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| 2. |
- Akner, Gunnar, 1953-, et al.
(författare)
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Glucocorticoid receptor inhibits microtubule assembly in vitro.
- 1995
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Ingår i: Molecular and cellular endocrinology. - : Elsevier BV. - 0303-7207 .- 1872-8057. ; 110:1-2, s. 49-54
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Tidskriftsartikel (refereegranskat)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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| 3. |
- Bondestam, Jonas, et al.
(författare)
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Engagement of activin and bone morphogenetic protein signaling pathway Smad proteins in the induction of inhibin B production in ovarian granulosa cells
- 2002
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Ingår i: Molecular and Cellular Endocrinology. - 0303-7207 .- 1872-8057. ; 195:1-2, s. 79-88
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Tidskriftsartikel (refereegranskat)abstract
- In the mammalian ovary cell growth and differentiation is regulated by several members of the transforming growth factor beta (TGF beta) superfamily including activins, inhibins, growth differentiation factors and bone morphogenetic proteins (BMPs). The effects of TGF beta family members are mediated to the target cells via heteromeric complexes of type I and II serine/threonine kinase receptors which activate Smad signaling protein pathways in various cell types. We have previously shown that inhibin B, a hormonally important product from human granulosa cells, is up regulated by activin and BMPs. Here, we report the use of adenoviral gene transfer methodology to manipulate the TGF beta growth factor signaling system in primary cultures of human granulosa cells. These cells are exceedingly difficult to transfect by conventional transfection methods, but were virtually 100% infected with recombinant adenoviruses expressing green fluorescent protein (GFP). Adenoviruses expressing constitutively active forms of the seven known mammalian type I activin receptor-like kinase receptors (Ad-caALK1 through Ad-caALK7) cause activation of endogenous and adenovirally transferred Smad signaling proteins so that Ad-caALK1/2/3/6 and Ad-caALK4/5/7 induced phosphorylation of the Smad1 and Smad2 pathways, respectively. Activin A and BMP-2 activated the Smad1 and Smad2 pathways as well as inhibin B production as did all the Ad-caALKs. Furthermore, overexpression of adenoviral Smad1 and Smad2 proteins without exogenously added ligands induced inhibin B production. The inhibitory Smad7 protein suppressed BMP-2 and activin induced inhibin B production. Collectively, the present data demonstrate that adenoviral gene transfer provides an effective approach for dissecting the TGF beta signaling pathways in primary ovarian cells in vitro and more specifically indicate that the Smad1 and Smad2 pathways are involved in the regulation of inhibin B production by TGF beta family ligands in the ovary.
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| 9. |
- Gustavsson, Bengt, et al.
(författare)
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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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Ingår i: Molecular and Cellular Endocrinology. - 0303-7207 .- 1872-8057. ; 111:2, s. 167-173
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Tidskriftsartikel (refereegranskat)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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| 14. |
- Liu, Kui, et al.
(författare)
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Expression pattern and functional studies of matrix degrading proteases and their inhibitors in the mouse corpus luteum
- 2003
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Ingår i: Molecular and Cellular Endocrinology. - 0303-7207 .- 1872-8057. ; 205:1-2, s. 131-140
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Tidskriftsartikel (refereegranskat)abstract
- The formation of the corpus luteum (CL) is accompanied with angiogenesis and tissue remodeling and its regression involves tissue degradation. Matrix degrading proteases such as plasminogen activators (PAs) and matrix metalloproteinases (MMPs) are thought to play important roles in such controlled proteolytic processes. In this study, in situ hybridization has been used to examine the regulation and expression pattern of mRNAs coding for proteases and protease inhibitors belonging to the PA- and MMP-systems during the life cycle of the CL in an adult pseudopregnant mouse model. Of the nine proteases and five protease inhibitors that were studied, the majority were found to be temporally expressed during the formation and/or the regression of the CL. However, the mRNAs coding for urokinase type PA (uPA), membrane-type 1 MMP (MT1-MMP), and tissue inhibitor of metalloproteinases type-3 (TIMP-3) were constantly expressed in the mouse CL throughout its whole life span. To study the functional role of uPA in the CL, we analyzed luteal formation and function in uPA deficient mice. Our results revealed no significant difference in ovarian weight, serum progesterone levels, and blood vessel density in the functional CL between uPA deficient and wild type control mice. The temporal and spatial expression pattern of proteases and protease inhibitors during the CL life span suggests that members of the PA- and MMP-systems may play important roles in the angiogenesis and tissue remodeling processes during CL formation, as well as in the tissue degradation during luteal regression. However, the absence of reproductive phenotypes in mice lacking uPA and several other matrix degrading proteases indicates that there are redundancies among different matrix degrading proteases or that tissue remodeling in the ovary may involve other additional unique elements.
