Adaptation of Hemopoietic Tissue Resulting From Estrone‐induced Osteosclerosis in Mice

Bs, Morse; Giuliani, Dennis; Soremekun, M; DiFino, Santo M.; Er, Giuliani

doi:10.1111/j.1365-2184.1974.tb00404.x

Cited by 11 publications

(9 citation statements)

References 25 publications

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“…Present data tend to support reported increases in marrow space (Drinker et al, 1922;Johnstone, 192%) associated with the loss of normal splenic hemopoietic activity following splenectomy. Animals treated with estrone show a slight decrease in hematocrit and hemoglobin concentration, which reflects a combination of mild hemolysis and decreased production, as previously reported by Morse et al (1974). Bone and marrow parameters are consistent with endosteal deposition of a denser mineral complex.…”

Section: Sesupporting

confidence: 83%

Strategies of hemopoietic stress adaptation within the medullary cavity

1986

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Gravimetric determination of total bone water space was used as an index of available bone marrow space in mice following various specific stressors, i.e., splenectomy, hypoxia, bone fracture, and estrone-induced osteosclerosis. Data was corrected for bone weight and was reported as specific bone marrow volume (total bone water space/mg dry bone X 100). A direct relationship was observed between specific bone marrow volume and medullary hemopoietic activity induced by stress. Absolute and/or relative marrow space increased following splenectomy, hypoxia, and fracture. Osteosclerotic animals shift most hemopoietic activity from marrow to spleen, and splenectomized osteosclerotic animals become anemic. Both intact and splenectomized hypoxic animals develop increased specific bone marrow volume and successfully compensate for hypoxia with enhanced erythropoiesis. Animals sustaining a fracture callus increase both specific bone marrow volume and hemopoietic activity at the callus without an increase in hemopoietic demand. Increased specific bone marrow volume extends the marrow bone interface, where primitive stem cells accumulate, while expanding marrow stromal space, where stem cells lodge, proliferate and differentiate. Therefore, it would appear that availability of competent marrow space may play an integral part in passively permitting hematopoiesis and in determining hemopoietic reserve capacity. Stem cell migration increases during intensified hemopoietic demand, which also may be related to available marrow space. Mice have a low medullary hemopoietic reserve capacity; subsequently, when available medullary hematopoietic stroma becomes occupied, stem cells are more likely to migrate from the marrow to extra-medullary sites where they mature before entering the circulating pool.

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Section: Sesupporting

confidence: 83%

Strategies of hemopoietic stress adaptation within the medullary cavity

1986

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“…Indeed, in support of this, a similar abnormal distribution of stem cells was observed in estrone-induced osteopetrosis of mice (37). Similarly, the effects of a poor nutritional status, caused by the absence of incisors in these mice, cannot be disregarded, although earlier studies (2) of all murine osteopetrotic mutants failed to identify any common abnormalities that could be related to starvation of these mice.…”

Section: Attempts To Transfer the Macrophage Defect Of The Op/op Mousmentioning

confidence: 62%

Hematological characterization of congenital osteopetrosis in op/op mouse. Possible mechanism for abnormal macrophage differentiation.

Wiktor-Jedrzejczak¹,

Ahmed²,

Szczylik³

et al. 1982

The Journal of Experimental Medicine

279

142

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Osteopetrosis is a disease of bone resorption that may be inherited with m a n y separate genes in various m a m m a l i a n species (1, 2). There are four distinct mutations in the mouse that can individually result in this disorder: osteopetrotic (op) (3), microopthalmic (mi) (4), gray-lethal (gl) (5), and osteosclerotic (oc) (6). A major advance in our understanding of osteopetrosis was provided by the experiments of Walker (7-9), demonstrating the ability of normal hemopoietic cells to cure this disorder in mi/mi and gl/gl mice. Additionally, it was shown that spleen cells from these mutants transfer the disease into irradiated normal littermate recipients (8, 9). The response of other murine osteopetrotic m u t a n t s in transplantation assays remains unknown. At the cellular level, osteopetrosis is a disease of a functionally a n d / o r quantitatively a b n o r m a l osteoclast (1, 10), The osteoclast is a multinuclear cell that is most p r o b a b l y formed through a fusion of cells of the m o n o c y t e -m a c r o p h a g e lineage (11). Therefore, the osteoclast belongs to the progeny of the hemopoietic stem cell (HSC) 1 (12, 13), and this explains the positive response of mi/mi and gl/gl mice to transplants of hemopoietic cells. This cure of osteopetrosis by hemopoietic grafts is a more general p h e n o m e n o n and was recently observed also in juvenile osteopetrosis in man (14, 15) and in two rat mutants: ia/ia (16) and op/op (17). Studies (18) in op rat additionally linked osteopetrosis with abnormalities in the T lymphocyte system. O n the other hand, the osteopetrosis in tl/tl rat failed to respond to the bone marrow transplant (19), suggesting that the p r i m a r y lesion in this m u t a n t resides beside the hemopoietic tissue, presumably in the hemopoietic microenvironment (HM). The H M is m a d e by stromal tissue of bones and spleen, histogenetically different from the hemopoietic system and largely derived from cells with fibroblast-like morphology (20). The classic example of the disorder of H M is a n e m i a in S1/S1 d mice, which is * Supported in part by a grant from the Polish Academy of Sciences to W. Wiktor-Jedrzeiczak , and by the Naval Medical Research and Development Command. The opinions and assertions contained herein are the private ones of the writers and are not to be construed as official or reflecting the views of the U. S. Navy Department or the naval service at large. The experiments reported herein were conducted according to the principles set forth in the current edition of the "Guide for the Care and Use

