| 1. |
- Akner, Gunnar, 1953-, et al.
(author)
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Glucocorticoid receptor inhibits microtubule assembly in vitro.
- 1995
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In: Molecular and cellular endocrinology. - : Elsevier BV. - 0303-7207 .- 1872-8057. ; 110:1-2, s. 49-54
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Journal article (peer-reviewed)abstract
- The effect of glucocorticoid hormones, purified glucocorticoid receptor (GR) and purified heat shock protein M(r) 90,000 (hsp90) on microtubule (MT) assembly in vitro was tested by a spectrophotometric MT assembly assay and electron microscopy. GR significantly prolonged the nucleation phase, slowed down the assembly rate and reduced the maximal amplitude of MT assembly compared with control. The effects were partially reversed by the addition of glucocorticoid hormone. GR associated with MTs. These results indicate that GR affects MT assembly in vitro, which may be a functional correlate to the structural association of GR with MTs. This implies that factors affecting GR may affect MT assembly in vivo.
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| 2. |
- Gustavsson, Bengt, et al.
(author)
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Functional analysis of a variant of the thyrotropin receptor gene in a family with Graves' disease
- 1995
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In: Molecular and Cellular Endocrinology. - 0303-7207 .- 1872-8057. ; 111:2, s. 167-173
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Journal article (peer-reviewed)abstract
- Nucleotide sequence analysis of PCR fragments corresponding to the TSH-receptor (TSHR) amplified from genomic DNA collected from the four members of a family, two of which had Graves' thyrotoxicosis, revealed a nucleotide substitution in the first position of codon 36 of the TSH-receptor gene in the two patients. The nucleotide substitution was from G to C, leading to a 36D-->36H change (D36H) in the predicted amino acid sequence of the receptor. The altered sequence was also found in DNA obtained from their mother, but not in DNA from their father. We stably expressed the two receptor variants in NIH 3T3 cells, by transfection of cDNA encoding the wildtype (WT) and D36H variants of the TSHR. Neither the binding of 125I-TSH nor the responsiveness to TSH measured as cAMP formation, appeared to be different in the TSHR-D36H compared to the TSHR-WT. Furthermore, the D36H-receptor also became desensitized when exposed to TSH as did the WT-receptor.
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| 3. |
- Öberg-Welsh, Charlotte, et al.
(author)
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Effects of vascular endothelial growth factor on pancreatic duct cell replication and the insulin production of fetal islet-like cell clusters in vitro
- 1997
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In: Molecular and Cellular Endocrinology. - 0303-7207 .- 1872-8057. ; 126:2, s. 125-132
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Journal article (peer-reviewed)abstract
- We have previously shown that the tyrosine kinase receptor Flk-1 and its ligand, vascular endothelial growth factor (VEGF), may play a role in the development of fetal rat islet-like structures in vitro, possibly by stimulating the maturation of endocrine precursor cells in the pancreatic ductal epithelium. In order to further assess this, adult rat pancreatic ducts and fetal porcine islet-like cell clusters (ICC) were cultured in the presence of VEGF. In ducts, VEGF stimulated the mitogenesis in the epithelium. Culture of ICC in the presence of VEGF significantly enhanced their insulin content, but decreased the insulin accumulation to the culture medium. Glucose-stimulated acute insulin release was not affected by VEGF. Northern blot analysis after partial pancreatectomy in adult rats revealed induction of VEGF mRNA 3 days after the operation. Immunohistochemistry of fetal rat pancreas showed staining mainly in the islets of Langerhans. We conclude that VEGF directly stimulates the replication of the ductal epithelium, a possible prerequisite for β-cell formation. This could require local production of VEGF, which may alter in response to physiological demands.
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| 4. |
- Liu, K, et al.
(author)
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Temporal expression of urokinase type plasminogen activator, tissue type plasminogen activator, plasminogen activator inhibitor type 1 in rhesus monkey corpus luteum during the luteal maintenance and regression.
- 1997
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In: Molecular and Cellular Endocrinology. - 0303-7207 .- 1872-8057. ; 133:2, s. 109-16
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Journal article (peer-reviewed)abstract
- Proteolytic activity generated by the plasminogen activator (PA) system has been associated with many biological processes. Using a pregnant mare serum gonadotropin (PMSG)/human chorionic gonadotropin (hCG)-induced rhesus monkey corpus luteum (CL) model, we have studied how urokinase-type plasminogen activator (uPA), tissue-type plasminogen activator (tPA), and plasminogen activator inhibitor type 1 (PAI-1), are temporally expressed in CL of rhesus monkey at the luteotropic and luteolytic periods. Slot blot analysis and in situ hybridization were performed to analyze the expression and distribution of uPA and PAI-1 messenger RNA (mRNA). Fibrin overlay was used to detect uPA and tPA activities. We found that uPA is the dominating PA in luteotropic CL in the monkey. Abundant expression of PAI-1 mRNA was detected. The highest expression of uPA and PAI-1 mRNA was observed at the luteotropic period, while their expression decreased approximately 50% at early luteal regression defined by considerably decreased serum progesterone levels, and remained at very low levels at the late stage of luteal regression. We also observed an increased tPA activity at the time of luteal regression. Moreover, the exogenous tPA could inhibit the progesterone production in cultured luteal cells from 13-day-old monkey CL. We also used LH receptor mRNA expression as a mark for the luteal phases. A highly expressed, evenly distributed LH receptor mRNA was detected in CL during the luteotropic phase, while its expression decreased at day 13 coinciding with the reduction of progesterone production. We conclude that proteolysis mediated by uPA and regulated by PAI-1 may play a role in the luteal maintenance, while tPA may participate in the luteal regression in the rhesus monkey.
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