ArticleIn vitro cellular & developmental biology. Animal2021
BAFF signaling drives interstitial transformation of mouse renal tubular epithelial cells in a Pin1-dependent manner.
Article in In vitro cellular & developmental biology. Animal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Pathogenesis of renal involvement in primary Sjögren's disease: convergence of multifactorial mechanisms on immune dysregulation.Frontiers in immunology · 2026Review
- Exploration of effective biomarkers and infiltrating immune cells in metastatic colorectal cancer based on bioinformatics analysis.Scientific reports · 2025Article
- Blocking BAFF Alleviates Hepatic Fibrosis inPathogens (Basel, Switzerland) · 2023Article
- Associations of serum keratin 1 with thyroid function and immunity in Graves' disease.PloS one · 2023Article
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4 authors at 1 institution in 1 country.
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Abstract
Aberrant expression of B cell-activating factor belonging to TNF superfamily (BAFF) and its receptors results in abnormal biological activities in hematopoietic and non-hematopoietic cells and is closely associated with the occurrence and development of various diseases. However, the biological significance and potential mechanisms underlying BAFF signaling in renal tubular epithelial cells (RTECs) remain unknown. This study aimed to investigate the biological role of BAFF signaling in RTECs. Mice primary RTECs were applied. The proliferation status and apoptotic rates were examined by MTS assay and flow cytometry, respectively. The expression of BAFF and its receptors was analyzed via flow cytometry and sodium ion transport function, and cytokeratin-18 expression was detected through immunofluorescence staining. In addition, Pin1 was knocked down via siRNA and its expression was assessed through reverse transcription PCR. Lastly, western blotting was performed to analyze E-cadherin, ɑ-SMA, and Pin1 expression. Results suggested that BAFF-R was significantly upregulated upon IFN-γ stimulation, and enhancement of BAFF signaling promoted cell survival and reduced their apoptotic rate, while simultaneously reducing the epithelial phenotype and promoting the interstitial transformation of cells. Furthermore, Pin1 was significantly increased, along with the upregulation of BAFF signaling in the RTECs, and participated in interstitial transformation induced by BAFF signaling. Collectively, the present results elucidate the potential mechanism of loss of normal function of RTECs under long-term high dose of BAFF stimulation provides a potential therapeutic target for renal interstitial fibrosis, and underlining mechanisms of shortening of long-term outcomes of kidney allografts via augmenting of BAFF signaling.
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