ArticleThe American journal of pathology1996
Apoptosis during an early stage of nephrogenesis induces renal hypoplasia in bcl-2-deficient mice.
Article in The American journal of pathology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
12 citing papers in PubMed, 54 citations in OpenAlex.
- Increase in podocyte number induced by SV40T antigen during the fetal stage does not expand glomerular size in mice.Physiological reports · 2026Article
- The regulation of apoptosis in kidney development: implications for nephron number and pattern?Frontiers in pediatrics · 2014Review
- Article
- Kidney and urinary tract development: an apoptotic balancing act.Pediatric nephrology (Berlin, Germany) · 2011Review
- Role of mitotic, pro-apoptotic and anti-apoptotic factors in human kidney development.Pediatric nephrology (Berlin, Germany) · 2006Article
- The reaper-binding protein scythe modulates apoptosis and proliferation during mammalian development.Molecular and cellular biology · 2005Article
- A familial case of multicystic dysplastic kidney.Pediatric nephrology (Berlin, Germany) · 2005Article
- Bim regulation of lumen formation in cultured mammary epithelial acini is targeted by oncogenes.Molecular and cellular biology · 2005Article
- Proapoptotic BH3-only Bcl-2 family member Bik/Blk/Nbk is expressed in hemopoietic and endothelial cells but is redundant for their programmed death.Molecular and cellular biology · 2004Article
- Cell cycle regulation and differentiation in the human podocyte lineage.The American journal of pathology · 1998Article
- The development of the kidney.Current topics in developmental biology · 1998Review
- D-glucose-induced dysmorphogenesis of embryonic kidney.The Journal of clinical investigation · 1996Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal development in bcl-2-deficient mice was monitored to examine the temporal and spatial function of this gene during nephrogenesis in vivo. Extensive apoptosis occurred during abnormal nephrogenesis in bcl-2-deficient mice. In embryos and newborn mice, the sequence of morphological events was monitored by morphology in conjunction with morphometry, and bcl-2 -/-, bcl-2 +/-, and bcl-2 +/+ mice were compared. In bcl-2 -/- mice, initial induction of nephrons was detected by embryonic day 13 (E-13) as normal. Then, apoptotic cells became five times more frequent at E-13 to E-16 with a significant reduction (1/5) in nephron number at E-17 to E-19 in bcl-2 -/- mice compared with bcl-2 +/+ mice. No morphological difference was evident between bcl-2 +/- mice and bcl-2 +/+ mice by morphometry. Apoptotic cells were found mainly among the mesenchyme and less frequently in tubuli. Little apoptosis among ureteric buds was noted. In bcl-2 -/- mice at E-17 to E-19, inactive branching and insufficient convolution of ureteric buds were accompanied by fulminant apoptosis in the mesenchyme. Neonatal bcl-2 -/- mice lacked the nephrogenic zone, exhibiting renal hypoplasia. Thus, bcl-2 seems to inhibit apoptosis in renal stem cells during the induction of nephrons in vivo.
Indexed as
Identifiers
8623928PMC1861554W1766380940What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.