Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.27.5 (RNase)
17,967 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

cDNA encoding the canine keratinocyte growth factor (KGF) was cloned from normal canine prostate tissue. The authentic canine KGF cDNA sequence, 686 bp in length, spans the protein-coding region and 88 bp of the 5' and 19 bp of the 3' untranslated regions of canine KGF. The predicted amino acid sequence of canine KGF is composed of 194 amino acid residues. Canine KGF exhibits highest homology with the human KGF cDNA and amino acid sequences (95.8% and 97.4%, respectively), while it demonstrates the lowest homology with the rat sequences at 88.0% and 92.3%, respectively. The degrees of homology with mouse cDNA and amino acid sequences are 91.8% and 95.9%, respectively. By using RNase protection assay, KGF was shown to be expressed in normal prostate tissues of both mature and young (5-month-old) dogs. In vitro, the recombinant canine KGF has mitogenic activity on cultured canine epithelial cells, whereas it has no effect on cultured canine prostatic stromal cells. This novel canine KGF cDNA may be a valuable tool in the study of human benign prostatic hyperplasia using the canine prostatic as a model.
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PMID:Keratinocyte growth factor (KGF/FGF-7) has a paracrine role in canine prostate: molecular cloning of mRNA encoding canine KGF. 863 53

During fetal and neonatal development and experimental obstruction, the bladder wall undergoes changes in both the amount and composition of the urothelium, extracellular matrix, and smooth muscle. We hypothesize that cell-cell signaling among the different layers of the bladder wall mediates these changes. Growth factors likely to be involved in this process are keratinocyte growth factor (KGF) and transforming growth factor (TGF)-alpha, -beta 2, and -beta 3. Whole rodent bladders were analyzed by RNase protection assays for KGF, KGF receptor, TGF alpha, epidermal growth factor receptor, and TGF beta 2 and -beta 3 transcripts at Fetal Day 14 (before smooth muscle differentiation) and Fetal Day 18 (after smooth muscle differentiation), at birth, and 60 days postnatal. Growth factor transcripts were also analyzed in partially obstructed rodent bladders and in sham-operated animals. TGF beta 2 and -beta 3 mRNA expression decreased as a function of gestational age, whereas TGF alpha mRNA increased. KGF mRNA was low before smooth muscle differentiation at 14 days' gestation, then increased. The mRNA of receptors for KGF and EGF remained essentially unchanged throughout bladder development. In bladders subjected to partial urethral outlet obstruction, there was a 2-fold increase in mRNA for TGF beta 2, a 5-fold increase in TGF beta 3, and a 10-fold increase TGF alpha mRNA. In contrast, there was no change in transcripts for either KGF or receptors for KGF and epidermal growth factor. Immunohistochemical localization of the protein for these growth factors showed selective localization to the epithelium and/or smooth muscle for TGF beta 2 and -beta 3, whereas TGF alpha and the epidermal growth factor receptor localized throughout the bladder wall. In conclusion, growth factor mRNA expression is modulated in bladder development and obstruction, which implies a possible mechanistic role of growth factors for the observed changes in the bladder wall and extracellular matrix.
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PMID:Growth factors and receptors in bladder development and obstruction. 876 16

We have previously identified and cloned a novel keratinocyte growth factor (KGF)-regulated gene in human keratinocytes that encodes the human homologue of a bovine non-selenium glutathione peroxidase (GPx). To gain insight into the regulation of this gene in vivo, we isolated the murine homologue from a mouse skin cDNA library. In vitro transcription/translation demonstrated that the cDNA encodes a 27 kDa protein. Furthermore, we amplified by PCR a partial cDNA that most likely corresponds to a related gene. RNase protection analysis revealed tissue-specific expression of both genes and the occurrence of alternative splicing or RNA editing of at least one of the primary transcripts. Similar to that of KGF, expression of GPx was strongly induced after cutaneous injury, and each isoform displayed unique kinetics of expression during the repair process. In situ hybridization studies demonstrated high levels of GPx mRNA in keratinocytes of the hyperproliferative epithelium at the wound edge. Since these cells express functional KGF receptors, induction of GPx expression by KGF might also occur in vivo. These data suggest a role for GPx in the protection of epithelial cells against oxidative stress, particularly during the inflammatory phase of wound repair.
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PMID:A novel type of glutathione peroxidase: expression and regulation during wound repair. 929 Nov 35

