Quantitative ultrastructural characteristics relating to transport between luteal cell cytoplasm and blood in the corpus luteum of the pregnant rat

1985 ◽  
Vol 172 (1) ◽  
pp. 87-99 ◽  
Author(s):  
A. M. Dharmarajan ◽  
N. W. Bruce ◽  
G. T. Meyer
Keyword(s):  
Corpus Luteum ◽  
Luteal Cell ◽  
Cell Cytoplasm ◽  
Pregnant Rat ◽  
Ultrastructural Characteristics

scholarly journals TAMANHO DA AMOSTRA PARA ESTUDO DA PROPORÇÃO VOLUMÉTRICA DOS CONSTITUINTES DO CORPO LÚTEO BOVINO

2002 ◽  
Vol 7 (2) ◽  
Author(s):  
M. M. NEVES ◽  
A. P. MARQUES JR.
Keyword(s):  
Endothelial Cells ◽  
Soybean Oil ◽  
Corpus Luteum ◽  
Cell Types ◽  
Luteal Cell ◽  
Cell Nuclei ◽  
Cell Cytoplasm ◽  
Bovine Corpus Luteum

O objetivo deste estudo foi estabelecer o número de campos histológicos necessários para quantificar os componentes celulares do corpo lúteo bovino. Para os parâmetros citoplasma das células luteínicas, núcleo das células luteínicas e fibroblasto são necessários 30 campos, enquanto que para células endoteliais e pericito são necessários 35, podendo-se padronizar a técnica em 35 campos e 875 pontos por corpo lúteo. Soybean oil replaced by acidulated soapstock in broiler diets Abstract The purpose of this study was to determine the number of fields necessary for the quantification of the cell types of the bovine corpus luteum. A total of 30 fields is necessary for the quantification of the luteal cell cytoplasm, luteal cell nuclei and fibroblast, and 35 fields for the quantification of endothelial cells and pericycles. For the analysis of both parameters is recommended the study of 35 fields and 875 points per corpus luteum.

scholarly journals Differential distribution of gelatinases and tissue inhibitor of metalloproteinase-1 in the rat ovary

1998 ◽  
Vol 158 (2) ◽  
pp. 221-228 ◽  
Author(s):  
P Bagavandoss
Keyword(s):  
Plasma Membrane ◽  
Corpus Luteum ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Neonatal Rat ◽  
Luteal Cell ◽  
Surface Epithelium ◽  
Tissue Inhibitor ◽  
Differential Distribution ◽  
Thecal Cells ◽  
Rat Ovary

The distribution of gelatinases/matrix metalloproteinases-2 and -9 (MMP-2 and MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in neonatal and gonadotropin-primed immature rat ovaries was studied by immunofluorescent microscopy. Immature female Long-Evans rats were primed with 15 IU pregnant mare's serum gonadotropin (PMSG) in 100 microliters PBS. Two days later, to induce ovulation, the rats were injected with human chorionic gonadotropin (hCG, 5 IU/100 microliters PBS). The animals were killed at appropriate times and the ovaries removed and processed for cryostat or paraffin sectioning. Ovaries were also obtained from 7-day-old neonatal rats and processed as above. In the neonatal rat ovary, MMP-2 was present in the follicle and in the ovarian surface epithelium. MMP-9 was not detectable in the neonatal ovary. TIMP-1 was present in the oocyte and in the surface epithelium. In the PMSG-primed ovary, MMP-2 was present in the granulosa and thecal cells of the ovary. MMP-9 distribution, however, was restricted to the interstitial and thecal cells. TIMP-1 was mainly present in the blood vessels and thecal cells, with minor staining in the granulosa cells. In the developing corpus luteum, luteal and endothelial cells were positive for MMP-2. MMP-9 localization was restricted to the plasma membrane of the luteal and interstitial cells. TIMP-1 was clearly observed in the luteal capillaries and, to a lesser extent, in the luteal cell plasma membrane. This distribution of MMP-2, MMP-9, and TIMP-1 in the corpus luteum persisted throughout the life span of the corpus luteum. The spatial and temporal distribution of the gelatinases and TIMP-1 suggests unique roles for these proteins in the rat ovary.

scholarly journals HIF-1α Activation Promotes Luteolysis by Enhancing ROS Levels in the Corpus Luteum of Pseudopregnant Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Zonghao Tang ◽  
Jiajie Chen ◽  
Zhenghong Zhang ◽  
Jingjing Bi ◽  
Renfeng Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Corpus Luteum ◽  
Cell Apoptosis ◽  
In Vitro Study ◽  
Luteal Cell ◽  
Independent Manner ◽  
Luteal Regression ◽  
Luteal Cells

The increase of oxidative stress is one of the important characteristics of mammalian luteal regression. Previous investigations have revealed the essential role of reactive oxygen species (ROS) in luteal cell death during luteolysis, while it is unknown how ROS is regulated in this process. Considering the decrease of blood flow and increase of PGF2α during luteolysis, we hypothesized that the HIF-1α pathway may be involved in the regulation of ROS in the luteal cell of the late corpus luteum (CL). Here, by using a pseudopregnant rat model, we showed that the level of both HIF-1α and its downstream BNIP3 was increased during luteal regression. Consistently, we observed the increase of autophagy level during luteolysis, which is regulated in a Beclin1-independent manner. Comparing with early (Day 7 of pseudopregnancy) and middle CL (Day 14), the level of ROS was significantly increased in late CL, indicating the contribution of oxidative stress in luteolysis. Inhibition of HIF-1α by echinomycin (Ech), a potent HIF-1α inhibitor, ameliorated the upregulation of BNIP3 and NIX, as well as the induction of autophagy and the accumulation of ROS in luteal cells on Day 21 of pseudopregnancy. Morphologically, Ech treatment delayed the atrophy of the luteal structure at the late-luteal stage. An in vitro study indicated that inhibition of HIF-1α can also attenuate PGF2α-induced ROS and luteal cell apoptosis. Furthermore, the decrease of cell apoptosis can also be observed by ROS inhibition under PGF2α treatment. Taken together, our results indicated that HIF-1α signaling is involved in the regression of CL by modulating ROS production via orchestrating autophagy. Inhibition of HIF-1α could obviously hamper the apoptosis of luteal cells and the process of luteal regression.

