Transcriptomic effects of early life and peripubertal dietary vitamin D deficiency on mouse ovaries and pituitary glands
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Dumitru Iacobas
PROVIDER: E-GEOD-48170 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Vitamin D2 (VD) and the VD3 receptor (VDR) are proposed to have multiple important physiological roles that include but are not limited to glucose homeostasis, bone health, immune competency and more recently maintenance of normal reproductive physiology. The prevalence of VD deficiency in the US is reported to be as high as 60% in some populations. Several recent studies suggest that reproductive-aged women and their offspring are at the greatest risk for VD deficiency. The objective of our study was to determine the effect of early life (intrauterine through preweaning) and peripubertal VD deficiency on female reproductive physiology. Profile and compare the ovarian transcriptomes of 2-month-old C57BL/6J mice that received a normal (OC samples) or a VD-deficient diet only during the early life (OE samples) or peripubertal (OP samples). Each diet group (OC, OE and OP) was composed of 4 females (biological replicas).
2013-06-21 | E-GEOD-48167 | biostudies-arrayexpress
Project description:Vitamin D2 (VD) and the VD3 receptor (VDR) are proposed to have multiple important physiological roles that include but are not limited to glucose homeostasis, bone health, immune competency and more recently maintenance of normal reproductive physiology. The prevalence of VD deficiency in the US is reported to be as high as 60% in some populations. Several recent studies suggest that reproductive-aged women and their offspring are at the greatest risk for VD deficiency. The objective of our study was to determine the effect of early life (intrauterine through preweaning) and peripubertal VD deficiency on female reproductive physiology. Profile and compare the hypophysis transcriptomes of 2-month-old C57BL/6J mice that received a normal (OC samples) or a VD-deficient diet only during the early life (OE samples) or peripubertal (OP samples). Each diet group (OC, OE and OP) was composed of 4 females (biological replicas).
2013-06-21 | E-GEOD-48169 | biostudies-arrayexpress
Project description:Clear cell renal carcinoma (CCRC) accounts for >80% of all kidney cancers but what triggers the tumorigenesis in the kidney and metastases in the bones are still under debate. Our hypothesis is that remodeling of the genomic fabrics of certain functional pathways and their interplay beyond critical limits are key causes of CCRC. We profiled the transcriptomes of metastatic chest wall and of two primary cancerous sites of the renal medulla and compared them with that of non-cancerous kidney resection margins. Samples were collected from a 74 years old male with metastatic carcinoma, consistent with renal cell carcinoma, clear cell type, Fuhrman grade 3, who undergone total right kidney nephrectomy and resection of a chest wall mass. Transcriptomic analysis pointed the tumor region in the right kidney that led to the chest wall metastases. The tumor proved heterogeneous not only in the expression level but also in the expression control, coordination and interplay of pathways responsible for cellular processes and genetic and environmental information processing. The differently regulated pathways in the two sides of the tumor: CCRC, and HIF-1, Vegfa and mTor signaling indicate activation of distinct mechanisms. Four-conditions (CTR = control - non-cancerous kidney resection margins, PTA = primary tumor side A, PTB = primary tumor side B, MET = chest wall metastasis. Four biological replicates of each condition.
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Project description:We used Agilent human gene expression arrays to test whether Capridine, a chemotherapeutic agent with specificity towards prostate cancer, deregulates the genomic fabric of acute myeloyd leukemia in HL-60 cells. This cell line was derived at the National Cancer Institute from a 36-year-old woman with acute promyelocytic leukemia. We found that Capridine down-regulates the pathways responsible for formation of hematopoietic progenitor cells, for anti-apoptosis and for proliferation of clonal neoplastic cells. Our results indicates the therapeutic potential of Capridine against acute myeloid leukemia. Two-conditions: HO = not treated, HA = Capridine-treated HL-60 cells. Four biological replicates of each condition. Differently labeled biological replicates were cohybridized with each array. Results of similarly labeled different conditions were compared then averaged for the two fluorescent labels. For instance: HO1 & HO3 were compared with HA1 & HA3, HO2 & HO4 were compared with HA2 & + HA4, and the results of the comparisons averaged. This design uses 100% of the resources, has a better normlaiztion and allows all possible comparisons among the conditions.
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Project description:Our preclinical developmental program identified Capridine as a chemotherapeutic agent that had specificity towards prostate cancer with minimal bone marrow toxicity. In human prostate cancer xenograft studies both androgen responsive and non-responsive tumors were inhibited by a weekly therapeutic regimen Capridine. The minimal bone marrow toxicity as seen in rodent and dog preclinical studies is in line with its twenty-fold differential activity in prostate cancer cells vs. the promyelocytic leukemic cell line HL-60. This differential activity was partly attributed to its activity on ?H2AX modulation, which was considered as one of the targets. Capridine structure is consistent with a classical DNA intercalating agent; however, its DNA intercalation property does not fully correlate with its anti prostate cancer specific activity. To identify the cellular targets of Capridine in a more comprehensive manner we analyzed its transcriptomic effects on androgen non-responsive DU145 cells. Agilent human gene expression microarray analysis indicated that expression of 97 unigenes genes was altered by Capridine. Our data confirm that, in addition to DNA intercalation, Capridine targets DNA transcription via histone modulation in a cell-specific manner. Two-conditions: DO = not treated, DA = Capridine-treated DU145 cells. Four biological replicates of each condition. Differently labeled biological replicates were cohybridized with each array. Results of similarly labeled different conditions were compared then averaged for the two fluorescent labels. For instance: DO1 & DO3 were compared with DA1 & DA3, DO2 & DO4 were compared with DA2 & + DA4, and the results of the comparisons averaged. This design uses 100% of the resources, has a better normlaiztion and allows all possible comparisons among the conditions.
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