Acute hyperoxic lung injury remains a major factor in the development of chronic lung disease in neonates. A critical step in the repair of acute lung injury is the proliferation of type II alveolar epithelial cells. Type II cell proliferation is stimulated by keratinocyte growth factor (KGF), an epithelial cell-specific mitogen. We sought to investigate KGF mRNA expression in relation to type II cell proliferation during hyperoxic lung injury. We studied a previously described newborn (NB) rabbit model of acute and chronic hyperoxic injury [C. T. D'Angio, J. N. Finkelstein, M. B. LoMonaco, A. Paxhia, S. A. Wright, R. B. Baggs, R. H. Notter, and R. M. Ryan. Am. J. Physiol. 272 (Lung Cell. Mol. Physiol. 16): L720-L730, 1997]. NB rabbits were placed in 100% O2 for 9 days and then recovered in 60% O2. RT-PCR was used to synthesize and amplify a 267-bp fragment of rabbit KGF cDNA from whole lung RNA. KGF mRNA expression was analyzed by ribonuclease protection assay, and mRNA abundance was quantified by phosphorimaging. Proliferating cell nuclear antigen immunohistochemistry was used on lung sections to identify proliferating cells. The rabbit partial cDNA sequenced was >95% homologous to human cDNA, and all amino acids were conserved. Whole lung KGF mRNA expression was increased 12-fold after 6 days of hyperoxia compared with control lungs, and remained increased throughout the 100% O2 exposure period. Proliferating cell nuclear antigen immunohistochemistry showed an increase in type II cell proliferation after 8-12 days of hyperoxia. NB rabbits exposed to hyperoxic injury exhibit increased whole lung KGF mRNA expression preceding type II cell proliferation. KGF may be an important mitogen in the regulation of alveolar epithelial repair after hyperoxic lung injury.
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PMID:Hyperoxia increases keratinocyte growth factor mRNA expression in neonatal rabbit lung. 988 62

The purpose of this study is to evaluate the role of keratinocyte growth factor (KGF), transforming growth factor-alpha (TGF-alpha), and their receptors in altered renal growth caused by complete ureteral obstruction in the developing kidney. Neonatal and adult rats underwent complete unilateral ureteral ligation or sham operation. The kidneys were harvested at 1, 5, 10, 20, and 30 days after obstruction. Renal growth and development was assessed by histology and immunohistocytochemical localization of vimentin, cytokeratin and smooth muscle-alpha actin. Cellular proliferation was measured by [3H]thymidine labeling index of all cells. RNase protection assays were used to quantify mRNA encoding for KGF, KGF receptor, TGF-alpha, and epidermal growth factor (EGF) receptor. Ureteral obstruction in the developing kidneys resulted in decreased DNA synthesis, rapid parenchymal loss, myofibroblast proliferation in the interstitium, decreased tubular epithelial cells formation, and development of cystic dysplasia. In comparison, obstruction in the mature kidneys resulted in transient growth in the medullary ductal cells, parenchymal loss, and myofibroblast proliferation at a later time, lymphocytic infiltration in the interstitium but not cystic dysplasia. KGF and KGF receptor mRNA levels were increased in obstructed neonatal kidneys. Similarly, TGF-alpha and EGF receptor mRNA levels were increased. Delayed and more moderate increases in KGF, KGF receptor, and TGF-alpha expression were also seen in the obstructed mature kidneys. Of importance, the amount of EGF receptor mRNA was not increased in the obstructed compared with the contralateral or sham-operated adult kidneys. This study suggests that obstruction alters the normal expression pattern of KGF, TGF-alpha, and their receptors in renal development. These changes may be responsible for the impaired renal growth and altered development seen in ureteral obstruction of the kidneys. Although some changes are similar to those seen in the adult kidney, the increased expression of TGF-alpha and cystic dysplasia are unique to neonatal obstruction.
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PMID:Growth factor expression in the obstructed developing and mature rat kidney. 1006 5

