PMID- 8853432
OWN - NLM
STAT- MEDLINE
DCOM- 19961205
LR  - 20191210
IS  - 0002-9513 (Print)
IS  - 0002-9513 (Linking)
VI  - 271
IP  - 3 Pt 2
DP  - 1996 Sep
TI  - Autocrine production and TGF-beta 1-mediated effects on metabolism and viability 
      in renal cells.
PG  - F689-97
AB  - Transforming growth factor-beta 1 (TGF-beta 1) treatment (0.2-2.0 ng/ml, 8-80 M) 
      of confluent primary cultures of rabbit renal proximal bular cells (RPTC) for 6 
      consecutive days resulted in both a benotypic transformation of the monolayer 
      into solid clus- rs of cells and apoptosis. TGF-beta 1 treatment stimulated 
      glycolysis before any effect on monolayer DNA content or morphology. TGF-beta 1 
      treatment also resulted in a 35% decrease in oxygen consumption, 50% inhibition 
      of Na(+)-K(+)- ATPase activity, and a 57% decrease in gluconeogenesis. A 
      concentration of 0.06 ng/ml TGF-beta 1 decreased oxygen consumption and induced 
      glycolysis but had no effect on morphology and viability of RPTC. Endogenous 
      production of TGF-beta 1 by RPTC increased 2.6-fold during 10 days of culture. 
      Control RPTC treated with anti-TGF-beta antibodies exhibited decreased 
      glycolysis, and lactate metabolism shifted from net production to net 
      consumption. These results show that TGF-beta 1 stimulates glycolysis, decreases 
      respiration, and, at higher concentrations, induces RPTC apoptosis and phenopic 
      changes. Inhibition of net lactate production in cells grown in the presence of 
      anti-TGF-beta antibodies suggests that increased endogenous production of 
      TGF-beta is responsible for the stimulation of glycolysis in long-term cultures 
      of RPTC.
FAU - Nowak, G
AU  - Nowak G
AD  - Department of Pharmacology and Toxicology, University of Arkansas for Medical 
      Sciences, Little Rock 72205-7199, USA.
FAU - Schnellmann, R G
AU  - Schnellmann RG
LA  - eng
GR  - ES-04110/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Physiol
JT  - The American journal of physiology
JID - 0370511
RN  - 0 (Antibodies)
RN  - 0 (Hormones)
RN  - 0 (Transforming Growth Factor beta)
RN  - EC 7.2.2.13 (Sodium-Potassium-Exchanging ATPase)
SB  - IM
MH  - Animals
MH  - Antibodies/immunology
MH  - Cell Division
MH  - Cell Survival
MH  - Female
MH  - Gluconeogenesis/drug effects
MH  - Glycolysis/drug effects
MH  - Hormones/*metabolism
MH  - Kidney Tubules, Proximal/cytology/*metabolism
MH  - Oxygen Consumption/drug effects
MH  - Rabbits
MH  - Sodium-Potassium-Exchanging ATPase/metabolism
MH  - Transforming Growth Factor beta/immunology/pharmacology/*physiology
EDAT- 1996/09/01 00:00
MHDA- 1996/09/01 00:01
CRDT- 1996/09/01 00:00
PHST- 1996/09/01 00:00 [pubmed]
PHST- 1996/09/01 00:01 [medline]
PHST- 1996/09/01 00:00 [entrez]
AID - 10.1152/ajprenal.1996.271.3.F689 [doi]
PST - ppublish
SO  - Am J Physiol. 1996 Sep;271(3 Pt 2):F689-97. doi: 
      10.1152/ajprenal.1996.271.3.F689.