Neuroprotection by estrogen against MPP+-induced dopamine neuron death is mediated by ERalpha in primary cultures of mouse mesencephalon.

Estrogen involvement in neuroprotection is now widely accepted, although the specific molecular and cellular mechanisms of estrogen action in neuroprotection remain unclear. This study examines estrogenic effects in a mixed population of cells in attempts to identify the contributing cells that result in estrogen-mediated neuroprotection. Utilizing primary mesencephalic neurons, we found expression of both estrogen receptor alpha (ERalpha) and estrogen receptor beta (ERbeta) with a predominance of ERalpha on both dopamine neurons and astrocytes.

Modulation of bradykinin signaling by EP24.15 and EP24.16 in cultured trigeminal ganglia.

Metalloendopeptidases expressed in neural tissue are characterized in terms of their neuropeptide substrates. One such neuropeptide, bradykinin (BK), is an important inflammatory mediator that activates the type-2 BK receptor (B2R) on the terminal endings of specialized pain-sensing neurons known as nociceptors. Among several metalloendopeptidases that metabolize and inactivate BK, EP24.

Regeneration of skeletal muscle from transplanted immortalised myoblasts is oligoclonal.

Myoblasts transplanted into muscles of recipient mice mostly die, only a minor stem cell-like subpopulation surviving and participating in muscle regeneration. To investigate this phenomenon further, we used a retrovirus expressing beta-galactosidase to provide a unique marker for satellite-cell-derived muscle precursor cells, before transplanting them into myopathic mdx nu/nu mouse muscle. We employed inverse polymerase chain reaction to identify viral integrations, to follow the fate of clones present within the injected cells.