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At least 487 records · Page 27Linked to original sources
PubMed1990

Ontogeny of gonadotropin-releasing hormone-containing neurons in early fetal development of rhesus macaques.

We studied the ontogeny of GnRH neurons in fetal rhesus macaques from days 36-135 of gestation. The nasal region, pituitary, and brain were dissected, fixed in 4% paraformaldehyde, sectioned on a cryostat at 10 microns, and mounted on slides. Immunocytochemistry and in situ hybridization were performed for GnRH, pro-GnRH, and pro-GnRH mRNA on nasal and brain tissues. Immunoreactive LH, FSH, and PRL were determined in developing pituitary glands. At 36 days, clusters of GnRH cells were found in the nasal region only. GnRH fibers extended into the brain, and large bundles projected laterally toward the basal hypothalamus. By day 38 GnRH cells were also localized in the olfactory region of the brain. With increasing fetal age a gradual caudal extension of GnRH cells occurred. These cells were first observed in the basal hypothalamus at 47 days. Cells containing PRL and gonadotropins (LH and FSH) were detected in the pituitary at 47 and 50 days, respectively. Low levels of pro-GnRH mRNA were present in the nasal epithelium and septum by day 38 of gestation. The levels of pro-GnRH mRNA in the nasal area and the brain remained low in the day 50 fetus, but were increased significantly by day 135. These data suggest that GnRH neurons in the primate brain originate in the nasal region. Furthermore, GnRH neurons exhibit low levels of synthetic activity at the early fetal stages, but higher synthetic activity close to term.

Animals↗
PubMed2003

Functional and morphological development of lymphoid tissues and immune regulatory and effector function in rhesus monkeys: cytokine-secreting cells, immunoglobulin-secreting cells, and CD5(+) B-1 cells appear early in fetal development.

Little is known regarding the timing of immune ontogeny and effector function in fetal humans and nonhuman primates. We studied the organization of lymphocyte and antigen-presenting cell populations in developing lymphoid tissues of rhesus monkey fetuses during the second and third trimesters (65 to 145 days of gestation; term = 165 days). Immunoglobulin-secreting and cytokine-secreting cells were detected at day 80. The thymus, spleen, lymph nodes, and intestinal mucosa were examined for cells expressing CD3, CD5, CD20, CD68, p55, and HLA-DR. In the spleens of 65-day-old fetuses (early second trimester), the overwhelming majority of total lymphocytes were CD5(+) CD20(+) B-1 cells. The remaining lymphocytes were CD3(+) T cells. By day 80, splenic B and T cells were equal in number. Intraepithelial CD3(+) CD5(-) T cells and lamina propria CD20(+) CD5(+) B cells were present in the intestines of 65-day-old fetuses. By day 80, numerous CD20(+) CD5(+) B cells were present in the jejunums and colons and early lymphocyte aggregate formation was evident. The spleens of 80- to 145-day-old fetuses contained immunoglobulin M (IgM)-secreting cells, while IgA-, IgG-, interleukin-6-, and gamma interferon-secreting cells were numerous in the spleens and colons. Thus, by the second trimester, the lymphoid tissues of the rhesus monkey fetus have a complete repertoire of properly organized antigen-presenting cells, T cells, and B cells.

Animals↗
PubMed1994

Relationships between maternal and fetal liver copper, iron, manganese, and zinc concentrations and fetal development in California Holstein dairy cows.

Associations between maternal trace element deficiencies and abortion have been made for many mammalian species. Objectives of this study were to estimate and correlate maternal and fetal hepatic Cu, Fe, Mn, and Zn concentrations through gestation. Additionally, aborted fetuses, stratified by cause of abortion (infectious or noninfectious), were compared to size-matched nonaborted fetuses to examine for magnitude and direction of change in hepatic trace element status. Dam and fetal liver were removed at slaughter from 103 Holstein dairy cows judged grossly normal by ante- and postmortem examination. Liver samples were collected from fetuses submitted by veterinarians for routine diagnosis of abortion (n = 80). Hepatic Cu, Fe, Mn, and Zn concentrations were determined by flame spectrophotometry. Comparisons of groups, estimations of correlations, and derived prediction equations were made by least-squares methods. Maternal liver Cu, Fe, Mn, and Zn concentrations did not vary during gestation. Compared with the dam, fetal liver Fe and Zn concentrations were higher (P < 0.05), fetal Cu concentrations were similar (P > 0.05), and fetal liver Mn concentrations were lower (P < 0.05). As fetal size increased, fetal liver Cu and Zn concentrations increased (P < 0.05), fetal liver Fe concentration decreased (P < 0.05), and fetal liver Mn did not change (P > 0.05). Aborted fetuses had lower liver Cu, Mn, and Zn concentrations than did nonaborted fetuses (P < 0.05). Liver Fe concentration was lower in aborted fetuses than in nonaborted fetuses in the second trimester only (P < 0.05). Consistently lower liver Cu, Fe, Mn, and Zn concentrations in aborted fetuses suggest a nonspecific change in trace element status, which implies an effect of abortion, not a cause of abortion.