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| 23. |
- Sundfeldt, Karin, 1962
(författare)
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Cell-cell adhesion in the normal ovary and ovarian tumors of epithelial origin; an exception to the rule.
- 2003
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Ingår i: Molecular and cellular endocrinology. - : Elsevier BV. - 0303-7207. ; 202:1-2, s. 89-96
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Forskningsöversikt (refereegranskat)abstract
- Cells are held together either by direct cell-cell contact or adhesion to extra-cellular matrix. Cell-cell adhesion in epithelial cell sheets consists of junctions, i.e. tight-, adherens- and gap-junctions. The adherens junctions, which are build up by the cadherin/catenin complex, are the main topic of this review, especially the aspect of its role in ovarian tumor biology. The ovarian surface epithelium is the origin for approximately 90% of the malignant ovarian tumors. The tumors arise from the inclusion cysts, localized in the ovarian stroma and grow solid, cystic or in mixed formations. Intra-abdominal spread of the ovarian cancer is common and this is a process that theoretically could be closely connected with impaired cell-cell adhesion. However, as we stand today, descriptive and functional studies on the cadherin-catenin complex and its cell signaling role in ovarian tumorigenesis reveals data that suggests a conversion of the mesothelial-like cells of the ovarian surface to a more epithelial phenotype with normal cell-cell adhesion prior to tumor differentiation. In later stages, invasive ovarian tumors still strongly express several cadherins, which are contrary to many other tumors, i.e. prostate and thyroid adenocarcinomas.
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| 25. |
- Vaskivuo, Tommi E, et al.
(författare)
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Role of apoptosis, apoptosis-related factors and 17beta-hydroxysteroid dehydrogenases in human corpus luteum regression
- 2002
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Ingår i: Molecular and Cellular Endocrinology. - 0303-7207 .- 1872-8057. ; 194:1-2, s. 191-200
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Tidskriftsartikel (refereegranskat)abstract
- The human corpus luteum (CL) is a transient endocrine organ with a life span of 14-16 days. Apoptosis has been suggested to be the mechanism of CL regression and the possible regulatory role of the bcl-2 family in this process has been studied in animals and, to some extent, in humans. In the present study, apoptosis was studied in the human CL and in luteinised granulosa cells by in situ 3'-end labelling and gel electrophoretic DNA fragmentation analysis. The apoptosis-regulating factors Bcl-2, Bax and TNF-alpha, transcription factor NF-kappaB and Caspase-3, a key executioner protein in apoptotic cell death, were studied by immunohistochemistry and in situ hybridisation. Furthermore, we analysed expression of 17beta hydroxysteroid dehydrogenase (17HSD) type 1 and 2, key enzymes in the estrogen metabolism. Apoptosis was found in the CL throughout the luteal phase, but a marked increase of apoptotic luteal cells was observed during the late luteal phase (CL day 11-14). This was preceded by a clear increase of 17HSD type 1 expression. The apoptosis-regulating proteins Bcl-2 and Bax were expressed constantly in the CL throughout the luteal phase. TNF-alpha expression was constant during the early and mid-luteal phases, but in the late luteal phase, some specimens showed increased immunostaining. NF-kappaB and Caspase-3 were present in the CL throughout the luteal phase and in individual specimens, the expression of Caspase-3 was associated with a high rate of apoptosis in the late luteal phase. In conclusion, apoptosis is involved in human luteal regression and estradiol (E(2)) may function as a trigger for this process. The expression of the pro- and anti-apoptotic factors studied in the CL suggest their part in this process, but the conclusive evidence for the exact molecular mechanisms remains open.
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