Effects of GH/IGF axis on bone and cartilage. (1st January 2021)

• Record Type: Journal Article
• Authors: Dixit, Manisha; Poudel, Sher Bahadur; Yakar, Shoshana
• Is Part Of: Molecular and cellular endocrinology. Volume 519(2021)
• Publication Date: 2021-01-01
• Subjects: Growth hormone -- Insulin-like growth factor-1 -- Bone -- Cartilage; Endocrinology -- Periodicals; Molecular biology -- Periodicals; Cytology -- Periodicals; Endocrinology -- Periodicals; Hormones -- Periodicals; Endocrinologie -- Périodiques; Cytology; Endocrinology; Molecular biology; Periodicals; 573.4
• DOI: 10.1016/j.mce.2020.111052
• Languages: English
• ISSNs: 0303-7207

Abstract

Abstract: Growth hormone (GH) and its mediator, the insulin-like growth factor-1 (IGF-1) regulate somatic growth, metabolism and many aspects of aging. As such, actions of GH/IGF have been studied in many tissues and organs over decades. GH and IGF-1 are part of the hypothalamic/pituitary somatotrophic axis that consists of many other regulatory hormones, receptors, binding proteins, and proteases. In humans, GH/IGF actions peak during pubertal growth and regulate skeletal acquisition through stimulation of extracellular matrix production and increases in bone mineral density. During aging the activity of these hormones declines, a state called somatopaguss, which associates with deleterious effects on the musculoskeletal system. In this review, we will focus on GH/IGF-1 action in bone and cartilage. We will cover many studies that have utilized congenital ablation or overexpression of members of this axis, as well as cell-specific gene-targeting approaches used to unravel the nature of the GH/IGF-1 actions in the skeleton in vivo . Highlights: GH/IGF axis plays central roles in skeletal growth and mineral acquisition. Cells of the osseous system express the GHR and the IGF-1R and secrete IGF-1 that acts in an autocrine/paracrine fashion. GH/IGF stimulate proliferation and differentiation of chondrocytes in the growth plate, thus mediating linear bone growth. IGF-1 enhances OB differentiation, collagen secretion, and bone matrix mineralization. IGF-1 couples OB-induced bone formation and OCL-mediated bone resorption via activation of the ephrinB2/Eph4 system.