scholarly journals Control of Steroidogenesis in Small and Large Bovine Luteal. Cells

1987 ◽  
Vol 40 (3) ◽  
pp. 331 ◽  
Author(s):  
William Hansel ◽  
Hector W Alila ◽  
Joseph P Dowd ◽  
Xiangzhong Yang
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Corpus Luteum ◽  
Luteal Cell ◽  
Lipoxygenase Pathway ◽  
Luteal Cells ◽  
Kinase C ◽  
Bovine Corpus Luteum ◽  
Progesterone Synthesis

Evidence was cited to show that: (1) prostacyclin (PGI2) plays a luteotrophic role in the bovine corpus luteum and that products of the lipoxygenase pathway of arachidonic acid metabolism, especially 5-hydroxyeicosatetraenoic acid play luteolytic roles; (2) oxytocin of luteal cell origin plays a role in development, and possibly in regression, of the bovine corpus luteum; and (3) luteal cells arise from two sources; the characteristic small luteal cells at all stages of the o~strous cycle and pregnancy are of theca cell origin; the large cells are of granulosa cell origin early in the cycle, but a population of theca-derived large cells appears later in the cycle. Results of in vitro studies with total dispersed cells and essentially pure preparations of large and small luteal cells indicate that : (1) the recently described Ca2+ -polyphosphoinositol-protein kinase C second messenger system is involved in progesterone synthesis in the bovine corpus luteum; (2) activation of protein kinase C is stimulatory to progesterone synthesis in the small luteal cells; (3) activation of protein kinase C has no effect on progesterone synthesis in the large luteal cells; and (4) protein kinase C exerts its luteotrophic effect in total cell preparations, in part at least, by stimulating the production of prostacyclin. The protein kinase C system may cause down regulation of LH receptors in the large cells.

scholarly journals Association of luteal cell degeneration and progesterone deficiency with lysosomal storage disorder mucolipidosis type IV in Mcoln1−/− mouse model†

2019 ◽  
Vol 101 (4) ◽  
pp. 782-790 ◽  
Author(s):  
Zidao Wang ◽  
Ahmed E El Zowalaty ◽  
Yuehuan Li ◽  
Christian L Andersen ◽  
Xiaoqin Ye
Keyword(s):  
Corpus Luteum ◽  
Lysosomal Storage Disorder ◽  
Luteal Cell ◽  
Lysosomal Storage ◽  
Cell Degeneration ◽  
Mucolipidosis Type Iv ◽  
Type Iv ◽  
Mitochondrial Functions ◽  
Storage Disorder ◽  
Mucolipidosis Type

Abstract Transient receptor potential cation channel, mucolipin subfamily, member 1 (TRPML1) (MCOLN1/Mcoln1) is a lysosomal counter ion channel. Mutations in MCOLN1 cause mucolipidosis type IV (MLIV), a progressive and severe lysosomal storage disorder with a slow onset. Mcoln1−/− mice recapitulate typical MLIV phenotypes but roles of TRPML1 in female reproduction are unknown. Despite normal mating activities, Mcoln1−/− female mice had reduced fertility at 2 months old and quickly became infertile at 5 months old. Progesterone deficiency was detected on 4.5 days post coitum/gestation day 4.5 (D4.5). Immunohistochemistry revealed TRPML1 expression in luteal cells of wild type corpus luteum (CL). Corpus luteum formation was not impaired in 5–6 months old Mcoln1−/− females indicated by comparable CL numbers in control and Mcoln1−/− ovaries on both D1.5 and D4.5. In the 5–6 months old Mcoln1−/− ovaries, histology revealed less defined corpus luteal cord formation, extensive luteal cell vacuolization and degeneration; immunofluorescence revealed disorganized staining of collagen IV, a basal lamina marker for endothelial cells; Nile Red staining detected lipid droplet accumulation, a typical phenotype of MLIV; immunofluorescence of heat shock protein 60 (HSP60, a mitochondrial marker) and in situ hybridization of steroidogenic acute regulatory protein (StAR, for the rate-limiting step of steroidogenesis) showed reduced expression of HSP60 and StAR, indicating impaired mitochondrial functions. Luteal cell degeneration and impaired mitochondrial functions can both contribute to progesterone deficiency in the Mcoln1−/− mice. This study demonstrates a novel function of TRPML1 in maintaining CL luteal cell integrity and function.

Regulation of Luteal Cell Lipoprotein Receptors, Sterol Contents, and Steroidogenesis by Estradiol in the Pregnant Rat*

Endocrinology ◽  
1984 ◽  
Vol 114 (2) ◽  
pp. 609-617 ◽  
Author(s):  
GEULA GIBORI ◽  
Y. -D. IDA CHEN ◽  
IQBAL KHAN ◽  
SALMAN AZHAR ◽  
G. M. REAVEN
Keyword(s):  
Luteal Cell ◽  
Lipoprotein Receptors ◽  
Pregnant Rat
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