Tamoxifen induces permanent growth arrest through selective induction of apoptosis in growth plate chondrocytes in cultured rat metatarsal bones

Chagin, Andrei S.; Karimian, Elham; Zaman, Farasat; Takigawa, Masaharu; Chrysis, Dionisios; Sävendahl, Lars

doi:10.1016/j.bone.2006.12.066

Cited by 37 publications

(50 citation statements)

References 40 publications

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“…One limitation of this approach is the potential confounding effects of tamoxifen. As an estrogen metabolite, tamoxifen promotes growth plate chondrocyte apoptosis and reduces the proliferation of articular chondrocytes (33,34). We did not observe any changes in growth plate depth or proliferative growth plate chondrocytes in tamoxifeninjected C57 animals.…”

Section: Discussioncontrasting

confidence: 57%

Histone Deacetylase 7 (Hdac7) Suppresses Chondrocyte Proliferation and β-Catenin Activity during Endochondral Ossification

Bradley

Carpio

Olson

et al. 2015

Journal of Biological Chemistry

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Background: Hdac7 is a transcriptional co-repressor in skeletal tissues, but its role in chondrocytes is undefined. Results: Proteasomal degradation reduced Hdac7 levels during chondrogenic maturation and conditional deletion of Hdac7 in chondrocytes increased proliferation and ␤-catenin levels. Conclusion: Hdac7 degradation enhances ␤-catenin transcriptional activity in growth plate chondrocytes. Significance: Suppressing Hdac7 levels increases chondrocyte proliferation and promotes cartilage formation and regeneration.

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Section: Discussioncontrasting

confidence: 57%

Histone Deacetylase 7 (Hdac7) Suppresses Chondrocyte Proliferation and β-Catenin Activity during Endochondral Ossification

Bradley

Carpio

Olson

et al. 2015

Journal of Biological Chemistry

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“…Recently, it has been shown that estrogen promotes growth plate fusion in female mice through estrogen receptor α (ERα) (101), and the same result was demonstrated earlier in ERα knockout male mice (102). Selective estrogen receptor modulators (SERM) have been studied in vitro (tamoxifen) (103) and in animal models (raloxifene) (104), and they successfully ceased growth. In another example, retinoids are commonly used to treat cancer and skin problems, such as acne and hyperkeratotic disorders.…”

Section: Treatmentmentioning

confidence: 86%

MANAGEMENT OF ENDOCRINE DISEASE: Diagnostic and therapeutic approach of tall stature

Albuquerque

Scalco

Jorge

2017

European Journal of Endocrinology

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Tall stature is defined as a height of more than 2 standard deviations (s.d.) above average for same sex and age. Tall individuals are usually referred to endocrinologists so that hormonal disorders leading to abnormal growth are excluded. However, the majority of these patients have familial tall stature or constitutional advance of growth (generally associated with obesity), both of which are diagnoses of exclusion. It is necessary to have familiarity with a large number of rarer overgrowth syndromes, especially because some of them may have severe complications such as aortic aneurysm, thromboembolism and tumor predisposition and demand-specific follow-up approaches. Additionally, endocrine disorders associated with tall stature have specific treatments and for this reason their recognition is mandatory. With this review, we intend to provide an up-to-date summary of the genetic conditions associated with overgrowth to emphasize a practical diagnostic approach of patients with tall stature and to discuss the limitations of current growth interruption treatment options.

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“…Immunodetection of type X collagen was performed as described previously (35) with the following modification: Prior to suppressing endogenous peroxidase activity, antigen retrieval was carried out in citrate buffer (0.1 M) at þ808C in a water bath for 1 hour and then remained in the citrate buffer overnight, cooling down to reach room temperature. Immunostaining of ERa was performed based on a standard protocol for immunohistochemistry.…”

Section: Immunohistostaining Of Type X Collagen and Eramentioning

confidence: 99%

“…Apoptotic cells in the growth plate sections were identified employing the terminal deoxynucleotidyl transferase (TdT)-mediated deoxy-UTP nick end-labeling (TUNEL) technique (TdT-FragELTM DNA Fragmentation Kit, Calbiochem, Damstadt, Germany), as described previously. (35) Results…”

Section: Evaluation Of Cell Proliferation and Apoptosismentioning

confidence: 99%

The role of estrogen receptor α in growth plate cartilage for longitudinal bone growth

Börjesson

Lagerquist

Liu

et al. 2010

Journal of Bone and Mineral Research

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Estrogens enhance skeletal growth during early sexual maturation, whereas high estradiol levels during late puberty result in growth plate fusion in humans. Although the growth plates do not fuse directly after sexual maturation in rodents, a reduction in growth plate height is seen by treatment with a high dose of estradiol. It is unknown whether the effects of estrogens on skeletal growth are mediated directly via estrogen receptors (ERs) in growth plate cartilage and/or indirectly via other mechanisms such as the growth hormone/ insulin-like growth factor 1 (GH/IGF-1) axis. To determine the role of ERa in growth plate cartilage for skeletal growth, we developed a mouse model with cartilage-specific inactivation of ERa. Although mice with total ERa inactivation displayed affected longitudinal bone growth associated with alterations in the GH/IGF-1 axis, the skeletal growth was normal during sexual maturation in mice with cartilagespecific ERa inactivation. High-dose estradiol treatment of adult mice reduced the growth plate height as a consequence of attenuated proliferation of growth plate chondrocytes in control mice but not in cartilage-specific ERa À/À mice. Adult cartilage-specific ERa À/À mice continued to grow after 4 months of age, whereas growth was limited in control mice, resulting in increased femur length in 1-year-old cartilage-specific ERa À/À mice compared with control mice. We conclude that during early sexual maturation, ERa in growth plate cartilage is not important for skeletal growth. In contrast, it is essential for high-dose estradiol to reduce the growth plate height in adult mice and for reduction of longitudinal bone growth in elderly mice. ß

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Tamoxifen induces permanent growth arrest through selective induction of apoptosis in growth plate chondrocytes in cultured rat metatarsal bones

Cited by 37 publications

References 40 publications

Histone Deacetylase 7 (Hdac7) Suppresses Chondrocyte Proliferation and β-Catenin Activity during Endochondral Ossification

Histone Deacetylase 7 (Hdac7) Suppresses Chondrocyte Proliferation and β-Catenin Activity during Endochondral Ossification

MANAGEMENT OF ENDOCRINE DISEASE: Diagnostic and therapeutic approach of tall stature

The role of estrogen receptor α in growth plate cartilage for longitudinal bone growth

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