ArticleEndocrinology2012
In vivo 17β-estradiol treatment contributes to podocyte actin stabilization in female db/db mice.
Article in Endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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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
10 citing papers in PubMed, 14 citations in OpenAlex.
- Catalase, a therapeutic target in the reversal of estrogen-mediated aging.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Sex Differences in Glomerular Protein Expression and Effects of Soy-Based Diet on Podocyte Signaling.Canadian journal of kidney health and disease · 2022Article
- Diabetic condition induces hypertrophy and vacuolization in glomerular parietal epithelial cells.Scientific reports · 2021Article
- Estrogen and estrogen receptors in kidney diseases.Renal failure · 2021Review
- Gender Differences in the Acute Kidney Injury to Chronic Kidney Disease Transition.Scientific reports · 2017Article
- Estrogen receptor subtype ratio change protects against podocyte damage.Current trends in endocrinology · 2017Article
- Parp1 protects against Aag-dependent alkylation-induced nephrotoxicity in a sex-dependent manner.Oncotarget · 2016Article
- A Podocyte-Based Automated Screening Assay Identifies Protective Small Molecules.Journal of the American Society of Nephrology : JASN · 2015Article
- Endogenous female sex hormones delay the development of renal dysfunction in apolipoprotein E-deficient mice.Lipids in health and disease · 2014Article
- Podocytes, signaling pathways, and vascular factors in diabetic kidney disease.Advances in chronic kidney disease · 2014Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
We recently showed that 17β-estradiol (E(2)) treatment ameliorated type 2 diabetic glomerulosclerosis in mice in part by protecting podocyte structure and function. Progressive podocyte damage is characterized by foot process effacement, vacuolization, detachment of podocytes from the glomerular basement membrane, and apoptosis. In addition, podocytes are highly dependent on the preservation of their actin cytoskeleton to ensure proper function and survival. Because E(2) administration prevented podocyte damage in our study on diabetic db/db mice and has been shown to regulate both actin cytoskeleton and apoptosis in other cell types and tissues, we investigated whether actin remodeling and apoptosis were prevented in podocytes isolated from E(2)-treated diabetic db/db mice. We performed G-actin/F-actin assays, Western analysis for Hsp25 expression, Ras-related C(3) botulinum toxin substrate 1 (Rac1) activity, and apoptosis assays on previously characterized podocytes isolated from both in vivo-treated placebo and E(2) female db/db mice. We found that in vivo E(2) protects against a phenotype change in the cultured podocytes characterized by a percent increase of F-actin vs. G-actin, suppression of Hsp25 expression and transcriptional activation, increase of Rac1 activity, and decreased apoptotic intermediates. We conclude from these studies that E(2) treatment protects against podocyte damage and may prevent/reduce diabetes-induced kidney disease.
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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.