Essential role of Ca2+-dependent phospholipase A2in estradiol-induced lysosome activation

2002 ◽  
Vol 283 (5) ◽  
pp. C1461-C1468 ◽  
Author(s):  
Bruno Burlando ◽  
Barbara Marchi ◽  
Isabella Panfoli ◽  
Aldo Viarengo
Keyword(s):  
Blood Cells ◽  
Neutral Red ◽  
Short Term ◽  
Estradiol Treatment ◽  
Lysosomal Membranes ◽  
A 23187 ◽  
17Β Estradiol ◽  
Dependent Mechanism ◽  
Sustained Increase

The mechanism of lysosome activation by 17β-estradiol has been studied in mussel blood cells. Cell treatment with estradiol induced a sustained increase of cytosolic free Ca2+that was completely prevented by preincubating the cells with the Ca2+chelator BAPTA-AM. Estradiol treatment was also followed by destabilization of the lysosomal membranes, as detected in terms of the lysosomes' increased permeability to neutral red. The effect of estradiol on lysosomes was almost completely prevented by preincubation with the inhibitor of cytosolic Ca2+-dependent PLA2(cPLA2), arachidonyl trifluoromethyl ketone (AACOCF3), and was significantly reduced by preincubation with BAPTA-AM. In contrast, it was virtually unaffected by preincubation with the inhibitor of Ca2+-independent PLA2, ( E)-6-(bromomethylene)tetrahydro-3-(1-naphtalenyl)-2 H-pyran-2-one (BEL). The Ca2+ionophore A-23187 yielded similar effects on [Ca2+]iand lysosomes. Exposure to estradiol also resulted in cPLA2translocation from cytosol to membranes, lysosome enlargement, and increased protein degradation. These results suggest that the destabilization of lysosomal membranes following cell exposure to estradiol occurs mainly through a Ca2+-dependent mechanism involving activation of Ca2+-dependent PLA2. This mechanism promotes lysosome fusion and catabolic activities and may mediate short-term estradiol effects.

Remodeling of hyperplastic pituitaries in hypothyroid α-subunit knockout mice after thyroxine and 17β-estradiol treatment: Role of apoptosis

1998 ◽  
Vol 9 (3) ◽  
pp. 261-274 ◽  
Author(s):  
Elzbieta Kulig ◽  
Sally A. Camper ◽  
Sara Kuecker ◽  
Long Jin ◽  
Ricardo V. Lloyd
Keyword(s):  
Knockout Mice ◽  
Estradiol Treatment ◽  
Α Subunit ◽  
17Β Estradiol

scholarly journals Protective role of 17β-estradiol treatment in renal injury on female rats submitted to brain death

2021 ◽  
Vol 0 (0) ◽  
pp. 0-0
Author(s):  
Roberto Armstrong-Jr ◽  
Fernanda Yamamoto Ricardo-da-Silva ◽  
Marina Vidal-dos-Santos ◽  
Cristiano de Jesus Correia ◽  
Lucas Ferreira Anunciação ◽  
...  
Keyword(s):  
Brain Death ◽  
Renal Injury ◽  
Protective Role ◽  
Female Rats ◽  
Estradiol Treatment ◽  
17Β Estradiol

scholarly journals Disruption of Tubulobulbar Complex by High Intratesticular Estrogens Leading to Failed Spermiation

Endocrinology ◽  
2008 ◽  
Vol 150 (4) ◽  
pp. 1861-1869 ◽  
Author(s):  
Ryan D'Souza ◽  
Shilpa Pathak ◽  
Rahul Upadhyay ◽  
Reshma Gaonkar ◽  
Serena D'Souza ◽  
...  
Keyword(s):  
Sertoli Cell ◽  
De Novo ◽  
Seminiferous Tubules ◽  
Estradiol Treatment ◽  
Electron Microscopic ◽  
Molecular Events ◽  
Cause Of Failure ◽  
17Β Estradiol ◽  
Ectoplasmic Specialization

Spermiation is the final phase of spermatogenesis leading to release of mature spermatids into the lumen of the seminiferous tubules. Morphologically, it involves a series of events, namely removal of excess spermatid cytoplasm, removal of ectoplasmic specialization, formation of tubulobulbar complex, and final disengagement of the spermatid from the Sertoli cell. Previous studies in our laboratory have shown that administration of 17β-estradiol at a dose of 100 μg/kg body weight for 10 d resulted in failure of spermiation. This was accompanied by a suppression of FSH and intratesticular testosterone with a concomitant rise in intratesticular 17β-estradiol. The present study was undertaken to determine the cause of failure and subsequently the molecular events in spermiation. Electron microscopic and confocal studies revealed an absence of tubulobulbar complex in step 19 spermatids after estradiol treatment, highlighting the significance of these structures in spermiation. It was further observed that treatment affected the Sertoli cell cytoskeleton and Arp2/3 complex that is critical for de novo polymerization of actin during tubulobulbar complex formation. In conclusion, the present study reports the role of 17β-estradiol in inhibiting the formation of tubulobulbar complex, which could be one of the mechanism by which environmental estrogens influence male fertility.

Role of affect in short-term memory for paired associates.

1968 ◽  
Vol 78 (3, Pt.1) ◽  
pp. 494-501 ◽  
Author(s):  
Calvin F. Nodine ◽  
James H. Korn
Keyword(s):  
Short Term Memory ◽  
Short Term ◽  
Term Memory ◽  
Paired Associates

The capacity of short term memory from an evolutionary perspective

2019 ◽  
Author(s):  
Majid Manoochehri
Keyword(s):  
Short Term Memory ◽  
Memory Span ◽  
Critical Role ◽  
Experimental Studies ◽  
Cognitive System ◽  
Evolutionary Approach ◽  
Evolutionary Perspective ◽  
Short Term ◽  
Term Memory

Memory span in humans has been intensely studied for more than a century. In spite of the critical role of memory span in our cognitive system, which intensifies the importance of fundamental determinants of its evolution, few studies have investigated it by taking an evolutionary approach. Overall, we know hardly anything about the evolution of memory components. In the present study, I briefly review the experimental studies of memory span in humans and non-human animals and shortly discuss some of the relevant evolutionary hypotheses.

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