Fibroblast growth factor (FGF)-10, a homologue of FGF-7, is expressed significantly in normal rat prostate tissue, well differentiated rat prostate tumors with an epithelial and stromal compartment and only in derived prostate stromal cells in culture. Similar to FGF-7, recombinant rat FGF-10 was a specific mitogen for prostate epithelial cells. In contrast to FGF-7 which is widely expressed among stromal cells in tissues, the expression of FGF-10 correlated with the presence of stromal cells of muscle origin. Radioreceptor binding assays and covalent cross-linking analysis revealed that FGF-10 binds with an affinity equal to FGF-7 to resident epithelial cell receptor, FGFR2IIIb, but unlike FGF-7 also binds the IIIb splice variant of FGFR1. Analysis of mRNA expression by RNase protection revealed that, similar to FGF-7, the expression of FGF-10 was responsive to androgen in stromal cells from normal prostate and non-malignant differentiated tumors. Although FGF-10 cDNA exhibits a signal sequence for secretion, cultured stromal cells exhibit strictly a cell-associated FGF-10 antigen that correlates with an alternately translated intracellular isoform. FGF-10 requires 1.4 times higher NaCl for elution from immobilized heparin than does FGF-7 and binds to four times the number of sites on the pericellular matrix of epithelial cells. The results show that prostate stromal cell-derived FGF-10, like FGF-7, exhibits the properties of an andromedin which may indirectly mediate control of epithelial cell growth and function by androgen. Although FGF-10 and FGF-7 bind and activate the same resident epithelial cell receptor (FGFR2IIIb), differences in cell type of origin, compartmentation by alternate translation, the affinity for FGFR1IIIb, and access to FGFR by differential interaction with pericellular matrix heparan sulfate suggest they may play both independent and compensatory roles in prostate homeostasis.
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PMID:Fibroblast growth factor-10. A second candidate stromal to epithelial cell andromedin in prostate. 1021 69

During fetal life, the pulmonary epithelium secretes liquid that distends the airways and is important for normal lung growth and development. The factors regulating human fetal lung liquid secretion are poorly understood; however, recent studies in murine models show that keratinocyte growth factor (KGF, FGF-7) and fibroblast growth factor 10 (FGF-10) stimulate liquid secretion. We asked whether KGF and FGF-10 stimulate liquid secretion in human fetal lung. First trimester fetal lung explants developed dose-dependent increases in intraluminal volume in response to KGF and FGF-10. Although there were no acute changes in explant transepithelial potential difference in response to KGF (0.1-1000 ng/mL), exposure to 5-50 ng/mL KGF over 60 h depolarized transepithelial potential difference compared with controls. We used ribonuclease protection assays to quantitate the ontogeny and regulation of mRNA expression for KGF and its receptor. Both mRNA were expressed in fetal and postnatal lung. Because the promoter region of the human KGF gene contains cAMP and IL-6 response elements, we asked whether cAMP or IL-6 stimulated expression of KGF or its receptor. We have previously shown that cAMP stimulates liquid secretion in this model. Both cAMP and IL-6 significantly increased expression of KGF but not KGF receptor during a 48-h experiment. Thus, stimulation of liquid secretion in explant models by cAMP may be mediated in part by induction of KGF expression. KGF and FGF-10 may be important paracrine factors regulating liquid secretion in human fetal lung.
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PMID:KGF and FGF-10 stimulate liquid secretion in human fetal lung. 1054 13

Fibroblast growth factor (FGF), a key regulatory factor of cell growth and differentiation, is involved in embryonic development, angiogenesis, and tumorigenesis. To date, four different FGF receptors (FGFRs) have been cloned and characterized. We examined the expression of four FGFRs in human gastric cancer tissues and cell lines using Northern analysis, ribonuclease protection assay, and immunohistochemistry. The mRNAs of FGFR-1 (10/14), FGFR-2 (9/14), and FGFR-4 (9/14) were up-regulated in cancer compared with normal tissues. FGFR-3 mRNAs were barely detectable in both normal and cancer tissues. These FGFR mRNAs were co-expressed in various combinations of two or three in the same tissue. Immunohistochemistry confirmed specific staining of multiple FGFRs, except FGFR-3, in the cancer specimens. To investigate the functional significance of FGFR co-expression we examined the invasive property of SNU-16 cells, which exhibited gene amplification of FGFR-2, -3, and -4 as well as over-expression of keratinocyte growth factor receptor (KGFR), a splice variant of FGFR-2, and FGFR-4 mRNA. KGF plus acidic FGF (aFGF), KGF, and aFGF treatment enhanced the invasive potential of SNU-16 cells over the control by 100%, 107%, and 47%, respectively, indicating that neither additive nor synergistic effect was induced by stimulation with aFGF plus KGF. These results suggest that co-expression of FGFRs in various combinations may cause subtle changes in the progression of gastric cancer.
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PMID:Up-regulation and co-expression of fibroblast growth factor receptors in human gastric cancer. 1100 64