Animals↗
PubMed2002

Detection of chondroitin sulfates and decorin in developing fetal and neonatal rat lung.

Chondroitin sulfates and their related proteoglycans are components of extracellular matrix that act as key determinants of growth and differentiation characteristics of developing lungs. Changes in their immunohistochemical distribution during progressive organ maturation were examined with monospecific antibodies to chondroitin sulfate, a nonbasement membrane chondroitin sulfate proteoglycan, and the specific chondroitin sulfate-containing proteoglycan decorin in whole fetuses and lungs from newborn and adult rats. Alveolar and airway extracellular matrix immunostained heavily in the prenatal rat for both chondroitin sulfate and chondroitin sulfate proteoglycan, whereas decorin was confined to developing airways and vessels. These sites retained their respective levels of reactivity with all antibodies through 1-10 days postnatal but thereafter became progressively more diminished and focal in alveolar regions. The heavy staining seen early in development was interpreted to reflect a significant and wide distribution of chondroitin sulfates, chondroitin sulfate proteoglycans, and decorin in rapidly growing tissues, whereas the reduced and more focal reactivity observed at later time points coincided with known focal patterns of localization of fibrillar elements of the extracellular matrix and a more differentiated state.

Aging↗
PubMed1997

Cardiac expression of 52beta, an alternative transcript of the congenital heart block-associated 52-kd SS-A/Ro autoantigen, is maximal during fetal development.

OBJECTIVE: Congenital heart block (CHB), associated with antibodies to SS-A/Ro and SS-B/La, is most often detected between 18 and 24 weeks of gestation, yet the maternal heart is unaffected. We recently described an alternatively spliced 52-kd SS-A/Ro messenger RNA (mRNA) derived from the skipping of exon 4 which encodes a smaller protein, 52beta (MW 45 kd), recognized by CHB maternal antisera. This study was designed to identify whether cardiac expression of 52beta and full-length 52alpha relates to the development of CHB. METHODS: Reverse transcriptase-polymerase chain reaction was performed using primers flanking exon 4 and mRNA from 22 human fetal hearts (age 11-25 weeks) and 3 adult hearts. The brain, kidney, liver, lung, and spleen were similarly evaluated in a 15-week, an 18-week, and a 24-week fetus. RESULTS: Expression of 52beta was greatest and 52alpha lowest between 14 and 16 weeks of gestation. In fetal hearts ages 22-25 weeks and adult heart, the 52beta transcript was markedly diminished and 52alpha clearly dominated. The 52beta mRNA was observed in a 15-week brain, kidney, lung, and spleen; however, its expression relative to 52alpha was greatest in the heart. CONCLUSION: Since expression of the alternative product 52beta is maximal at the time of cardiac ontogeny when maternal antibodies gain access to the fetal circulation, just prior to the clinical detection of bradyarrhythmia, a role for 52beta in the development of CHB is implicated. Although other fetal tissues express 52beta, there may be differences in accessibility of antigen or regenerative capacities.

Adult↗
PubMed2006

Acute and long-term effects of clinical doses of antenatal glucocorticoids in the developing fetal sheep kidney.

OBJECTIVES: The controversy regarding potential long-term side effects of antenatal steroid administration for accelerating fetal lung maturation is still unresolved despite more than 30 years of experience. Studies in animals have demonstrated that administration of glucocorticoids during pregnancy alters renal expression of several key regulatory molecules at different developmental stages followed in most cases with the development of hypertension in the adult. We studied the effects of betamethasone on the expression of (1) NA,K-ATPAse pump; (2) the Na/H exchanger 3 (NAHE3); (3) angiotensin receptor (AT1 and AT2); and (4) the type 1 dopamine receptor (D1R). METHODS: Pregnant sheep were treated with either 0.17 mg/kg betamethasone or vehicle 24 hours apart at 80 and 81 days' gestation. Fetal kidneys were harvested at 81 and 135 days' gestation. Protein and mRNA levels were measured in kidney cortex. RESULTS: Betamethasone had acute and long-term effects on fetal kidney cortex gene expression. Acutely, mRNA abundance for AT2 was significantly lower and that of NHE3 significantly higher than in controls (0.4 +/- 0.02 vs 0.7 +/- 0.05; 1.2 +/- 0.16 vs 0.4 +/- 0.04; P < .05). At 135 days' gestation, AT2 receptor abundance remained lower than control (0.2 +/- 0.02 vs 0.4 +/- 0.02; P < .05), whereas D1R expression was higher (0.8 +/- 0.17 vs 0.5 +/- 0.06; P < .05). No changes in Na,K-ATPase of AT1 receptor at either of the two time points studied were observed. Antenatal steroid administration was not associated with premature labor or a reduction in either body weight or kidney weight. CONCLUSION: Our findings strongly suggest that antenatal glucocorticoid administration according to National Institutes of Health (NIH) consensus guidelines may alter human fetal renal development. Further studies are needed to establish a direct relationship between alterations in fetal renal gene expression and the development of hypertension in adulthood.

Animals↗