Regulation of Gastrointestinal Peptide Hormone Gene Expression

Author(s):  
R. K. Pearson
1982 ◽  
Vol 5 ◽  
pp. 314-317 ◽  
Author(s):  
James L. Roberts ◽  
Ching-Ling C. Chen ◽  
France T. Dionne ◽  
Connie E. Gee

Gut ◽  
1998 ◽  
Vol 42 (6) ◽  
pp. 795-798 ◽  
Author(s):  
D F McWilliams ◽  
S A Watson ◽  
D M Crosbee ◽  
D Michaeli ◽  
R Seth

Background—The peptide hormone gastrin is a recognised growth factor for gastrointestinal (GI) tumour cells. Carboxyamidated gastrins bind to the cell surface gastrin/cholecystokinin B (CCK-B) receptor which can be expressed as either a normal or a truncated isoform (ΔCCK-B).Aims—To compare gastrin gene expression with ΔCCK-B and total CCK-B (both isoforms) gene expression in both GI and non-GI tract derived human tumour cell lines.Methods—Total RNA was extracted and gene expression was assayed by the reverse transcription-polymerase chain reaction followed by Southern blotting and hybridisation with specific oligo probes.Results—Gastrin was expressed by 5/5 gastric and 7/8 colorectal cell lines. Coexpression of gastrin CCK-B isoform was found in 80% of gastric and 75% of colorectal cell lines. Non-GI cell lines, with the exception of a lymphoblastic leukaemia cell line, showed no coexpression. The truncated receptor, ΔCCK-B, was shown in 3/5 gastric and 5/8 colorectal cell lines and was always coexpressed with gastrin.Conclusions—The truncated gastrin receptor, ΔCCK-B, is coexpressed with gastrin in 8/13 GI tumour cell lines. Gastrin and CCK-B receptor isoforms may be involved in maintaining autocrine/paracrine growth pathways in GI cancer cells.


2016 ◽  
Vol 56 (1) ◽  
pp. 11-22 ◽  
Author(s):  
Anji Lian ◽  
Keqiang Wu ◽  
Tianqiang Liu ◽  
Nan Jiang ◽  
Quan Jiang

The peptide hormone adropin plays a role in energy homeostasis. However, biological actions of adropin in non-mammalian species are still lacking. Using tilapia as a model, we examined the role of adropin in lipoprotein lipase (LPL) regulation in hepatocytes. To this end, the structural identity of tilapia adropin was established by 5′/3′-rapid amplification of cDNA ends (RACE). The transcripts of tilapia adropin were ubiquitously expressed in various tissues with the highest levels in the liver and hypothalamus. The prolonged fasting could elevate tilapia hepatic adropin gene expression, whereas no effect of fasting was observed on hypothalamic adropin gene levels. In primary cultures of tilapia hepatocytes, synthetic adropin was effective in stimulating LPL release, cellular LPL content, and total LPL production. The increase in LPL production also occurred with parallel rises in LPL gene levels. In parallel experiments, adropin could elevate cAMP production and up-regulate protein kinase A (PKA) and PKC activities. Using a pharmacological approach, cAMP/PKA and PLC/inositol trisphosphate (IP3)/PKC cascades were shown to be involved in adropin-stimulated LPL gene expression. Parallel inhibition of p38MAPK and Erk1/2, however, were not effective in these regards. Our findings provide, for the first time, evidence that adropin could stimulate LPL gene expression via direct actions in tilapia hepatocytes through the activation of multiple signaling mechanisms.


2018 ◽  
Vol 40 (2) ◽  
pp. 101-108 ◽  
Author(s):  
G V Gerashchenko ◽  
L V Mevs ◽  
L I Chashchina ◽  
M V Pikul ◽  
O P Gryzodub ◽  
...  

