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GROWTH HORMONE (GH) RECEPTOR IMMUNOREACTIVITY IN CARTILAGE AND BONE OF GROWTH-RETARDED HYPOTHYROID (HT) RATS

HT results in diminished GH synthesis, increased liver GH receptors, growth retardation with narrowing of the growth plate and osteopenia. We examined the immunoreactivity (IR) of GH receptors (R) in tibiae of normal young rats, and compared them with rats, rendered HT by methymazole for 7 wk, with or without GH or L-thyroxine (T4) replacement over the last 2 wk, to demonstrate ‘catchup’ growth. The avidin-biotin-peroxydase method was used to localize GH-R, tagged with monoclonal antibody to the GH-R (MAb 263), Quantitative analysis was made by antibody dilution. HT and replacement efficacy were varified by serum T4 and T3 levels. HT rats' growth was stunted, and GH therapy induced ‘catch-up’ growth, to half of that of T4 replacement. Pituitary GH levels were nullified in HT. In normal rats GH-R IR was localized at the resting chondroprogenitor cells and in mature hypertrophic cells of the growth plate, but not in proliferating chondrobllsts. It was also present in articular cartilage, in osteoblasts, osteoclasts, some osteocytes of the metaphyseal bone, and various components of the bone marrow. In HT bones GH-R were also evident in proliferating flat chondroblasts of the growth plate. GH-R IR was >4-folds higher in HT growth plate and bone compared with normal. GH replacement decreased the intensity of GH-R in both chondrocytes and osteoblasts, and T4 replacement normalized it. It is concluded that bone and cartilage GH-R increase in HT, due partly to the accompanied GH-deficiency, and partly through direct T4 effect in cartilage and bone.