Effect of Estrogen on Acidification in Osteoclasts

Kief, Nancy L; Bekker, Petrus J.

doi:10.1006/bbrc.1993.1551

Cited by 32 publications

(20 citation statements)

References 33 publications

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“…Though it is unclear whether Kupffer and endothelial cells take up the administered steroid-BSAs as steroid hormone, denaturated BSA or both, the existence of BSA in these cell nuclei indicates that these cells may recognize the steroid-BSAs as hormone, and it is possible that there is some mechanism that disturbs the digestion of steroid-BSAs by lysosomal enzymes. Estrogen is likely to decrease acidification of the early endosomes (Gay et al, 1993;Van Dyke and Root, 1993).…”

Section: Discussionmentioning

confidence: 99%

Immunocytochemical Localization of Bovine Serum Albumin (BSA) in the Liver and Testis of Rats injected with Testosterone-BSA, Hydrocortisone-BSA or Corticosterone-BSA.

Nishimura

Nakano

2000

Cell Struct. Funct.

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ABSTRACT. Through observations of colloidal gold with silver enhancement, we have demonstrated that 2-nm colloidal gold labeled-testosterone-bovine serum albumin (BSA) conjugate or hydrocortisone-BSA conjugate injected intravenously enters the hormone-target cell nuclei of rats (Nishimura and Ichihara, 1997; Nakano, 1997, 1999). To confirm immunocytochemically whether the nature of BSA in the steroid hormone-BSA conjugates (steroid-BSAs) remains intact in the hormone-target cell nuclei, testosterone-BSA, hydrocortisone-BSA or corticosterone-BSA was injected into the vascular system of rats, then the liver and testes of rats killed 2 h postinjection were reacted with FITC-conjugated anti-BSA antibody, and examined under fluorescence microscopy and confocal laser scanning microscopy. In the liver of rat injected with testosterone-BSA, the fluorescence was observed in the nuclei of endothelial cells, but not in the nuclei of hepatocytes, hepatic stellate cells and Kupffer cells. In the liver of rat injected with hydrocortisone-BSA, intense fluorescence was seen in the nuclei of hepatic stellate cells, but did not seem to be present in the nuclei of the other three kinds of cells. In the liver of rat injected with corticosterone-BSA, the fluorescence seemed to be in a few nuclei of hepatic stellate cells, and appeared as speckles in a few nuclei of the hepatocytes and Kupffer cells. In some seminiferous tubules of rat injected with testosterone-BSA, fluorescence was observed in the nuclei of spermatocytes and spermatids. These results suggest that BSA conjugated with steroid hormone can enter the hormone-target cell nuclei with its antigenicity kept intact, and that the fate of steroid-BSAs is decided at the cell membrane level.Key words: testosterone-BSA/hydrocortisone-BSA/corticosterone-BSA/target cell nuclei/ in vivo/immunocytochemistry Steroid hormones circulate in blood plasma in three physical states: free, albumin-bound, and bound to serum steroid binding proteins such as sex hormone-binding globulin (SHBG) and corticosteroid-binding globulin (CBG) (Kuhn,

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Section: Discussionmentioning

confidence: 99%

Immunocytochemical Localization of Bovine Serum Albumin (BSA) in the Liver and Testis of Rats injected with Testosterone-BSA, Hydrocortisone-BSA or Corticosterone-BSA.

Nishimura

Nakano

2000

Cell Struct. Funct.

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“…(16,36) The upregulation of CLC-7 and H + -ATPase, transporters known to be involved in resorption pit acidification, observed in our study coincided with a significant rise in serum PTH levels in TRPV5 −/− mice. Because the stimulatory effect of PTH on osteoclast acidification as well as H + -ATPase and ClC-7 has been previously shown, (16,34,(37)(38)(39)(40)(41) the increased PTH levels are likely responsible.…”

Section: Alendronate In Trpv5mentioning

confidence: 96%

Bone Resorption Inhibitor Alendronate Normalizes the Reduced Bone Thickness of TRPV5−/− Mice

