1.Fibroblast Growth Factor 21: A Novel Metabolic Regulator.
Diabetes & Metabolism Journal 2012;36(1):26-28
No abstract available.
Fibroblast Growth Factors
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Fibroblasts
2.Mouse fibroblast growth factors-21 (MFGF-21) isolation
Journal of Practical Medicine 2003;442(2):109-111
Adult made IRC white mouse of 21 week age, weighing 22-25 g underwent an operation for removing the liver, which was washed with PBS buffer. Total ARN extracted from clean mouse liver composes of 3 characteristic band 28S, 18S and 5S. Total ARN concentration received was 10Ug/Ul approximatively. Received PCR product is a characteristic band of the size of some 630bp corresponded to the size of mFGF-21. It is a total gene of mFGF-21 with a sequence 100% corresponding to the registered sequence in the gene international data Bank Number NM-020013
Fibroblast Growth Factors
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Mice
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Liver
4.Difference of Fibroblast Growth Factor Receptor-1(FGFR-1) and Progesterone Receptor(PR) Expression between Classic and Aggressive Meningiomas.
Tai Hyoung CHO ; Jung Yul PARK ; Yang Suk CHAI ; Youn Kwan PARK ; Yong Gu CHUNG ; Hung Seob CHUNG ; Hoon Kap LEE ; Ki Chan LEE
Journal of Korean Neurosurgical Society 1996;25(8):1555-1560
Fibroblast growth factor(FGF) is a mitogen and a potent antigenic factor. It is also known as a differentiation factor for neuroectodermal-derived cell. It has been observed to be expressed in more than 90% of m-RNA of human meningiomas and gliomas. Progesterone receptor(PR) is well known surface receptor of meningioma and its number is greater than that of estrogen receptor. It is one os the known prognostic factors of meningioma. Meningiomas themselves are regarded as benign tumors in general, however some types show aggressive features. In the present study, authors examined the expression of FGF-1 and PR in meningioma tissues using immunohistochemical techniques with monoclonal antibody against human FGF-1 and PR. FGF-1 was detected in 25 of 35 classic meningiomas and in 7 of 9 aggressive ones. PR is expressed in 5 cases of classic and 2 cases of aggressive meningiomas. These results suggest FGF-1 may be involved in aggressive progression of meningioma. There was no significant difference of aggressiveness and expression of FGFR-1 and PR between classic and aggressive meningiomas, including their subtypes.
Estrogens
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Fibroblast Growth Factor 1
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Fibroblast Growth Factors*
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Fibroblasts*
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Glioma
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Humans
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Meningioma*
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Progesterone*
5.Dynamic expression of wnt and fibroblast growth factor ligands in cleft palate induced by retinoic acid.
Lu SHEN ; Wei CONG ; Ru WANG ; Jing XIAO
West China Journal of Stomatology 2011;29(1):62-65
OBJECTIVETo screen the wnt and fibroblast growth factor (FGF) ligands involved in palatogenesis and cleft palate, and to study the dynamic expression of them in the different stages of palatal development and cleft palate formation.
METHODSMouse model of retinoic acid (RA)-induced cleft palate was set up. At embryo day (ED) 14.5, the palatal tissues of RA-treated group and wild type were collected and prepared for gene-chip analysis. According to the gene-chip results, wnt3, wnt8a, fgf9 and fgf10 were selected and their expression level was detected at ED13.5-15.5 by using semi-quantitative reverse transcription-PCR (RT-PCR).
RESULTS(1) Gene-chip analysis showed that in RA-induced cleft palate group wnt8a and fgf9 were down-regulated, wnt3 and fgf10 were up-regulated in conversely. (2)During the different stage of the control group palatogenesis, intense expression of wnt3, wnt8a, fgf9 and fgf10 were detected with a continuous dynamic pattern. (3)Compared with the control group, the expression level of wnt3, wnt8a, fgf9 and fgf10 in RA-induced cleft palate showed significant difference, respectively (P < 0.05).
CONCLUSIONwnt and FGF signaling molecules participate in the palatogenesis, and RA pathway may interact with wnt and FGF signaling pathway.