Aim: To analyze an expression pattern of the steroid and peptide hormone receptors, metabolic enzymes and EMT-related genes in prostate tumors in relation to the presence of the TMPRSS2/ERG fusion; and to examine a putative correlation between gene expression and clinical characteristics, to define the molecular subtypes of prostate cancer. Materials and Methods: The relative gene expression (RE) of 33 transcripts (27 genes) and the presence/absence of the TMPRSS2/ERG fusion were analyzed by a quantitative PCR. 37 prostate cancer tissues (T) paired with conventionally normal prostate tissue (CNT) and 21 samples of prostate adenomas were investigated. RE changes were calculated, using different protocols of statistics. Results: We demonstrated differences in RE of seven genes between tumors and CNT, as was calculated, using the 2−ΔCT model and the Wilcoxon matched paired test. Five genes (ESR1, KRT18, MKI67, MMP9, PCA3) showed altered expression in adenocarcinomas, in which the TMPRSS2/ERG fusion was detected. Two genes (INSR, isoform B and HOTAIR) expressed differently in tumors without fusion. Comparison of the gene expression pattern in adenomas, CNT and adenocarcinomas demonstrated that in adenocarcinomas, bearing the TMPRSS2/ ERG fusion, genes KRT18, PCA3, and SCHLAP1 expressed differently. At the same time, we detected differences in RE of AR (isoform 2), MMP9, PRLR and HOTAIR in adenocarcinomas without the TMPRSS2/ERG fusion. Two genes (ESR1 and SRD5A2) showed differences in RE in both adenocarcinoma groups. Fourteen genes, namely AR (isoforms 1 and 2), CDH1, OCLN, NKX3-1, XIAP, GCR (ins AG), INSR (isoform A), IGF1R, IGF1R tr, PRLR, PRL, VDR and SRD5A2 showed correlation between RE and tumor stage. RE of four genes (CDH2, ESR2, VDR and SRD5A2) correlated with differentiation status of tumors (Gleason score). Using the K-means clustering, we could cluster adenocarcinomas in three groups, according to gene expression profiles. A specific subtype of prostate tumors is characterized by the activated ERG signaling, due to the presence of TMPRSS2/ERG fusion, and also by high levels of the androgen receptor, prolactin, IGF, INSR and PCA3. Conclusions: We have found the specific differences in expression of the steroid and peptide hormone receptors, metabolic enzymes and EMT-related genes, depending on the presence/absence of the TMPRSS2/ERG fusion in prostate adenocarcinomas, CNT and adenomas. We showed three different gene expression profiles of prostate adenocarcinomas. One of them is characteristic for adenocarcinomas with the TMPRSS2/ERG fusion. Further experiments are needed to confirm these data in a larger cohort of patients.


2004 ◽  
Vol 16 (9) ◽  
pp. 282
Author(s):  
J. Gwyther ◽  
H. M. Gehring ◽  
L. J. Parry

Growth and development of the mammary apparatus (nipple and mammary gland) are important aspects of lactation. Macropodid marsupials can suckle young of two different ages simultaneously, a phenomenon known as asynchronous lactation. As a result, the type of milk produced and the structure of the two mammary glands supporting young of different ages vary considerably. A role for the peptide hormone relaxin in lactation has been demonstrated in relaxin receptor (LGR7)-deficient mice, which fail to deliver milk to their offspring due to impaired nipple development (1). This study investigated the distribution of LGR7 in the different mammary glands and nipples during asynchronous lactation in the tammar wallaby. The specific aim was to determine if the age of the pouch young influences LGR7 gene expression. Tissues were collected from the mammary apparatus sustaining the neonate and an older pouch young in the same mother, between Days 0 and 21 of lactation (n = 5/stage). A partial sequence (250-bp) of the tammar LGR7 was first obtained from a region close to the N-terminus of the soluble ectodomain, with 82% amino acid homology compared to the human LGR7 sequence. LGR7 gene expression was then measured by quantitative-PCR, using a TaqMan probe in the Opticon 2 thermal cycler (MJ Research, GeneWorks). Expression of LGR7 was upregulated in both the nipple and mammary gland supporting the neonate between 5 and 11 days after birth. There was no difference in LGR7 expression between these two tissues. However, LGR7 mRNA concentrations were significantly (P < 0.05: paired t-test) higher in the mammary apparatus supporting the neonate compared with that of the older young. These data suggest that a local stimulus, such as the continuous sucking by the neonate, may influence LGR7 expression in the mammary apparatus. (1) Krajnc-Franken et al. (2004) Mol. Cell. Biol. 24, 687–696.


