PMID- 12675841
OWN - NLM
STAT- MEDLINE
DCOM- 20031217
LR  - 20131121
IS  - 0085-2538 (Print)
IS  - 0085-2538 (Linking)
VI  - 63
IP  - 5
DP  - 2003 May
TI  - Imprinted mesodermal specific transcript (MEST) and H19 genes in renal 
      development and diabetes.
PG  - 1658-70
AB  - BACKGROUND: Imprinted genes, mesodermal specific cDNA or transcript (MEST) and 
      H19, are implicated in peri-implantation embryogenesis, and their expression was 
      assessed in embryonic kidneys undergoing glucose-induced dysmorphogenesis. 
      METHODS: MEST and H19 mRNA expression was assessed by Northern blot analysis in 
      embryonic kidneys of mice harvested at day 15 to day 19 of gestation and of 
      1-week-old mice obtained from hyperglycemic mothers. A full-length mouse MEST 
      cDNA was isolated, subcloned into an expression vector, a recombinant protein 
      prepared and an antibody raised; the latter was used to assess protein expression 
      by immunoprecipitation and immunofluorescence microscopy in day 13 metanephric 
      explants subjected to high glucose ambience. Also, MEST mRNA expression was 
      assessed in high d glucose-treated explants by competitive reverse 
      transcription-polymerase chain reaction (RT-PCR) analyses and by in situ tissue 
      autoradiography. RESULTS: A high expression of MEST and H19 with respective 
      transcript size of approximately 2.7 and approximately 2.4 kb was observed in 
      fetal kidneys, and their expression decreased during the successive stages of 
      gestation and was undetectable in the postnatal period. At day 13, the MEST mRNA 
      was expressed in the mesenchyme, while H19 was expressed in the ureteric bud 
      branches and epithelial elements of the metanephros. Their expression decreased 
      with progression of gestation. By competitive RT-PCR and Northern blot and in 
      situ autoradiographic analyses, both MEST and H19 expressions decreased in day 13 
      explants treated with high glucose and in the kidneys of fetuses obtained from 
      diabetic mothers. The MEST protein expression was observed in the metanephric 
      epithelial elements and ureteric bud branches instead of in the mesenchyme, and 
      its expression decreased in glucose-treated dysmorphogenetic explants, as 
      assessed by immunofluorescence and immunoprecipitation methods. CONCLUSION: MEST 
      and H19 imprinted genes are strategically located in the mammalian embryonic 
      metanephros. They are developmentally regulated and their concomitant decreased 
      expression in high glucose ambience or diabetic state did not follow the 
      prevailing dogma of reciprocal inactivation/activation of imprinted genes, and 
      such a decrease may be responsible for the perturbed epithelial:mesenchymal 
      interactions leading to dysmorphogenesis of the mammalian metanephros.
FAU - Kanwar, Yashpal S
AU  - Kanwar YS
AD  - Departments of Pathology, Northwestern University Medical School, Chicago, 
      Illinois 60611, USA. y-kanwar@northwestern.edu
FAU - Pan, Xiaomin
AU  - Pan X
FAU - Lin, Sun
AU  - Lin S
FAU - Kumar, Anil
AU  - Kumar A
FAU - Wada, Jun
AU  - Wada J
FAU - Haas, Christian S
AU  - Haas CS
FAU - Liau, Gene
AU  - Liau G
FAU - Lomasney, Jon W
AU  - Lomasney JW
LA  - eng
GR  - DK28492/DK/NIDDK NIH HHS/United States
GR  - DK60635/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Kidney Int
JT  - Kidney international
JID - 0323470
RN  - 0 (Antibodies)
RN  - 0 (H19 long non-coding RNA)
RN  - 0 (Proteins)
RN  - 0 (RNA, Long Noncoding)
RN  - 0 (RNA, Messenger)
RN  - 0 (RNA, Untranslated)
RN  - 0 (Recombinant Fusion Proteins)
RN  - 0 (mesoderm specific transcript protein)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Antibodies/pharmacology
MH  - Diabetic Nephropathies/*physiopathology
MH  - Female
MH  - Gene Expression Regulation, Developmental/drug effects
MH  - *Genomic Imprinting
MH  - Glucose/pharmacology
MH  - Hyperglycemia/physiopathology
MH  - Kidney/embryology/*physiology
MH  - Male
MH  - Mice
MH  - Mice, Inbred ICR
MH  - Organ Culture Techniques
MH  - Pregnancy
MH  - Pregnancy in Diabetics/physiopathology
MH  - Proteins/*genetics/immunology/pharmacology
MH  - RNA, Long Noncoding
MH  - RNA, Messenger/analysis
MH  - RNA, Untranslated/*genetics
MH  - Recombinant Fusion Proteins/pharmacology
EDAT- 2003/04/05 05:00
MHDA- 2003/12/18 05:00
CRDT- 2003/04/05 05:00
PHST- 2003/04/05 05:00 [pubmed]
PHST- 2003/12/18 05:00 [medline]
PHST- 2003/04/05 05:00 [entrez]
AID - S0085-2538(15)49055-6 [pii]
AID - 10.1046/j.1523-1755.2003.00905.x [doi]
PST - ppublish
SO  - Kidney Int. 2003 May;63(5):1658-70. doi: 10.1046/j.1523-1755.2003.00905.x.