Amyloid $sZ-protein stimulates parallel increases in cellular levels of its precursor and amyloid precursor-like protein 2 (APLP2) in human cerebrovascular smooth muscle cells

Abstract

The amyloid β-protein (Aβ) which accumulates in cerebral vascular and senile plaque deposits in the brains of patients with Alzheimer's disease (AD) is proteolytically derived from a larger precursor protein, the amyloid β-protein precursor (AβPP). AβPP is a member of a multigene family which includes amyloid precursor-like protein 2 (APLP2). Recently, we showed that Aβ1-42, but not the shorter Aβ1-40 induces cellular levels of AβPP in degenerating cultured human cerebrovascular smooth muscle (HCSM) cells. Here we report that Aβ1-42 stimulates a parallel increase in the cellular levels of APLP2 in cultured HCSM cells. in contrast, the levels of smooth muscle cell α-actin or total cellular protein did not appreciably change. These findings suggest a common regulatory mechanism for increased levels of HCSM cellular AJPP and APLP2 in response to pathologic Aβ1-42 induced stress.