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Response of hydra to tunicamycin
Cell Surface InteractionsDuring Development(83-95)
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RESPONSE OF HYDRA TO TUNICAMYCIN. L. De P e t r o c e l l i s , B. De P e t r o c e l l i s , V. Maharajan, R. Minei. CNR I n s t i t u t e s of Cybernetics and Molecular Embryology, 80072 Arco F e l i c e , Naples. We have studied the e f f e c t of Tunicamycin (TM) on regeneration and budding in Hydra attenuata. TM is known to i n h i b i t g l y c o s y l a t i o n of surface proteins in other c e l l s systems. Exposure to 0.5 ug/ml TM for 48hrs preceding decapitat i o n caused i n h i b i t i o n of head and tentacle regeneration u n t i l 5 days post decap i t a t i o n (pdc.). Beginning about 6 days pdc only 15% of the animals regenerated head and normal number of t e n t a c l e s . 60% of the animals f a i l e d to regenerate head, however they showed budding and by 8 days pdc they had an average of 1.6 buds per animal. Since c e l l u l a r movements and reo r i e n t a t i o n of these c e l l s plays import a n t role in regeneration in hydra, we suggest that p r o t e i n ~ l y c o s y l a t i ~ n plays a c r u c i a l role in regeneration in hydra.
ENDOTHELIAL CELL REGULATION OF PULMONARY ARTERIAL SMOOTH MUSCLE PROLIFERATION. W. B e n i t z a n d M. B e r n f i e l d . Dept. of Pediatrics, Stanford University School o f M e d i c i n e , S t a n f o r d , CA 94305. Endothelial cells (EC) andsmooth muscle cells (SMC) grown from the pulmonary arteries of near-term fetal calves were used to study the regulation o f SMC p r o l i f e r a t i o n b y EC i__nn v i t r o . Medium s u p p l e m e n t e d w i t h 10% f e t a l calf s e r u m (FCS) w a s c o n d i t i o n e d b y EC m o n o layers for 48 hours and mixed 1:1 with fresh medium. After 5 days in culture, sparsely plated SMC c u l t u r e d in that medium achieved a d e n s i t y which was only 59% o f t h a t in control cultures (p < 0.001). T h e DNA c o n t e n t o f SMC c o c u l t u r e d w i t h EC u n d e r s e r u m - d e p r i v e d conditions ( 2 . 5 % FCS) m o r e t h a n d o u b l e d in 2 days, but that of control cultures increased b y o n l y 30% (p < 0 . 0 0 1 ) . EC therefore produce both an inhibitor and a promoter o f SMC p r o l i f e r a t i o n . These mediators may r e p r e s e n t a mechanism by w h i c h EC r e g u l a t e extension o f t h e SMC investment of the pulmonary arteries during development. (Supported b y NIH grant HD06763 and American Heart Association CSA 8 4 - 4 4 3 . )
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RESPONSE OF HYDRA TO TUNICAMYCIN. L. De P e t r o c e l l i s , B. De P e t r o c e l l i s , V. Maharajan, R. Minei. CNR I n s t i t u t e s of Cybernetics and Molecular Embryology, 80072 Arco F e l i c e , Naples. We have studied the e f f e c t of Tunicamycin (TM) on regeneration and budding in Hydra attenuata. TM is known to i n h i b i t g l y c o s y l a t i o n of surface proteins in other c e l l s systems. Exposure to 0.5 ug/ml TM for 48hrs preceding decapitat i o n caused i n h i b i t i o n of head and tentacle regeneration u n t i l 5 days post decap i t a t i o n (pdc.). Beginning about 6 days pdc only 15% of the animals regenerated head and normal number of t e n t a c l e s . 60% of the animals f a i l e d to regenerate head, however they showed budding and by 8 days pdc they had an average of 1.6 buds per animal. Since c e l l u l a r movements and reo r i e n t a t i o n of these c e l l s plays import a n t role in regeneration in hydra, we suggest that p r o t e i n ~ l y c o s y l a t i ~ n plays a c r u c i a l role in regeneration in hydra.
ENDOTHELIAL CELL REGULATION OF PULMONARY ARTERIAL SMOOTH MUSCLE PROLIFERATION. W. B e n i t z a n d M. B e r n f i e l d . Dept. of Pediatrics, Stanford University School o f M e d i c i n e , S t a n f o r d , CA 94305. Endothelial cells (EC) andsmooth muscle cells (SMC) grown from the pulmonary arteries of near-term fetal calves were used to study the regulation o f SMC p r o l i f e r a t i o n b y EC i__nn v i t r o . Medium s u p p l e m e n t e d w i t h 10% f e t a l calf s e r u m (FCS) w a s c o n d i t i o n e d b y EC m o n o layers for 48 hours and mixed 1:1 with fresh medium. After 5 days in culture, sparsely plated SMC c u l t u r e d in that medium achieved a d e n s i t y which was only 59% o f t h a t in control cultures (p < 0.001). T h e DNA c o n t e n t o f SMC c o c u l t u r e d w i t h EC u n d e r s e r u m - d e p r i v e d conditions ( 2 . 5 % FCS) m o r e t h a n d o u b l e d in 2 days, but that of control cultures increased b y o n l y 30% (p < 0 . 0 0 1 ) . EC therefore produce both an inhibitor and a promoter o f SMC p r o l i f e r a t i o n . These mediators may r e p r e s e n t a mechanism by w h i c h EC r e g u l a t e extension o f t h e SMC investment of the pulmonary arteries during development. (Supported b y NIH grant HD06763 and American Heart Association CSA 8 4 - 4 4 3 . )
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