2018 ◽  
Author(s):  
Sreesha R. Sudhakar ◽  
Jishy Varghese

AbstractInsulin, a highly conserved peptide hormone, links nutrient availability to metabolism and growth in animals. Besides this, in fed states insulin levels are high and insulin acts as a satiety hormone. In animals that are food deprived insulin levels remain low which facilitates hunger induced feeding. Contrary to expectations, we present evidence for persistent Drosophila insulin-like peptide gene expression and insulin signalling during initial phases of starvation. Maintenance of insulin signalling is crucial to sustain feeding responses during initial stages of starvation. Insulin signalling acts in a feedback loop involving the abdominal fatbody to maintain dilp gene expression in the early stages of food deprivation. Furthermore, another feedback regulatory loop between insulin-producing cells (IPCs) and neurons that produce the orectic hormone short-neuropeptide-F (sNPF), maintains sNPF levels and triggers feeding behavior. Thus, insulin acts through multiple feedback regulatory loops to elicit orexigenic responses and aid in efficient utilization of energy stores during early starvation.


2002 ◽  
Vol 103 (s2002) ◽  
pp. 84S-89S ◽  
Author(s):  
Kaname SAIDA ◽  
Naoko KOMETANI ◽  
Tsuyoshi UCHIDE ◽  
Youji MITSUI

Vasoactive intestinal contractor (VIC)/endothelin-2 (ET2) is a vasoactive peptide hormone comprising 21 amino acids. The complete nucleotide sequence of the full-length gene encoding preproVIC (PPVIC) was determined. The PPVIC gene contains five exons that span 6kb and shows a duplication on exons 2 and 3, coding for the VIC and VIC-like peptides respectively. Similarities between the genomic organization of the PPVIC/preproET2 and preproendothelin-1 genes suggest that the two are distantly related. PPVIC gene expression was observed in foetal and adult mouse intestine. The expression level in adults was approx. 10-fold higher than in the foetus, suggesting an involvement of VIC in intestinal development.


2016 ◽  
Author(s):  
Amanda K. Broz ◽  
Rafael F. Guerrero ◽  
April M. Randle ◽  
You Soon Baek ◽  
Matthew W. Hahn ◽  
...  

AbstractUnilateral incompatibility (UI) is an asymmetric reproductive barrier that unidirectionally prevents gene flow between species and/or populations. UI is characterized by a compatible interaction between partners in one direction, but in the reciprocal cross fertilization fails, generally due to pollen tube rejection by the pistil. Although UI has long been observed in crosses between different species, the underlying molecular mechanisms are only beginning to be characterized. The wild tomato relative Solanum habrochaites provides a unique study system to investigate the molecular basis of this reproductive barrier, as populations within the species exhibit both interspecific and interpopulation UI. Here we used a transcriptomic approach to identify genes in both pollen and pistil tissues that may be probable key players in UI. We confirmed UI at the pollen-pistil level between a self-incompatible population and a self-compatible population of S. habrochaites. A comparison of gene expression between pollinated styles exhibiting the incompatibility response and unpollinated controls revealed only a small number of differentially expressed transcripts. Many more differences in transcript profiles were identified between UI-competent versus UI-compromised reproductive tissues. A number of intriguing candidate genes were highly differentially expressed, including a putative pollen arabinogalactan protein, a stylar Kunitz family protease inhibitor, and a stylar peptide hormone Rapid Alkalinization Factor. Our data also provide transcriptomic evidence that fundamental processes including reactive oxygen species signaling are likely key in UI pollen-pistil interactions between both populations and species. Our transcriptomic analysis highlighted specific genes, including those in ROS signaling pathways that warrant further study in investigations of UI. To our knowledge, this is the first report to identify candidate genes involved in unilateral barriers between populations of the same species.


2003 ◽  
Vol 88 (3) ◽  
pp. 1394-1397 ◽  
Author(s):  
Shigeo Yura ◽  
Norimasa Sagawa ◽  
Hiroaki Itoh ◽  
Kazuyo Kakui ◽  
Mercy A. Nuamah ◽  
...  

The mechanism for decreased insulin sensitivity in pregnant women is not fully clarified. Resistin, a novel peptide hormone, is specifically expressed in the adipose tissue and decreases insulin sensitivity in rodents. In the present study, we demonstrate resistin gene expression in the human placental tissue, mainly in trophoblastic cells. The resistin gene expression in term placental tissue was more prominent than was seen in the first trimester chorionic tissue. In contrast resistin gene expression in adipose tissue was rather weak and remained unchanged by pregnancy. Thus, resistin is a newly isolated placental hormone in humans which may modulate insulin sensitivity during pregnancy.


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