Growth inhibition and morphological changes of LLC-PK1 induced by ultimobranchial calcitonins.
Ultimobranchial calcitonins (CTs), known to stimulate cAMP production, inhibited the growth of a porcine kidney cell line LLC-PK1. This inhibition was accompanied by degenerative changes including vacuole formation and cell detachment. The electron microscopic study revealed marked swelling of rough endoplasmic reticulum (RER). Other cAMP-increasing agents such as human CT, arginine, vasopressin, and forskolin showed less growth inhibitory activities and no induction of the degenerative changes. These results indicate that the growth inhibition of LLC-PK1 by ultimobranchial CTs is mainly due to cellular death caused by the swelling of RER via a signalling pathway other than the cAMP-dependent event(s).
Inoue
A
A
Sagami Chemical Research Center, Kanagawa, Japan.
Komatsu
Y
Y
Ochiai
J
J
Itagaki
S
S
Nishide
H
H
Shikano
M
M
Hemmi
H
H
Numao
N
N
D015124:8-Bromo Cyclic Adenosine Monophosphate / Q000494:pharmacology; D000818:Animals; D001127:Arginine Vasopressin / Q000494:pharmacology; D002116:Calcitonin / Q000302:isolation & purification / Q000494:pharmacology*; D002455:Cell Division / Q000187:drug effects; D002460:Cell Line; D005576:Colforsin / Q000494:pharmacology; D000242:Cyclic AMP / Q000378:metabolism; D007668:Kidney / Q000166:cytology / Q000187:drug effects*; D013552:Swine; D014460:Ultimobranchial Body / Q000737:chemistry
D001127:Arginine Vasopressin; D005576:Colforsin; D015124:8-Bromo Cyclic Adenosine Monophosphate; D002116:Calcitonin; D000242:Cyclic AMP