The ghrelin paradox in the control of equine chondrocyte function: The good and the bad

Ceriotti S, Consiglio AL, Casati L, Cremonesi F, Sibilia V, Ferrucci F · Peptides

Ghrelin acted in both directions depending on concentration: at 10 to the minus 7 mol/L it left basal viability unchanged and prevented lipopolysaccharide-induced apoptosis and necrosis, so that viability did not differ from controls; at 10 to the minus 11 mol/L it reduced basal viability, raised apoptosis and necrosis through caspase activation, and worsened the lipopolysaccharide injury. The protective effect was lost with GHS-R1a antagonism, and the receptor was detected on the chondrocytes by western blot at every passage.

Population

Primary equine articular chondrocytes in culture, with and without lipopolysaccharide injury

Intervention

Ghrelin at 10 to the minus 7 through 10 to the minus 11 mol/L, with a caspase inhibitor, a des-acyl ghrelin comparison and GHS-R1a antagonism

Comparator

Untreated chondrocytes

Limitations

Cultured horse cells with viability endpoints only; no cartilage matrix measurement, no animal and no ipamorelin, which is the secretagogue that acts on the receptor tested. Earlier binding studies failed to find GHS-R1a on mouse and human chondrocyte lines, which the authors attribute to methods. Funded by a University of Milan research grant.