PMID- 12967341
OWN - NLM
STAT- MEDLINE
DCOM- 20031204
LR  - 20211203
IS  - 0022-0795 (Print)
IS  - 0022-0795 (Linking)
VI  - 178
IP  - 3
DP  - 2003 Sep
TI  - Thyroid hormone modulates ClC-2 chloride channel gene expression in rat renal 
      proximal tubules.
PG  - 503-11
AB  - Thyroid hormones has its main role in controlling metabolism, but it can also 
      modulate extracellular fluid Volume (ECFV) through its action on the expression 
      and activity of Na(+) transporters. Otherwise, chloride is the main anion in the 
      ECFV and the influence of thyroid hormones in the regulation of chloride 
      transporters is not yet understood. In this work, we studied the effect of 
      thyroid hormones in the expression of ClC-2, a cell Volume-, pH- and 
      voltage-sensitive Cl(-) channel, in rat kidney. To analyze the modulation of 
      ClC-2 gene expression by thyroid hormones, we used hypothyroid (Hypo) rats with 
      or without thyroxine (T(4)) replacement and hyperthyroid (Hyper) rats as our 
      experimental models. Total RNA was isolated and the expression of ClC-2 mRNA was 
      evaluated by a ribonuclease protection assay, and/or semi-quantitative RT-PCR. 
      Renal ClC-2 expression decreased in Hypo rats and increased in Hyper rats. In 
      addition, semi-quantitative RT-PCR of different nephron segments showed that 
      these changes were due exclusively to the modulation of ClC-2 mRNA expression by 
      thyroid hormone in convoluted and straight proximal tubules. To investigate 
      whether thyroid hormones action was direct or indirect, renal proximal tubule 
      primary culture cells were prepared and subjected to different T(4) 
      concentrations. ClC-2 mRNA expression was increased by T(4) in a dose-dependent 
      fashion, as analyzed by RT-PCR. Western blotting demonstrated that ClC-2 protein 
      expression followed the same profile of mRNA expression.
FAU - Santos Ornellas, D
AU  - Santos Ornellas D
AD  - Instituto de Biofisica Carlos Chagas Filho, Universidade Federal do Rio de 
      Janeiro, RJ, Brazil, CEP 21949-900.
FAU - Grozovsky, R
AU  - Grozovsky R
FAU - Goldenberg, R C
AU  - Goldenberg RC
FAU - Carvalho, D P
AU  - Carvalho DP
FAU - Fong, P
AU  - Fong P
FAU - Guggino, W B
AU  - Guggino WB
FAU - Morales, M
AU  - Morales M
LA  - eng
GR  - DK 32753/DK/NIDDK NIH HHS/United States
GR  - HL47122/HL/NHLBI NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - J Endocrinol
JT  - The Journal of endocrinology
JID - 0375363
RN  - 0 (CLC-2 Chloride Channels)
RN  - 0 (Chloride Channels)
RN  - 0 (RNA, Messenger)
RN  - 0 (Thyroid Hormones)
RN  - Q51BO43MG4 (Thyroxine)
SB  - IM
MH  - Animals
MH  - Blotting, Western/methods
MH  - CLC-2 Chloride Channels
MH  - Cells, Cultured
MH  - Chloride Channels/analysis/*genetics
MH  - *Gene Expression Regulation/drug effects
MH  - Hyperthyroidism/*metabolism
MH  - Hypothyroidism/*metabolism
MH  - Kidney Tubules, Proximal/*metabolism
MH  - Male
MH  - Models, Animal
MH  - RNA, Messenger/analysis
MH  - Rats
MH  - Rats, Wistar
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Thyroid Hormones/*physiology
MH  - Thyroxine/pharmacology
EDAT- 2003/09/12 05:00
MHDA- 2003/12/05 05:00
CRDT- 2003/09/12 05:00
PHST- 2003/09/12 05:00 [pubmed]
PHST- 2003/12/05 05:00 [medline]
PHST- 2003/09/12 05:00 [entrez]
AID - 10.1677/joe.0.1780503 [doi]
PST - ppublish
SO  - J Endocrinol. 2003 Sep;178(3):503-11. doi: 10.1677/joe.0.1780503.