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“…Early results obtained in mice indicated an inhibitory effect of physiological doses of estrogens on several hematopoietic lineages, including granulopoiesis and thrombocytopoiesis (Fried et al, 1974). It was initially thought that the in vivo suppression of hematopoiesis was secondary to replacement of the bone-marrow cavity by new bone because estrogens induce osteosclerosis (Morse et al, 1974). However, Perry et al (2000) showed that the effects of estrogens on murine hematopoiesis preceded those on bone formation, thus providing evidence for a primary action of the hormone on the hematopoietic marrow.…”

Section: Discussionmentioning

confidence: 99%

Differential Effects of Steroids and Retinoids on Bovine Myelopoiesis in Vitro

Merris

Meyer

Duchateau

et al. 2004

Journal of Dairy Science

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Pregnancy and parturition are associated with physiological changes caused by steroid hormones. Alterations in number, maturity, and function of polymorphonuclear leukocytes observed in dairy cows at parturition suggest a common causative relationship with steroid hormones. This study was designed to investigate the effects of progesterone, 17-β-estradiol, and hydrocortisone on the proliferation of bovine progenitor cells. An in vitro culturing system was used, and colonies were scored after 7 d of incubation. At low concentrations, 17-β-estradiol inhibited proliferation of granulocyte progenitor cells. Hydrocortisone reduced growth of granulocyte and monocyte colonies, whereas myelopoiesis was not altered by progesterone. Furthermore, we studied the effect of retinoids on colony formation of bovine bone marrow cells. All-trans-and 9-cis-retinoic acid stimulated growth of granulocyte colonies and inhibited proliferation of the monocyte lineage. The addition of the 13-cis-isomer also increased numbers of granulocyte colony-forming units. This study indicates that steroid hormones may be responsible for alterations in the bovine hematopoietic profiles observed in circulation during the postpartum period. White blood cells, especially polymorphonuclear leukocytes, which are derived from bone marrow, are an important first line defense against mastitis. Therefore, these effects of steroids might contribute to the increased susceptibility of dairy cows to Escherichia coli mastitis. We furthermore hypothesize that an important role might be attributed to retinoic acid in its regulation of bovine myelopoiesis. Modulation of myelopoiesis in favor of the granulocyte lineage during the acute-phase reaction may be an adaptive mechanism designed to increase the capacity of first-line defense to intramammary infections. Received: October 8, 2003. Accepted: November 6, 2003 Corresponding author: C. Burvenich; e-mail: Christian.Burvenich @UGent.be. 1188(Key words: steroid hormone, retinoic acid, bone marrow, myelopoiesis) Abbreviation key: cfu-G = colony-forming unit-granulocyte, cfu-GM = colony-forming unit-granulocyte and monocyte, cfu-M = colony-forming unit-monocyte, cfutotal = colony-forming unit-total myeloid, FBS = fetal bovine serum, IMDM = Iscove's modified Dulbecco's Minimal Essential, PMN = polymorphonuclear leukocytes, RAR = retinoic acid receptor, RXR = retinoid X receptor.

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Adaptation of Hemopoietic Tissue Resulting From Estrone‐induced Osteosclerosis in Mice

Cited by 11 publications

References 25 publications

Strategies of hemopoietic stress adaptation within the medullary cavity

Strategies of hemopoietic stress adaptation within the medullary cavity

Hematological characterization of congenital osteopetrosis in op/op mouse. Possible mechanism for abnormal macrophage differentiation.

Differential Effects of Steroids and Retinoids on Bovine Myelopoiesis in Vitro

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