B-cell activating factor-receptor specific activation of tumor necrosis factor receptor associated factor 6 and the phosphatidyl inositol 3-kinase pathway in lymphoma B cells

Secreto, Frank J.; Manske, Michelle K.; Price-Troska, Tammy; Ziesmer, Steven C.; Hodge, Lucy S.; Ansell, Stephen M.; Cerhan, James R.; Novak, Anne J.

doi:10.3109/10428194.2013.862619

Cited by 7 publications

(7 citation statements)

References 61 publications

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“…Upon binding to BAFF-R, BAFF activates protein kinase B (Akt) and extracellular signal-regulated kinase (Erk) in an IκB kinase (IKK)-1-dependent manner in primary B cells, thereby promoting B cell survival [ 10 ]. Notably, activation of BAFF-R recruits TNF receptor associated factor 6 (TRAF6) and induces activation of the phosphatidylinositol-3-kinases (PI3K) pathway through Akt and glycogen synthase kinase 3 beta (GSK3β) in malignant B cells [ 11 ]. Moreover, mitogen-activated protein kinase (MAPK) p38 signaling is also involved in BAFF/BAFF-R-mediated B cell chemotaxis [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

BAFF promotes proliferation of human mesangial cells through interaction with BAFF-R

Zheng

Wang

Ming³

et al. 2015

BMC Nephrol

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BackgroundB cell activating factor belonging to the TNF family (BAFF) is vital for B cell survival, proliferation and activation. Evidence indicates that BAFF is systemically or locally increased in glomerulonephritis (e.g. lupus nephritis, IgA nephropathy). However, the effect of BAFF on human mesangial cells is not known.MethodsThe impact of BAFF on the proliferation of a human mesangial cell line in vitro was investigated. The expression of BAFF receptor (BAFF-R) and downstream signal transduction were explored. The influence of BAFF on the expression of related genes was also studied.ResultsOur data indicated that BAFF had a proliferative effect on human mesangial cells, as supported by the results of cell proliferation assays and the inhibited expression of the pro-apoptotic gene Bim. BAFF-R was expressed on the cell membrane of human mesangial cells and blockade of BAFF/BAFF-R binding abrogated the proliferative effect of BAFF on human mesangial cells. BAFF stimulation led to rapid phosphorylation of NF-κBp65, Akt and MAPK p38 kinase in human mesangial cells, whereas it had no effect on the expression of NF-κB p100 and phosphorylation of Erk. The phosphorylation of Akt was very sensitive to blockade of BAFF/BAFF-R ligation, although activation of MAPK p38 and NF-κBp65 was not. BAFF treatment resulted in decreased expression of BAFF-R, which implied negative feedback regulation after its binding.ConclusionsBAFF promoted proliferation of human mesangial cells, which was mediated via BAFF-R. The BAFF/BAFF-R interaction triggered Akt, p65 and p38 activation, with Akt phosphorylation being tightly dependent on BAFF/BAFF-R interaction.

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Section: Introductionmentioning

confidence: 99%

BAFF promotes proliferation of human mesangial cells through interaction with BAFF-R

Zheng

Wang

Ming³

et al. 2015

BMC Nephrol

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“…Claudio et al ( 21 ) demonstrated that BAFF regulates B cell maturation via the NEMO-independent NF-κB2 pathway. In the present study, associated studies ( 22 – 24 ) demonstrated that the expression of BAFF-R in the B malignancy cells can be detected and BAFF can promote cell proliferation, however how Act1 affects the expression of BAFF and regulates of the growth of B-cell malignancy has not yet been reported. Therefore, three B malignancy cell lines were selected for the functional study, including Raji, Daudi (derived from Burkitt's lymphoma) and BALL-1 (derived from acute lymphoblastic leukemia), they are standard cell lines for B-cell malignancy research and have been widely used in previous studies ( 25 – 30 ).…”

Section: Discussionmentioning

confidence: 57%

Regulatory effect of Act1 on the BAFF pathway in B‑cell malignancy

Wang

et al. 2019

Oncol Lett

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The aim of the present study was to ascertain whether nuclear factor (NF)-κB Activator 1 (Act1) was involved in B cell-activating factor (BAFF) regulation in B-cell malignancy. The human B-cell malignancy cell lines Raji, Daudi and BALL-1 were cultured and the expression of BAFF receptor (BAFF-R) mRNA and protein was analyzed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting, respectively. NF-κB signaling was also assessed using western blotting. Act1 silencing was performed using Act1 small interfering RNA. BAFF-R levels were assessed using flow cytometry. It was demonstrated that BAFF-R was upregulated in all three cell lines and RT-qPCR, and western blotting confirmed these results. Act1 overexpression was demonstrated to induce BAFF-R upregulation, whereas Act1 knockdown resulted in BAFF-R downregulation. Furthermore, the NF-κB pathway was activated by Act1 overexpression and inhibited following Act1 knockdown. The results of the present study demonstrated that Act1 can regulate BAFF via targeting NF-κB signaling, which suggests that Act1 may be a promising therapeutic target for the treatment of B-cell malignancy.

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“…Pin1 reportedly affects substrate stability, and regulates TGF-β1 expression, thus enhancing TGF-β1-mediated fibrogenesis signaling (Matsuura et al 2010;Inoue et al 2019). In cells expressing BAFF-R H159Y , rBAFF stimulation increased the growth and survival of cells through the regulation of relevant genes including Pin1 (Secreto et al 2014).…”

Section: Baff-r Was Significantly Upregulated On Primarymentioning

confidence: 99%

“…Such information would not only facilitate further studies on the mechanism underlying the mesenchymal transition of RTECs, the biological function of BAFF signaling but also elucidate the progression of renal tubular atrophy and renal interstitial fibrosis in renal transplant allografts. Pin1 is one of the molecules regulated by BAFF signaling in malignant B cells (Secreto et al 2014), and it may play key role during EMT induction (Nakada et al 2019). While no direct evidence is available regarding the role of Pin1 on the characteristics of RTECs upon upregulation of BAFF signaling.…”

Section: Introductionmentioning

confidence: 99%

BAFF signaling drives interstitial transformation of mouse renal tubular epithelial cells in a Pin1-dependent manner

Song

et al. 2021

In Vitro Cell.Dev.Biol.-Animal

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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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B-cell activating factor-receptor specific activation of tumor necrosis factor receptor associated factor 6 and the phosphatidyl inositol 3-kinase pathway in lymphoma B cells

Cited by 7 publications

References 61 publications

BAFF promotes proliferation of human mesangial cells through interaction with BAFF-R

BAFF promotes proliferation of human mesangial cells through interaction with BAFF-R

Regulatory effect of Act1 on the BAFF pathway in B‑cell malignancy

BAFF signaling drives interstitial transformation of mouse renal tubular epithelial cells in a Pin1-dependent manner

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