To study biological character and function of epithelial rests of Malassez (ERM) in human periodontal ligament, we have developed a serum-free culture system of epithelial cells (ME) derived from ERM. The mitogenic effects of fibroblast growth factor (FGF)-1, FGF-2, and FGF-7/keratinocyte growth factor (KGF) on ME, human periodontal ligament-derived fibroblasts (PLF), human oral epithelial cells (OE), and human submandibular gland-derived epithelial cells (SGE) were investigated under a serum-free culture condition. FGF-1 and FGF-7/KGF stimulated the growth of both ME and SGE but FGF-2 had no effect. On the other hand, FGF-1, FGF-2, and FGF-7/KGF increased the OE proliferation. These results suggested that the divergent requirement of FGF ligands among these cells would be attributed to the different expression pattern of FGF receptor (FGFR) messenger ribonucleic acid (mRNA) isotypes. Therefore, we examined the expression of FGFR isotypes in these cells. Reverse transcription-polymerase chain reaction (RT-PCR) analysis of ME-and SGE-derived mRNAs revealed the presence of mRNA encoding FGFR2-IIIb, a high affinity receptor for FGF-1 and FGF-7/KGF. However, no mRNAs for other FGFR isotypes were detected in both ME and SGE. On the contrary, OE expressed FGFR1-IIIc, FGFR3-IIIb, and FGFR4 mRNAs as well as FGFR2-IIb. These results indicate that FGF binding sites on ME dominantly bind to FGF-1 and FGF-7/KGF, which transduce their signals via FGFR2-IIIb. Immunohistochemical analysis, PCR-Southern, ribonuclease protection assay (RPA), and Western blotting revealed that PLF expressed FGF-7/KGF mRNA and its peptide. These observations suggest that FGF-7/KGF might mediate epithelial-mesenchymal interactions between ME and PLF to maintain normal structure and function of periodontal ligament.
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PMID:Isolation and serum-free culture of epithelial cells derived from epithelial rests of Malassez in human periodontal ligament. 1114 56

Mammary gland development is regulated by complex interactions among mammogenic hormones and locally derived paracrine growth factors. In epithelial tissues, keratinocyte growth factor (KGF or FGF-7) originates in the stroma while its receptor (KGFR or FGFR2-IIIb) is present only in the epithelium. Previous work showed that estrogen but not progesterone could stimulate the synthesis of KGF in mammary stroma in vivo. The effects of 17 beta-estradiol and progesterone on KGFR expression in vivo were examined in these studies. Peripubertal and mature virgin mice received subcutaneous injections of hormone in sesame oil after which KGFR mRNA levels were assayed by ribonuclease protection analysis of mammary gland RNA. Estradiol treatment caused a dose- and time-dependent decrease in KGFR mRNA level in mice from both age groups while stimulating ductal growth after 7 days of treatment. Inhibition of KGFR expression was near maximal at an estradiol dose of 2 microg after 1 day of treatment. Progesterone injection increased KGFR mRNA levels but this effect correlated with the stimulation of ductal growth. However, when progesterone was co-administered with estradiol, KGFR mRNA levels were maintained in the absence of any effect on ductal growth. Thus, estradiol inhibited KGFR mRNA only when elevated unopposed by progesterone. These data show that KGFR expression is determined by the ratio of estradiol and progesterone and suggests a mechanism through which these hormones can co-operate to optimize their growth-promoting effects. Consequences of hormone imbalance are also implicated.
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PMID:In vivo inhibition of keratinocyte growth factor receptor expression by estrogen and antagonism by progesterone in the mouse mammary gland. 1169 52


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