Animals ; Cleft Palate ; Fibroblast Growth Factor 10 ; Fibroblast Growth Factors ; Genotype ; Ligands ; Mice ; Tretinoin ; Wnt3 Protein
6.Fibroblast Growth Factor-23 is associated with High-density lipoprotein in Systemic sclerosis Female patients
Antonio Alvarez-Cienfuegos ; Lucia Cantero-Nieto ; Jose Alberto Garcí ; a-Gomez ; Jose Luis Callejas-Rubio ; Javier Martin ; Norberto Ortego-Centeno
Philippine Journal of Internal Medicine 2020;59(1):9-13
INTRODUCTION: Fibroblast growth factor-23 (FGF23) is a circulating regulator of phosphate and vitamin D metabolism and has been implicated as a putative pathogenic factor in cardiovascular disease. The objectives of this study were: to compare serum FGF23 levels between systemic sclerosis (SSc) patients and healthy controls and to investigate possible associations between FGF23 and serum lipid profile in SSc patients.
METHODS: This cross-sectional study was performed in San Cecilio Hospital, Granada (Spain) from November 2017 to May 2019. We enrolled 62 consecutive female patients affected by SSc and 62 healthy women who served as controls. Cardiovascular risk factors and related biochemical parameters were collected. Serum FGF23 was analyzed using enzyme- linked immunosorbent assay (ELISA). Linear regression was used to examine the cross-sectional associations of serum FGF23 concentrations with high density lipoprotein-cholesterol (HDL-c).
RESULTS: There was no significant differences in FGF23 levels between the patients and controls (78.2 ± 60.5 vs. 80.3 ± 56.3 pg/mL, p= 0.662), but we found a statistically significant inverse relationship between FGF23 and HDL-c measurements (r= -0.27; p= 0.03) in women with SSc. In addition, in the linear regression model, higher FGF23 concentrations were associated with lower HDL-c [β = -1.45 95% CI (-2.81, -0.08); p < 0.05].
CONCLUSIONS: We report an association between circulating FGF23 and HDL-c in SSc female patients, representing a novel pathway linking high FGF23 to an increased cardiovascular risk.
Lipoproteins, HDL
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fibroblast growth factor 23
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Scleroderma, Systemic
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Fibroblast Growth Factors
7.Value of serum fibroblast growth factor 23 in diagnosis of hypophosphatemic rickets in children.
Sha-Sha DONG ; Ruo-Chen CHE ; Bi-Xia ZHENG ; Ai-Hua ZHANG ; Chun-Li WANG ; Mi BAI ; Ying CHEN
Chinese Journal of Contemporary Pediatrics 2023;25(7):705-710
OBJECTIVES:
To study the value of serum fibroblast growth factor 23 (FGF23) in the diagnosis of hypophosphatemic rickets in children.
METHODS:
A total of 28 children who were diagnosed with hypophosphatemic rickets in Children's Hospital of Nanjing Medical University from January 2016 to June 2021 were included as the rickets group. Forty healthy children, matched for sex and age, who attended the Department of Child Healthcare of the hospital were included as the healthy control group. The serum level of FGF23 was compared between the two groups, and the correlations of the serum FGF23 level with clinical characteristics and laboratory test results were analyzed. The value of serum FGF23 in the diagnosis of hypophosphatemic rickets was assessed.
RESULTS:
The rickets group had a significantly higher serum level of FGF23 than the healthy control group (P<0.05). In the rickets group, the serum FGF23 level was positively correlated with the serum alkaline phosphatase level (rs=0.38, P<0.05) and was negatively correlated with maximum renal tubular phosphorus uptake/glomerular filtration rate (rs=-0.64, P<0.05), while it was not correlated with age, height Z-score, sex, and parathyroid hormone (P>0.05). Serum FGF23 had a sensitivity of 0.821, a specificity of 0.925, an optimal cut-off value of 55.77 pg/mL, and an area under the curve of 0.874 in the diagnosis of hypophosphatemic rickets (P<0.05).
CONCLUSIONS
Serum FGF23 is of valuable in the diagnosis of hypophosphatemic rickets in children, which providing a theoretical basis for early diagnosis of this disease in clinical practice.
