Endothelinergic signaling during recovery of brain cortical lesions.

Objectives: Recovery of brain lesions has been associated with increased activation and migration of endogenous neural stem cells, glia, and endothelium. To understand the role of endothelinergic signaling in these phenomena we studied devascularizing lesions of mouse brain cortex. Our specific aims were to: (i) describe the endothelinergic cell phenotypes appearing within the lesions; and (ii) evaluate the effect of endothelinergic blockade on the injured cortex.

Endothelins participate in the central and peripheral regulation of submandibular gland secretion in the rat.

We previously reported that endothelins (ETs) are involved in the rat central and peripheral regulation of bile secretion. In this study we sought to establish whether ET-1 and ET-3 modulated submandibular gland secretion when locally or centrally applied. Animals were prepared with gland duct cannulation to collect saliva samples and jugular cannulation to administer sialogogues.

Endothelinergic cells in the subependymal region of mice.

Endothelin (ET) is a small peptide that activates astrocyte proliferation, regulates proliferation and migration of embryonic neural precursor cells and stimulates glioblastoma growth. We found that in mouse brain, ET and its receptor B (ETRB) were highly expressed in the subependymal zone (SEZ), an adult neurogenic niche. Cells with ET immunoreactivity (ET+ cells) selectively appeared along the lateral and dorsal walls of the lateral ventricle.