Localization of estrogen receptors-alpha and -beta and androgen receptor in the human growth plate at different pubertal stages

Nilsson, Ola; Chrysis, Dionisios; Pajulo, Olli; Boman, Anders; Holst, Mikael; Rubinstein, Joanna; Ritzén, E. M.; Sävendahl, Lars

doi:10.1677/joe.0.1770319

Cited by 124 publications

(71 citation statements)

References 46 publications

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“…Immunohistochemistry was performed as previously described (19) with the following modifications. After antigen retrieval by incubating with trypsin (Invitrogen) for 10 min at 37°C, the sections were additionally treated with 5 mg/mL hyaluronidase (Sigma Chemical Co.-Aldrich, Inc, Steinheim, Germany) for 30 min at 37°C.…”

Section: Methodsmentioning

confidence: 99%

Epiphyseal Fusion in the Human Growth Plate Does not Involve Classical Apoptosis

et al. 2009

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By the end of puberty, growth ceases and epiphyseal fusion occurs through mechanisms not yet completely understood. Human growth plate tissues were collected in various pubertal stages including a unique late pubertal growth plate, which was about to fuse. Apoptosis was studied by TUNEL staining, immunolocalization of pro-and antiapoptotic proteins, and electron microscopy (EM). Morphologic analyses of the fusing growth plate revealed disorganized, large chondrocytes surrounded by a border of dense, corticallike bone. In the unfused growth plates, few chondrocytes were TUNEL positive. In contrast, the fusing growth plate contained no single TUNEL-positive cell. Antiapoptotic (Bcl-2 and Bcl-X L ) and proapoptotic (Bax, Bad, and cleaved caspase-3) proteins were detected in all growth plate zones without change in intensity during pubertal progression. Expression of antiapoptotic proteins was found in the fusing growth plate but of the proapoptotic proteins only Bad was detected. EM revealed no typical signs of apoptosis or autophagy in any of the growth plates. In contrast, morpohological signs of hypoxia and necrosis were observed. We conclude that classical apoptosis is not likely to be involved in the process of human growth plate fusion. (Pediatr Res 66: 654-659, 2009)

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Section: Methodsmentioning

confidence: 99%

Epiphyseal Fusion in the Human Growth Plate Does not Involve Classical Apoptosis

et al. 2009

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“…Some organs are capable of synthesising sex steroids from sulphated precursors which are present in high amounts in the circulation. The term 'intracrinology' was introduced, suggesting that sex steroids can be synthesised locally and act in the same cell without being released, indicating that a more complicated mechanism may be available in the physis [12,13,18,29].…”

Section: Endocrinology Of Growth and Pubertymentioning

confidence: 99%

Slipped capital femoral epiphysis and its association with endocrine, metabolic and chronic diseases: A systematic review of the literature

Witbreuk

Kemenade

Sluijs

et al. 2013

Journal of Children's Orthopaedics

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Purpose Puberty, obesity, endocrine and chronic systemic diseases are known to be associated with slipped capital femoral epiphysis (SCFE). The mechanical insufficiency of the physis in SCFE is thought to be the result of an abnormal weakening of the physis. However, the mechanism at the cellular level has not been unravelled up to now. Methods To understand the pathophysiology of endocrine and metabolic factors acting on the physis, we performed a systematic review focussing on published studies reporting on hormonal, morphological and cellular abnormalities of the physis in children with SCFE. In addition, we looked for studies of the effects of endocrinopathies on the human physis which can lead to cause SCFE and focussed in detail on hormonal signalling, hormone receptor expression and extracellular matrix (ECM) composition of the physis. We searched in the PubMed, EMBASE.com and The Cochrane Library (via Wiley) databases from inception to 11thSeptember 2012. The search generated a total of 689 references: 382 in PubMed, 232 in EMBASE.com and 75 in The Cochrane Library. After removing duplicate papers, 525 papers remained. Of these, 119 were selected based on titles and abstracts. After excluding 63 papers not related to the human physis, 56 papers were included in this review. Results Activation of the gonadal axis and the subsequent augmentation of the activity of the growth hormone-insulin-like growth factor 1 (GH-IGF-1) axis are important for the pubertal growth spurt, as well as for cessation of the physis at the end of puberty. The effects of leptin, thyroid hormone and corticosteroids on linear growth and on the physis are also discussed. Children with chronic diseases suffer from inflammation, acidosis and malnutrition. These consequences of chronic diseases affect the GH-IGF-1 axis, thereby, increasing the risk of the development of SCFE. The risk of SCFE and avascular necrosis in children with chronic renal insufficiency, growth hormone treatment and renal osteodystrophy remains equivocal. Conclusions SCFE is most likely the result of a multifactorial event during adolescence when height and weight increase dramatically and the delicate balance between the various hormonal equilibria can be disturbed. Up to now, there are no screening or diagnostic tests available to predict patients at risk.

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“…(9) The two nuclear ERs, ERa and ERb, as well as the membrane Gprotein-coupled receptor GPR30 proposed to be an ER, are expressed in growth plate cartilage. (10)(11)(12)(13)(14)(15)(16) ERa is the main functional ER in the mouse growth plate, although ERb slightly modulates longitudinal bone growth in female but not in male mice. (17,18) We recently demonstrated that female GPR30 À/À mice displayed reduced longitudinal bone growth and reduced growth plate height that could not be reduced further by E2 treatment.…”

Section: J Jbmrmentioning

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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Localization of estrogen receptors-alpha and -beta and androgen receptor in the human growth plate at different pubertal stages

Cited by 124 publications

References 46 publications

Epiphyseal Fusion in the Human Growth Plate Does not Involve Classical Apoptosis

Epiphyseal Fusion in the Human Growth Plate Does not Involve Classical Apoptosis

Slipped capital femoral epiphysis and its association with endocrine, metabolic and chronic diseases: A systematic review of the literature

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

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