Expression of adiponectin in the calcaneus growth plate
Location
Philadelphia, PA
Start Date
17-4-2026 1:30 PM
End Date
17-4-2026 2:30 PM
Description
INTRODUCTION: Cartilaginous structures called growth plates are the site of longitudinal bone growth in the developing skeleton. Growth plates contain chondrocytes arranged into reserve, proliferative, and hypertrophic zones. The calcaneus, a tarsal bone in the ankle, forms a single growth plate with an associated secondary ossification center.
We used RNA sequencing data from the growth plate-forming and non-forming ends of the calcaneus to identify differentially expressed genes (DEGs) associated with growth plate formation in the calcaneus. Adiponectin is one gene that is more highly expressed in the growth plate forming end of the calcaneus in postnatal day (P) 0 and P4 mice.
Adiponectin, encoded by the Adipoq gene, is an adipose derived hormone. Adiponectin is primarily known to be secreted by adipocytes and binds to the receptorsAdipoR1 and AdipoR2 in muscle and liver, respectively. Adiponectin also signals through these receptors to activate key pathways involved in the regulation of chondrocyte proliferation and differentiation in growth plates.
OBJECTIVES: The primary objective of this study is to investigate the expression pattern of adiponectin as it relates to the developing calcaneus and calcaneal growth plate.
METHODS: Histological specimens consisted of FVB/NJ mouse hind limbs collected at postnatal days 0, 4, and 9 (P0, P4, P9). Samples were fixed in an RNase-free preparation of 4% paraformaldehyde and decalcified in RNase-free Morse’s solution (22.5% formic acid and 10% sodium citrate) for 24 hours. Specimens were embedded and sectioned following standard procedures. We performed in situ hybridization using RNAscope™ 2.5 HD Assay – RED (ACD Bio) for Adipoq following RNAscope™ standard protocol, except replacing standard antigen retrieval processes with the use of an RNAscope™ proprietary antigen retrieval enzyme for bone and cartilage tissue.
RESULTS: At postnatal day (P)0, we observed minimal expression of Adipoq in the cartilage and perichondrium. By P4, Adipoq expression is increased compared to P0 with low level expression throughout cartilage and is present throughout the perichondrium surrounding the calcaneus. These expression patterns appear similar in the growth plate-forming and non-forming sides of the calcaneus. An increase in Adipoq expression is also apparent in the bone marrow cavity over time.
CONCLUSION: Adiponectin promotes chondrocyte proliferation and differentiation therefore acting as a potential regulator of cartilage development. We observe expression of adiponectin at low levels throughout the chondrocytes, and moderate levels throughout the P4 perichondrium of the calcaneus. These results suggest that this gene likely plays a role in cartilage proliferation and/or differentiation; however, we do not observe a noticeable difference in expression between the growth plate-forming and non-forming sides. This may be, in part, due to the low total number of transcripts observed in the RNA-seq data.
Embargo Period
5-19-2026
Expression of adiponectin in the calcaneus growth plate
Philadelphia, PA
INTRODUCTION: Cartilaginous structures called growth plates are the site of longitudinal bone growth in the developing skeleton. Growth plates contain chondrocytes arranged into reserve, proliferative, and hypertrophic zones. The calcaneus, a tarsal bone in the ankle, forms a single growth plate with an associated secondary ossification center.
We used RNA sequencing data from the growth plate-forming and non-forming ends of the calcaneus to identify differentially expressed genes (DEGs) associated with growth plate formation in the calcaneus. Adiponectin is one gene that is more highly expressed in the growth plate forming end of the calcaneus in postnatal day (P) 0 and P4 mice.
Adiponectin, encoded by the Adipoq gene, is an adipose derived hormone. Adiponectin is primarily known to be secreted by adipocytes and binds to the receptorsAdipoR1 and AdipoR2 in muscle and liver, respectively. Adiponectin also signals through these receptors to activate key pathways involved in the regulation of chondrocyte proliferation and differentiation in growth plates.
OBJECTIVES: The primary objective of this study is to investigate the expression pattern of adiponectin as it relates to the developing calcaneus and calcaneal growth plate.
METHODS: Histological specimens consisted of FVB/NJ mouse hind limbs collected at postnatal days 0, 4, and 9 (P0, P4, P9). Samples were fixed in an RNase-free preparation of 4% paraformaldehyde and decalcified in RNase-free Morse’s solution (22.5% formic acid and 10% sodium citrate) for 24 hours. Specimens were embedded and sectioned following standard procedures. We performed in situ hybridization using RNAscope™ 2.5 HD Assay – RED (ACD Bio) for Adipoq following RNAscope™ standard protocol, except replacing standard antigen retrieval processes with the use of an RNAscope™ proprietary antigen retrieval enzyme for bone and cartilage tissue.
RESULTS: At postnatal day (P)0, we observed minimal expression of Adipoq in the cartilage and perichondrium. By P4, Adipoq expression is increased compared to P0 with low level expression throughout cartilage and is present throughout the perichondrium surrounding the calcaneus. These expression patterns appear similar in the growth plate-forming and non-forming sides of the calcaneus. An increase in Adipoq expression is also apparent in the bone marrow cavity over time.
CONCLUSION: Adiponectin promotes chondrocyte proliferation and differentiation therefore acting as a potential regulator of cartilage development. We observe expression of adiponectin at low levels throughout the chondrocytes, and moderate levels throughout the P4 perichondrium of the calcaneus. These results suggest that this gene likely plays a role in cartilage proliferation and/or differentiation; however, we do not observe a noticeable difference in expression between the growth plate-forming and non-forming sides. This may be, in part, due to the low total number of transcripts observed in the RNA-seq data.