other organ systems (e.g., FGF and epithelial branching morphogenesis), were co-opted to take on new functions (e.g., AP-2gamma, Dlx3, Hand1), or arose via gene duplication to take on a specialized placental function (e.g., Gcm1, Mash2). Many of the human orthologues of these critical genes show restricted expression patterns that are consistent with a conserved function. Such information is aiding the comparison of the human and mouse placenta. In addition, the prospect of a conserved function clearly suggests potential mechanisms for explaining complications of human placental development.

Adult↗