Abstract:
:An acetylcholine (ACh) agonist, carbachol (Cch), causes hepatocytes to proliferate in the presence of hepatic nonparenchymal cells (HNPCs). To identify the HNPCs and ACh receptor subtypes involved in carbachol-induced hepatocyte proliferation (CIHP), we examined two types of vascular cells as candidates for HNPCs mediating CIHP in cocultures of hepatocytes using the Transwell filter insert. In the coculture with vascular smooth muscle cells (VSMCs) or endothelial cells (VECs), but not in the monoculture, 72 h treatment with Cch significantly increased the numbers of hepatocytes. The results suggest that both VSMCs and VECs are involved in CIHP through soluble factors secreted from these cells. Interestingly, coculture with VECs, but not with VSMCs, markedly increased the number of hepatocytes, even in the absence of Cch. Cell proliferation assays using an analogue of thymidine, bromodeoxyuridine (BrdU), demonstrated that the hepatocytes in both cocultures transiently replicated their chromosomes 12 h after Cch administration. Blocking the muscarinic type 1 ACh receptor (M1), M3/5, intracellular inositol triphosphate (IP3) receptor, or protein kinase C (PKC) pathways inhibited VSMC-mediated CIHP, whereas blocking the M3/5, IP3 receptor, or PKC pathways inhibited VEC-mediated CIHP. Co-culturing hepatocytes with both types of vascular cells markedly increased their albumin content, but addition of Cch had no effect. In conclusion, VSMCs among vascular cells mediate CIHP through M1, M3/5, and IP3/PKC signal transduction pathways, whereas VECs do so through M3/5, and IP3/PKC pathways.
journal_name
Cell Biol Intjournal_title
Cell biology internationalauthors
Yoshimura R,Arai J,Endo Ydoi
10.1016/j.cellbi.2009.01.018subject
Has Abstractpub_date
2009-04-01 00:00:00pages
516-23issue
4eissn
1065-6995issn
1095-8355pii
S1065-6995(09)00034-1journal_volume
33pub_type
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