The roles of activins in repair processes of the skin and the brain.

A recent study from our laboratory demonstrated a strong upregulation of activin expression during cutaneous wound healing. To further analyze the role of activin A in skin morphogenesis and wound repair, we generated transgenic mice that overexpress activin A under the control of the keratin 14 promoter. The latter targets expression of transgenes to the basal, proliferating layer of the epidermis.

Induction of activin A is essential for the neuroprotective action of basic fibroblast growth factor in vivo.

Exogenous application of neurotrophic growth factors has emerged as a new and particularly promising approach not only to promote functional recovery after acute brain injury but also to protect neurons against the immediate effect of the injury. Among the various growth factors and cytokines studied so far, the neuroprotective and neurotrophic profile of basic fibroblast growth factor (bFGF) is the best documented. Using an animal model of acute excitotoxic brain injury, we report here that the neuroprotective action of bFGF, which is now being tested in stroke patients, depends on the induction of activin A, a member of the transforming growth factor-beta superfamily.

Connective tissue growth factor: a novel player in tissue reorganization after brain injury?

Recent studies have suggested a role of connective tissue growth factor (CTGF) in repair processes of the skin as well as in various types of fibrotic disease. However, a function of this molecule in central nervous system (CNS) repair has not been demonstrated yet. In this study we analysed the temporal and spatial expression pattern of CTGF after unilateral kainic acid lesions of the hippocampal CA3 region in mice.

Spread of excitation in chronically lesioned mouse hippocampus determined by laser scanning microscopy.

Fast optical recordings by means of laser scanning microscopy in conjunction with a voltage-sensitive dye (RH 414) were performed to monitor the spatio-temporal spread of neuronal activity in CA3/CA4-lesioned C57BL6 mouse hippocampal slices prepared approximately 3 months after intracerebroventricular kainic acid (KA) injection. The aim of our study was to assess the effects of a circumscribed neuronal loss on the propagation of electrical activity along the trisynaptic hippocampal circuit. Both in physiological bathing solution and in bicuculline (10 microM), hilar stimulation failed to activate the downstream pathway, so that, under these conditions, the chronically disinhibited CA1 region appeared to be effectively isolated from burst activity arising upstream; however, epileptiform discharges evoked in zero Mg2+ solution were reliably transmitted from the dentate gyrus to the CA1 region.