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Am J Physiol Renal Physiol (December 4, 2001). doi:10.1152/ajprenal.00200.2001
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Articles in PresS, published online ahead of print December 4, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.00200.2001
Submitted on July 2, 2001
Accepted on November 28, 2001

Identification of developmentally regulated Mesodermal Specific Transcript (MEST) in mouse embryonic metanephros

Yashpal S Kanwar1*, Anil Kumar1, Kosuke Ota2, Sun Lin1, Jun Wada2, Sumant Chugh3, and Elisabeth I Wallner3

1 Pathology, Northwestern University Medical School, Chicago, IL, USA
2 Medicine, Okayama University, Okayama, Japan
3 Medicine, Northwestern University Medical School, Chicago, IL, USA

* To whom correspondence should be addressed. E-mail: y-kanwar{at}northwestern.edu.

Mesodermal specific cDNA or transcript (MEST) was identified by suppression subtractive hybridization-PCR of cDNA isolated from embryonic day-13 versus newborn mice kidneys. At day-13 of mouse gestation, a high expression of MEST with single ~2.7 kb size transcript was observed, which was exclusively localized to the metanephric mesenchyme. The MEST mRNA expression gradually decreased during the later stages, followed by an abrupt decrease in the newborn kidneys and subsequent postnatal life, after which a very mild expression persisted in the glomerular mesangium. The regression in the mRNA expression during embryonic renal development appears to be related to methylation of the MEST gene. Treatment of metanephroi, harvested at day-13 of gestation, with MEST-specific antisense oliogodeoxynucleotide resulted in a dose-dependent decrease in size of the explants and nephron population. This was associated with a selective decrease of MEST mRNA expression and accelerated apoptosis of the mesenchyme. These findings suggest that MEST, a gene with a putative mesenchymal-derived protein, conceivably plays a role in mammalian metanephric development.






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