ArticleAmerican journal of physiology. Renal physiology2012
BIM deficiency differentially impacts the function of kidney endothelial and epithelial cells through modulation of their local microenvironment.
Article in American journal of physiology. Renal physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Identification of genes involved in energy metabolism in preeclampsia and discovery of early biomarkers.Frontiers in immunology · 2025Article
- Bim Expression Influences Choroidal Endothelial Cell Characteristics and Their Response to Therapeutic Intervention.International journal of molecular sciences · 2024Article
- Bim Expression Modulates Branching Morphogenesis of the Epithelium and Endothelium.Biomolecules · 2022Article
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- Endothelial cell apoptosis in angiogenesis and vessel regression.Cellular and molecular life sciences : CMLS · 2017Review
- The contribution of the programmed cell death machinery in innate immune cells to lupus nephritis.Clinical immunology (Orlando, Fla.) · 2017Review
- Pro-apoptotic BIM is an essential initiator of physiological endothelial cell death independent of regulation by FOXO3.Cell death and differentiation · 2014Article
- Cyp1b1 mediates periostin regulation of trabecular meshwork development by suppression of oxidative stress.Molecular and cellular biology · 2013Article
- Over-production of nitric oxide by oxidative stress-induced activation of the TGF-β1/PI3K/Akt pathway in mesangial cells cultured in high glucose.Acta pharmacologica Sinica · 2013Article
- Aberrant production of extracellular matrix proteins and dysfunction in kidney endothelial cells with a short duration of diabetes.American journal of physiology. Renal physiology · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The extracellular matrix (ECM) acts as a scaffold for kidney cellular organization. Local secretion of the ECM allows kidney cells to readily adapt to changes occurring within the kidney. In addition to providing structural support for cells, the ECM also modulates cell survival, migration, proliferation, and differentiation. Although aberrant regulation of ECM proteins can play a causative role in many diseases, it is not known whether ECM production, cell adhesion, and migration are regulated in a similar manner in kidney epithelial and endothelial cells. Here, we demonstrate that lack of BIM expression differentially impacts kidney endothelial and epithelial cell ECM production, migration, and adhesion, further emphasizing the specialized role of these cell types in kidney function. Bim -/- kidney epithelial cells demonstrated decreased migration, increased adhesion, and sustained expression of osteopontin and thrombospondin-1 (TSP1). In contrast, bim -/- kidney endothelial cells demonstrated increased cell migration, and decreased expression of osteopontin and TSP1. We also observed a fivefold increase in VEGF expression in bim -/- kidney endothelial cells consistent with their increased migration and capillary morphogenesis. These cells also had decreased endothelial nitric oxide synthase activity and nitric oxide bioavailability. Thus kidney endothelial and epithelial cells make unique contributions to the regulation of their ECM composition, with specific impact on adhesive and migratory properties that are essential for their proper function.
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