Oestrogen‐deficiency inducing haematopoiesis dysfunction via reduction in haematopoietic stem cells and haematopoietic growth factors in rats

Qiu, Xi; Yuan, Xianggui; Jin, Xiaoli; He, Xin; Zhu, Lihong; Zhao, Xiaoying

doi:10.1111/j.1365-2613.2012.00815.x

Cited by 13 publications

(14 citation statements)

References 24 publications

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“…This result is in accordance with our previous study in vivo (Qiu et al 2012). The exact mechanism of E2 on HSCs is still obscure.…”

Section: Discussionsupporting

confidence: 93%

“…Nakada et al (2014) recently confirmed that estrogen increases the self-renewal of HSCs in females during pregnancy. In our previous study in rats, when estrogendeficiency was established by ovariectomy, hematopoiesis dysfunction occurred due to the decreased number of HSCs in the bone marrow (Qiu et al 2012). Further, a reduction of osteoblasts also occured, which positively correlated A.…”

Section: Discussionmentioning

confidence: 83%

“…Briefly, CD90 + cells were segregated and harvested with a magnetic particle separator according to the manufacturers' instructions. CD45RC was then used for magnetic activated cell sorting again in order to remove CD90 McCarthy et al 1987;Pu and Yang 2002;Qiu et al 2012) were obtained and seeded into 75 cm 2 culture flasks. More than 95% cell viability was achieved as assessed by trypan blue staining.…”

Section: Cell Culture and Isolation Of Mscs And Hscsmentioning

confidence: 99%

“…Moreover, estrogen was shown to play an important role in the differentiation and maturation of early hematopoietic progenitor cells (Shim et al 2003). In our previous studies, we found that estrogen-deficiency caused by ovariectomy leads to hematopoiesis dysfunction in rats, which is related with the reduction of hematopoietic stem cells (HSCs) in the bone marrow (Qiu et al 2012). However, the mechanism whereby estrogen stimulates the proliferation of HSCs remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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17<i>β</i>-Estradiol Induces the Proliferation of Hematopoietic Stem Cells by Promoting the Osteogenic Differentiation of Mesenchymal Stem Cells

Qiu

Jin

et al. 2014

Tohoku J. Exp. Med.

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The process of hematopoiesis is associated with hematopoietic stem cells (HSCs) and the hematopoietic microenvironment. Osteoblasts, derived from mesenchymal stem cells (MSCs), are one of the most important components in the hematopoietic microenvironment. Osteoblasts secrete a variety of cytokines including interleukin-6 (IL-6) and granulocyte-macrophage colony-stimulating factor (GM-CSF), thereby regulating the biological activities of HSCs. It has been shown that hematopoiesis dysfunction can be induced by estrogen-deficiency through the exhaustion of HSCs. However, the effect of estrogen on the proliferation of HSCs is not fully understood. The aim of this study was to investigate the role of estradiol in the process of hematopoiesis, especially regarding the proliferation of HSCs in vitro. Bone marrow-derived MSCs and HSCs were isolated from 3-month-old female Sprague-Dawley rats. Mineralization ability and osteocalcin assays demonstrated that treatment with 17β -estradiol (E2) significantly enhanced the osteogenic differentiation of MSCs. HSCs and MSCs were then cocultured with or without E2 treatment. Colony forming assays demonstrated that E2 increased the number of colony forming units-granulocyte/ macrophage in a dose-dependent manner when HSCs were co-cultured with MSCs in Osteogenic Medium that is suitable for the in vitro osteogenic differentiation. Further, increased concentrations of GM-CSF and IL-6 were detected by enzyme linked immunosorbent assay (ELISA). These results indicate that E2 induces the proliferation of HSCs, which depends on the promotion of osteogenic differentiation of MSCs, and that process is mediated by both GM-CSF and IL-6.

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“…This result is in accordance with our previous study in vivo (Qiu et al 2012). The exact mechanism of E2 on HSCs is still obscure.…”

Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 83%

Section: Cell Culture and Isolation Of Mscs And Hscsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

17<i>β</i>-Estradiol Induces the Proliferation of Hematopoietic Stem Cells by Promoting the Osteogenic Differentiation of Mesenchymal Stem Cells

Qiu

Jin

et al. 2014

Tohoku J. Exp. Med.

Self Cite

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“…Oestrogen also maintains the number and activity of HSCs in bone (Qiu et al 2012), and increases the ratio of OPG/RANKL (Yan & Ye 2015).…”

Section: Endocrine Effects In Bonementioning

confidence: 99%

The endocrine influence on the bone microenvironment in early breast cancer

Wilson

Brown

Holen

2016

Endocrine-Related Cancer

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Multiple factors influence the survival of disseminated breast tumour cells (DTCs) in bone. Whereas gene signature studies have identified genes that predict a propensity of tumours to metastasise to bone, the bone environment is key in determining the fate of these tumour cells. Breast cancer cells locate to specific niches within the bone that support their survival, regulated by host factors within the bone microenvironment including bone cells, cells of the bone micro vasculature, immune cells and the extracellular matrix. Reproductive endocrine hormones that affect bone and clinical studies across the menopausal transition have provided comprehensive understanding of the changes in the bone microenvironment during this time. Menopause is characterized by a decrease in ovarian oestradiol and inhibins, with an increase in pituitary follicle-stimulating hormone and this review will focus on the role of these three hormones in determining the fate of DTCs in bone. Both in vivo and clinical data suggest that premenopausal bone is a conducive environment for growth of breast cancer cells in bone. Adjuvant cancer treatment aims to reduce the risk of tumour recurrence by affecting DTCs. Drugs targeting the bone resorbing osteoclasts, such as bisphosphonates, have therefore been evaluated in this setting. Both preclinical and adjuvant clinical studies have shown that bisphosphonates' ability to decrease tumour growth in bone is influenced by the levels of endocrine hormones, with enhanced effects in a postmenopausal bone microenvironment. The challenge is to understand the molecular mechanisms behind this phenomenon and to evaluate if alternative adjuvant bone-targeted therapies may be effective in premenopausal women.

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