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. 2015 Jan 23;16(2):2663-77.
doi: 10.3390/ijms16022663.

Bone-remodeling transcript levels are independent of perching in end-of-lay white leghorn chickens

Maurice D Dale  1 , Erin M Mortimer  2 , Santharam Kolli  3 , Erik Achramowicz  4 , Glenn Borchert  5 , Steven A Juliano  6 , Scott Halkyard  7 , Nick Seitz  8 , Craig Gatto  9 , Patricia Y Hester  10 , David A Rubin  11
Affiliations

Bone-remodeling transcript levels are independent of perching in end-of-lay white leghorn chickens

Maurice D Dale et al. Int J Mol Sci. .

Abstract

Osteoporosis is a bone disease that commonly results in a 30% incidence of fracture in hens used to produce eggs for human consumption. One of the causes of osteoporosis is the lack of mechanical strain placed on weight-bearing bones. In conventionally-caged hens, there is inadequate space for chickens to exercise and induce mechanical strain on their bones. One approach is to encourage mechanical stress on bones by the addition of perches to conventional cages. Our study focuses on the molecular mechanism of bone remodeling in end-of-lay hens (71 weeks) with access to perches. We examined bone-specific transcripts that are actively involved during development and remodeling. Using real-time quantitative PCR, we examined seven transcripts (COL2A1 (collagen, type II, alpha 1), RANKL (receptor activator of nuclear factor kappa-B ligand), OPG (osteoprotegerin), PTHLH (PTH-like hormone), PTH1R (PTH/PTHLH type-1 receptor), PTH3R (PTH/PTHLH type-3 receptor), and SOX9 (Sry-related high mobility group box)) in phalange, tibia and femur. Our results indicate that the only significant effect was a difference among bones for COL2A1 (femur > phalange). Therefore, we conclude that access to a perch did not alter transcript expression. Furthermore, because hens have been used as a model for human bone metabolism and osteoporosis, the results indicate that bone remodeling due to mechanical loading in chickens may be a product of different pathways than those involved in the mammalian model.

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Figures

Figure 1
Figure 1
Summary of cellular events and transcription factors that regulate bone development and remodeling. Mesenchymal stem cells give rise to pathways for chondrogenesis and osteogenesis. During chondrocyte development and maturation, SOX9 promotes the expression of PTHLH [22] and COL2A1 (collagen, type II, alpha 1) [23]. When Indian hedgehog (IHH) is secreted by chondrocytes, it not only induces further development of prehypertrophic chondrocytes, but also increases the expression of PTHLH [24]. Subsequently, PTHLH regulates the differentiation of prehypertrophic chondrocytes into hypertrophic chondrocytes, while runt-related transcription factor 2 (RUNX2) acts on prehypertrophic chondrocytes, stimulating their development into hypertrophic chondrocytes [24,25]. During endochondral bone development, hypertrophic chondrocytes are stimulated by vascular endothelial growth factor (VEGF), which promotes vascularization of the cartilage [25]. RANKL is secreted by hypertrophic chondrocytes to recruit osteoclasts to the region of cartilage development. The recruited osteoclast develop the marrow region of the bone. Once osteoblasts arrive at the vascularized cartilage, they begin depositing minerals [25] and subsequently mature into osteocytes, which become imbedded in the lacunae of trabecular and cortical bone. To regulate bone remodeling in vertebrates, RANKL expression by osteoblasts and osteocytes is necessary for osteoclast progenitors to differentiate into osteoclast by binding to the RANK receptor [26]. Osteocytes also regulate osteoclast activity by expressing OPG, which acts as a decoy that binds directly to RANKL [26]. Thus, OPG inhibits RANKL from binding to the receptor on osteoclasts and preosteoclasts, resulting in the inhibition of their activity and differentiation. Osteoclast regulation occurs directly and indirectly by PTH, which binds and activates the PTH/PTHLH receptor. Although the PTH/PTHLH type-1 receptor (PTH1R) is common throughout all vertebrates, birds and fish (and not humans) express a PTH/PTHLH type-3 receptor (PTH3R). While PTH1R is primarily activated by PTH for calcium regulation throughout all vertebrates, it appears that the PTH3R in fish is primarily activated in PTHLH, whereas the activation of PTH3R in birds is not fully understood [27]. In vertebrates, bone resorption occurs when PTH directly activates the PTH/PTHLH receptors on osteoclasts [28]. However, when PTH binds to PTH/PTHLH receptors on osteoblast, calcium is secreted, and the calcium released is sensed by calcium-sensing receptors (CaSR) on the surface of osteoclast [28]. Osteoclast activity is inhibited by the calcium secreted by osteoblasts and by PTHLH, but the mechanism is not completely understood [28]. Osteoclasts in medullary bone are resistant to many factors that inhibit their activity in trabecular and cortical bone [4]. (Abbreviations: SOX9, SRY (sex-determining region Y)-box 9; PTHLH, parathyroid hormone like-hormone; COL2A1, collagen, type II, alpha 1; IHH, Indian Hedgehog, NM_204957; RUNX2, Runt-related transcription factor 2, NM_204128; VEGF, vascular endothelial growth factor, AB011078; RANKL, receptor activator of nuclear factor kappa-B ligand; OPG, osteoprotegerin; PTH, parathyroid hormone; PTHLH, PTH-like hormone; PTH1R, PTH/PTHLH type-1 receptor; PTH3R, PTH/PTHLH type-3 receptor; CaSR, calcium-sensing receptor, XM_416491.4).
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