Prolactin induced expression of glial fibrillary acidic protein and tumor necrosis factor-alpha at a wound site in the rat brain

To determine if PRL stimulates astrocyte proliferation and cytokine expression in vivo, we examined the effect of PRL on the wound-induced increase in the expression of glial fibrillary acid protein (GFAP) and tumor necrosis factor-α (TNF-α) in the CNS. Low levels of GFAP detected by Western blot analysis were identified in the non-wounded controls. Five days after the inflicition of the wound, the relative abundance of GFAP in the tissue surrounding the wound site was greater than those of intact controls. Injection of PRL into the wound site markedly increased GFAP expression in the hypothalamus. Western blot analysis failed to detect TNF-α in the hypothalamus of non-wounded animals. In contrast, TNF-α was easily detected in the hypothalamus of wounded rats, and was markedly increased in PRL injected animals. To confirm the PRL-induced increase in TNF-α levels, TNF-α levels in hypothalamic extracts were measured by bioassay. In non-wounded controls, low but detectable TNF-α levels were found in the hypothalamus by bioassay (0.13 ± 0.02 ng/mg protein). Infliction of a hypothalamic wound markedly increased TNF-α levels to 1.4 ± 0.3 ng/mg protein. Injection of PRL into the wound site resulted in a further increase in TNF-α levels to 11.4 ± 2.6 ng/mg protein. Further, infliction of the hypothalamic wound increased hypothalamic PRL content and PRL mRNA levels. The PRL-induced enhancement of GFAP and TNF-α expression, and the wound-induced increase in PRL content and mRNA levels in the tissue surrounding a CNS wound site, suggest that an increase in local PRL concentrations may be involved in regulating astrogliosis and cytokine expression in response to injury.