Child
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Humans
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Fibroblast Growth Factor-23
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Fibroblast Growth Factors
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Familial Hypophosphatemic Rickets/diagnosis*
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Rickets, Hypophosphatemic/diagnosis*
8.Recent Progress in Osteocyte Research.
Endocrinology and Metabolism 2013;28(4):255-261
The last decade has seen an exponential increase in our understanding of osteocytes function and biology. These cells, once considered inert by-standers trapped into the mineralized bone, has now risen to be key regulators of skeletal metabolism, mineral homeostasis, and hematopoiesis. As tools and techniques to study osteocytes improved and expanded, it has become evident that there is more to these cells than initially thought. Osteocytes are now recognized not only as the key responders to mechanical forces but also as orchestrators of bone remodeling and mineral homeostasis. These cells are the primary source of several important proteins, such as sclerostin and fibroblast growth factor 23, that are currently target as novel therapies for bone loss (as the case for antisclerostin antibodies) or phosphate disorders. Better understanding of the intricate cellular and molecular mechanisms that govern osteocyte biology will open new avenue of research and ultimately indentify novel therapeutics to treat bone and mineral disorders. This review summarizes novel findings and discusses future avenues of research.
Biology
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Bone Remodeling
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Fibroblast Growth Factors
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Hematopoiesis
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Homeostasis
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Metabolism
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Osteocytes*
9.Recent Progress in Osteocyte Research.
Endocrinology and Metabolism 2013;28(4):255-261
The last decade has seen an exponential increase in our understanding of osteocytes function and biology. These cells, once considered inert by-standers trapped into the mineralized bone, has now risen to be key regulators of skeletal metabolism, mineral homeostasis, and hematopoiesis. As tools and techniques to study osteocytes improved and expanded, it has become evident that there is more to these cells than initially thought. Osteocytes are now recognized not only as the key responders to mechanical forces but also as orchestrators of bone remodeling and mineral homeostasis. These cells are the primary source of several important proteins, such as sclerostin and fibroblast growth factor 23, that are currently target as novel therapies for bone loss (as the case for antisclerostin antibodies) or phosphate disorders. Better understanding of the intricate cellular and molecular mechanisms that govern osteocyte biology will open new avenue of research and ultimately indentify novel therapeutics to treat bone and mineral disorders. This review summarizes novel findings and discusses future avenues of research.
Biology
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Bone Remodeling
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Fibroblast Growth Factors
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Hematopoiesis
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Homeostasis
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Metabolism
;
Osteocytes*
10.The Effect of Mitomycin C and Daunorubicin on the Healing Process in Rabbit Extraocular Muscle Surgery.
Journal of the Korean Ophthalmological Society 1998;39(3):591-597
One of the most serious complications following strabismus surgery is the formation of adhesions that may result in restrictive ocular motility dysfunction. Management of the postoperative adhesions is often difficult. We investigated the effect of mitomycin c(MMC) and daunorubicin(DR) on postoperative would healing in rabbit extraocular muscle surgery after single intraoperative application. Sixteen white rabbits(32 eyes), weighing 2.0~2.5kg were used. These rabbits were divided into 4 groups; control group(BSS for 5 minutes exposure), group 1 (0.5mg/ml MMC for 1 minute exposure), group 2 (0.5mg/ml MMC for 5 minutes exposure), and group 3(25microgram/ml DR for 5 minutesexposure). Histopathologically, there was a more significant reduction of fibroblast and collagen fiber proliferation in group 1 and 2 than the control group. In group 3, these effects were better than the control group, but less than group 1 or 2. Immunohistochemically, group 1 and 2 showed greater effects of fibroblast growth factor (FGF) than the control group. In group 3, less effect was shown than group 1 or 2, but no difference was noted compare with the control group. These results suggest that intraoperative application of mitomycin c in strabismus surgery can increase a surgical success rate. However, daunorubicin is still controversial and more studies are needed on the dose and exposure time.
Collagen
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Daunorubicin*
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Fibroblast Growth Factors
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Fibroblasts
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Mitomycin*
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Rabbits
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Strabismus