Influence of estradiol treatment on bone marrow cell differentiation in collagenase-induced arthritis

Ganova, Petya; Zhivkova, R; Kolarov, Anton; Ivanovska, Nina

doi:10.1007/s00011-020-01338-w

Cited by 7 publications

(7 citation statements)

References 33 publications

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“…For example, estrogen is one of the most deeply investigated sex hormones in OA [12]. Although estrogen is considered to have protective potency against OA, the effects of estrogen replacement therapy and selective estrogen receptor modulators in preserving and/or restoring joint tissue in OA are controversial among currently published reports [13,14]. Besides estrogen, sex hormone-binding globulin [15], follicle-stimulating hormone [16], dehydroepiandrosterone [17], progesterone [18], and testosterone [19] may all influence OA progression.…”

Section: Introductionmentioning

confidence: 99%

Males and Females Have Distinct Molecular Events in the Articular Cartilage during Knee Osteoarthritis

Zheng

2021

IJMS

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Osteoarthritis (OA) is a major public health challenge that imposes a remarkable burden on the affected individuals and the healthcare system. Based on the clinical observation, males and females have different prevalence rates and severity levels of OA. Thus, sex-based differences may play essential roles in OA’s prognosis and treatment outcomes. To date, the comprehensive understanding of the relationship between sex and OA is still largely lacking. In the current study, we analyzed a published transcriptome dataset of knee articular cartilage (GSE114007) from 18 healthy (five females, 13 males) and 20 OA (11 females, nine males) donors to provide a slight insight into this important but complex issue. First, comparing female healthy cartilage samples with those of males revealed 36 differential expression genes (DEGs), indicating the fundamental sex-related differences at the molecular level. Meanwhile, 923 DEGs were distinguished between OA and healthy female cartilage, which can be enriched to 15 Reactome pathways. On the other hand, when comparing OA and healthy male cartilage, there are only 419 DEGs were identified, and only six pathways were enriched against the Reactome database. The different signaling response to OA in the male and female cartilage was further enforced by recognizing 50 genes with significantly different OA-responsive expression fold changes in males and females. Particularly, 14 Reactome pathways, such as “Extracellular matrix organization”, “Collagen biosynthesis and modifying enzymes”, “Dissolution of fibrin clot”, and “Platelet Aggregation (Plug formation)”, can be noted from these 50 sex-dependent OA-responsive genes. Overall, the current study explores the Sex as a Biological Variable (SABV) at the transcriptomic level in the knee articular cartilage in both healthy status and OA event, which could help predict the differential OA prognosis and treatment outcome of males and female patients.

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Section: Introductionmentioning

confidence: 99%

Males and Females Have Distinct Molecular Events in the Articular Cartilage during Knee Osteoarthritis

Zheng

2021

IJMS

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“…Estradiol (17β-estradiol, Sigma-Aldrich) was administered orally as described previously. 24 Briefly, 4 μg of substance was dissolved in 0.3 ml sesame oil (Sigma-Aldrich) and mixed with 60 mg Nutella (Ferrero Co, UK). Another group of CIOA mice was treated with ED for 30 days starting with collagenase injection at a dose of 4 µg from day 0 of CIOA ( n = 10 per group in two experiments).…”

Section: Methodsmentioning

confidence: 99%

“…Previously, we have established that the administration of 4 μg estradiol/mouse for 30 days in mice with collagenase-induced osteoarthritis resulted in reduced synovitis and cartilage destruction which correlated with attenuated glycosaminoglycan and proteoglycan loss, and osteophyte formation. 24 In the present study we investigated in parallel the capacity of ED and FSH to alter osteoblast/osteoclast balance in arthritic mice.…”

Section: Introductionmentioning

confidence: 99%

Follicle stimulating hormone and estradiol alter immune response in osteoarthritic mice in an opposite manner