Nijenhuis

Eerden

Hoenderop

et al. 2008

Journal of Bone and Mineral Research

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TRPV5 is a Ca 2+ -selective channel involved in transcellular Ca 2+ absorption expressed in kidney and in the ruffled border of osteoclasts. Studies in hypercalciuric TRPV5 knockout (TRPV5 −/− ) mice, which display significantly increased vitamin D levels, showed that TRPV5 ablation increases number and size of osteoclasts but impairs osteoclast-mediated bone resorption. The latter is not in line with the observed decreased bone thickness in TRPV5 −/− mice. Bisphosphonates also inhibit osteoclast-mediated bone resorption. The aim of this study was to evaluate the effect of alendronate on the expression of the Ca 2+ transporters in bone, kidney, and duodenum and, importantly, the bone phenotype in TRPV5 −/− mice. Wildtype (TRPV5 +/+ ) and TRPV5−/− mice were treated during 10 wk with 2 mg/kg alendronate or vehicle weekly and housed in metabolic cages at the end of treatment. Urine and blood samples were taken for biochemical analysis, and duodenum, kidney, and femur were sampled. Expression of Ca 2+ transporters and osteoclast ruffled border transporters in bone and cultured osteoclasts was determined by QPCR analysis. Femurs were scanned using CT, and resorption pit assays were performed in bone marrow cultures isolated from TRPV5 +/+ and TRPV5 −/− mice. Alendronate treatment enhanced bone thickness in TRPV5 +/+ mice but also normalized the disturbed bone morphometry parameters in TRPV5 −/− mice. Bone TRPV5 expression was specifically enhanced by alendronate, whereas the expression of Ca 2+ transporters in kidney and intestine was not altered. The expression of the osteoclast ruffled border membrane proteins chloride channel 7 (CLC-7) and the vacuolar H + -ATPase did not differ between both genotypes, but alendronate significantly enhanced the expression and PTH levels in TRPV5 −/− mice. The expression of TRPV5, CLC-7, and H + -ATPase in osteoclast cultures was not affected by alendronate. The number of resorption pits was reduced in TRPV5 −/− bone marrow cultures, but the response to vitamin D was similar to that in TRPV5 +/+ cultures. The alendronate-induced upregulation of TRPV5 in bone together with the decreased resorptive capacity of TRPV5 −/− osteoclasts in vitro suggests that TRPV5 has an important role in osteoclast function. However, our data indicate that significant bone resorption still occurs in TRPV5 −/− mice, because alendronate treatment normalized bone thickness in these mice. Thus, TRPV5 −/− mice are able to rescue the resulting defect in osteoclast-mediated bone resorption, possibly mediated by the long-term hypervitaminosis D or other (non)hormonal compensatory mechanisms.

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“…Most studies on matrix degradation have involved biochemical analyses. However, the spatial precision afforded by microscopy has shown that osteoclasts synthesize B, L and D cathepsins on the basis of immunolocalization and that the B and L forms are secreted, whereas D cathepsin remains as an intracellular enzyme (Goto et al, 1992). An ultrastructural study has shown that matrix is not destroyed when bone explants have been cultured in the presence of the cysteine proteinase inhibitor, leupeptin (Everts et al, 1988).…”

Section: Detection Of Specific Binding Of Calciotrophicmentioning

confidence: 98%

Role of microscopy in elucidating the mechanism and regulation of the osteoclast resorptive apparatus

Gay¹

1996

Microsc. Res. Tech.

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Effect of Estrogen on Acidification in Osteoclasts

Cited by 32 publications

References 33 publications

Immunocytochemical Localization of Bovine Serum Albumin (BSA) in the Liver and Testis of Rats injected with Testosterone-BSA, Hydrocortisone-BSA or Corticosterone-BSA.

Immunocytochemical Localization of Bovine Serum Albumin (BSA) in the Liver and Testis of Rats injected with Testosterone-BSA, Hydrocortisone-BSA or Corticosterone-BSA.

Bone Resorption Inhibitor Alendronate Normalizes the Reduced Bone Thickness of TRPV5−/− Mice

Role of microscopy in elucidating the mechanism and regulation of the osteoclast resorptive apparatus

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