Belenska-Todorova

Zhivkova

Markova

et al. 2021

Int J Immunopathol Pharmacol

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Although a number of studies have shown that the occurrence and progression of osteoarthritis (OA) is related to endocrine system dysfunction, there is limited evidence about what roles sex hormones play. The aim of the present study was to examine the capacity of 17β-estradiol (ED) and follicle stimulating hormone (FSH) to alter the differentiation of bone marrow (BM) cells in arthritic mice. The experiments were conducted in collagenase-induced osteoarthritis in mice. Cartilage degradation was observed by safranin and toluidine blue staining. Flow cytometry was used to define different BM and synovial cell populations. The influence of FSH and ED on osteoclastogenesis was studied in BM cultures and on the osteoblastogenesis in primary calvarial cultures. The levels of IL-8, TNF-α, FSH, and osteocalcin were estimated by ELISA. FSH increased cartilage degradation and serum osteocalcin levels, while ED abolished it and lowered serum osteocalcin. FSH elevated the percentage of monocytoid CD14+/RANK+ and B cell CD19+/RANK+ cells in contrast to ED which inhibited the accumulation of these osteogenic populations. Also, ED changed the percentage of CD105+/F4/80+ and CD11c+ cells in the synovium. FSH augmented and ED suppressed macrophage colony-stimulating factor (M-CSF) + receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast (OC) formation, and this correlated with a respective increase and decrease of IL-8 secretion. FSH did not influence osteoblast (OB) formation while ED enhanced this process in association with changes of TNF-α, IL-8, and osteocalcin production. ED reduced osteoclast generation in bone. The key outcome of the current study is that both hormones influenced BM cell differentiation, with FSH favoring osteoclast formation and ED favoring osteoblast accumulation.

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“…In the course of osteoporosis, bone mass decreases and there is a micro-architectonic degradation of bone tissue, which carries the risk of fractures [39,40]. Estrogen, which inhibits the formation of osteoclasts, has a positive effect on osteoporosis inhibition [41]. Moreover, estrogen blocks osteoblast apoptosis and increases their viability by Sema3A secretion induction in osteocytes [42,43].…”

Section: Hormone-dependent Diseases With Bone Density Lossmentioning

confidence: 99%

“…It is known that treatment with IL-1 receptor antagonist or TNF-binding protein decreases osteoclast formation and bone resorption in ovariectomized mice, which indicates that both factors are highly relevant for estrogenrelated bone loss [46]. Effects of estrogen on TNF level is indirectly meditated by T cells, revealing the importance of T cells for estrogen-mediated bone protection [41,42,[47][48][49].…”

Section: Hormone-dependent Diseases With Bone Density Lossmentioning

confidence: 99%

New Generation of Meso and Antiprogestins (SPRMs) into the Osteoporosis Approach

Woźniczka

Błaszczak-Świątkiewicz

2021

Molecules

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Receptor activator of nuclear factor κB (RANK) and its ligand (RANKL) play key roles in bone metabolism and the immune system. The RANK/RANKL complex has also been shown to be critical in the formation of mammary epithelia cells. The female hormones estradiol and progesterone closely control the action of RANKL with RANK. Blood concentration of these sex hormones in the postmenopausal period leads to an increase in RANK/RANKL signaling and are a major cause of women’s osteoporosis, characterized by altered bone mineralization. Knowledge of the biochemical relationships between hormones and RANK/RANKL signaling provides the opportunity to design novel therapeutic agents to inhibit bone loss, based on the anti-RANKL treatment and inhibition of its interaction with the RANK receptor. The new generation of both anti- and mesoprogestins that inhibit the NF-κB-cyclin D1 axis and blocks the binding of RANKL to RANK can be considered as a potential source of new RANK receptor ligands with anti-RANKL function, which may provide a new perspective into osteoporosis treatment itself as well as limit the osteoporosis rise during breast cancer metastasis to the bone.

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Influence of estradiol treatment on bone marrow cell differentiation in collagenase-induced arthritis

Cited by 7 publications

References 33 publications

Males and Females Have Distinct Molecular Events in the Articular Cartilage during Knee Osteoarthritis

Males and Females Have Distinct Molecular Events in the Articular Cartilage during Knee Osteoarthritis

Follicle stimulating hormone and estradiol alter immune response in osteoarthritic mice in an opposite manner

New Generation of Meso and Antiprogestins (SPRMs) into the Osteoporosis Approach

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